Laboratory and instrumental research methods. Glomerulonephritis Is it possible to cure chronic glomerulonephritis forever

82 Acute glomerulonephritis: symptomatology, examination data, laboratory data.

Symptomatology: 1. edema, 2. arterial hypertension, 3. urine changes. In addition, the patient may complain of: weakness, headache, visual disturbances, urination (oliguria, polyuria, urine the color of meat slops), decreased performance, severe suffocation, shortness of breath.

Inspection: edematous, puffy face, limbs, pale skin, due to shortness of breath, patients are in a semi-sitting or sitting position

Palpation helps to determine the severity, localization of edema, displacement of the kidneys, their increase, the pulse is tense, often slow.

Percussion allows you to identify free fluid in the cavities (pleural)

Auscultation auscultated wheezing in the pleural cavity, possibly hard or unchanged breathing, auscultation of the heart - bradycardia, I tone is weakened, a gallop rhythm is possible, blowing systolic murmur.

Laboratory data: proteinuria, cylindruria, hematuria, tests for the purification of insulin and PAH give data on a decrease in the function of the glomerular apparatus of the kidney.

Burnok the beginning of the disease, weakness, pastosity of the eyelids and face

Anamnesis: suffered streptococcus inf.

syndromes: nephrotic, hypertensive

LII: hematuria, cylinruria, leukocyturia, leukocytosis, accelerated ESR, anemia

inflamed pr-ki-C-reactive protein +, increase alpha12 globulin protein fractions

bioh blood test: hypoproteinemia, hypoalbuminemia, hypercholesterolemia, hyperlipidemia,

visual impairment

immune pr-ki: lower complement level, lower T-lymphocyte level

kidney biopsy-diff glomeral nephritis

TRIAD OF SYMPTOMS: NEPHROTIC, HYPERTENSION, URINARY

clinical manifestations: acute cyclic, nephrotic, latent

by severity: mild, moderate, severe,

83Chronic glomerulonephritis: symptomatology, examination data, laboratory data.

Symptoms appear 3-7 days after exposure to a provoking factor (latent period), they can also be detected by chance during a medical examination. Recurrent episodes of hematuria. Edema, urinary syndrome, arterial hypertension in various forms - nephrotic or acute nephritic syndrome (nephrotic form, mixed form - up to 10%, hypertonic form - 20-30%). A combination of manifestations of acute nephritic and nephrotic syndromes is possible. Complaints of headache, darkening of urine, edema and decreased diuresis. Objectively - pastosity or edema, increased blood pressure, expansion of the borders of the heart to the left. Body temperature is normal or subfebrile.

Clinical manifestations in various clinical forms

Latent CGN(50-60%) . Edema and arterial hypertension are absent. In the urine, proteinuria is not more than 1-3 g / day, microhematuria, leukocyturia, casts (hyaline and erythrocyte) ”Can be transformed into nephrotic or hypertonic forms. The development of CRF occurs within 10-20 years. Hypertensive CGN. Clinical manifestations of the syndrome of arterial hypertension. In the urine there is a slight proteinuria, sometimes microhematuria, cylindruria. CRF is formed within 15-25 years. Hematuric CGN. In the urine - recurrent or persistent hematuria and minimal proteinuria (less than 1 g / day). There are no extrarenal symptoms. CRF develops in 20-40% within 5-25 years. Nephrotic form- Clinical and laboratory manifestations of nephrotic syndrome. mixed form. The combination of nephrotic syndrome, arterial hypertension and / or hematuria. Usually it is noted in secondary CGN, systemic diseases (SLE, systemic vasculitis), CRF is formed within 2-3 years.

Clinical picture depending on the morphological form

Mesangioproliferative CGN. Isolated urinary syndrome. Acute nephritic or nephrotic syndrome. Macro or microhematuria - Berger's disease. CKD develops slowly. Membranous CGN manifested by nephrotic syndrome (80%). Membranoproliferative CGN Begins with acute nephritic syndrome, 50% of patients have nephrotic syndrome. Isolated urinary syndrome with hematuria. Arterial hypertension, hypocomplementemia, anemia, cryoglobulinemia are characteristic. The course is progressive, sometimes rapidly progressive. Glomerulonephritis with minimal changes. Nephrotic syndrome, in 20-30% of cases with microhematuria. Arterial hypertension and renal failure are rare. Focal segmental glomerulosclerosis. nephrotic syndrome. In the urine, erythrocyturia, leukocyturia. Arterial hypertension. The development of chronic renal failure is natural. Fibroplastic glomerulonephritis. Nephrotic syndrome (up to 50%). HPN. Arterial hypertension.

Laboratory data In blood- moderate increase in ESR(with secondary CGN, a significant increase may be detected, which depends on the primary disease), an increase in the level of the CEC, antistreptolysin O, a decrease in the complement content in the blood (immunocomplex CGN), with Berger's disease, an increase in the content of IgA is detected. Reduced concentrations of total protein and albumin(significantly - with nephrotic syndrome), increased concentrations of a7 and B globulins, hypogammaglobulinemia with nephrotic syndrome. In secondary CGN caused by systemic diseases of the connective tissue (lupus nephritis), uglobulins can be increased. Hyper and dyslipidemia (nephrotic form). Decreased GFR, increased urea and creatinine levels, anemia, metabolic acidosis, hyperphosphatemia, etc. (ARF against the background of chronic renal failure or chronic renal failure). In the urine, erythrocyturia, proteinuria(massive with nephrotic syndrome), leukocyturia, cylinders - granular, waxy (with nephrotic syndrome).

instrumental data With ultrasound or survey urography, the size of the kidneys is normal or reduced (in chronic renal failure), the contours are smooth, echogenicity is diffusely increased. X-ray of the chest organs - expansion of the borders of the heart to the left (with arterial hypertension). ECG - signs of left ventricular hypertrophy. Kidney biopsy (light, electronic microscopy, immunofluorescence study) allows to clarify the morphological form, activity of CGN, to exclude kidney diseases with similar symptoms.

Diagnostics With a decrease in diuresis, the appearance of dark urine, edema or pasty ™ face, an increase in blood pressure (may be normal), a set of studies is carried out: measurement of blood pressure, total OAK, OAM, determination of daily proteinuria, total protein concentration and evaluate the proteinogram, blood lipids. An in-depth physical and clinical laboratory examination is aimed at identifying a possible cause of CGN - a general or systemic disease. Ultrasound (radiography) of the kidneys allows you to clarify the size and density of the kidneys. Assessment of kidney function - Reberg-Tareev test, determination of the concentration of urea and / or creatinine in the blood. The diagnosis is confirmed by kidney biopsy.

Differential Diagnosis with chronic pyelonephritis, acute glomerulonephritis, nephropathy of pregnancy, chronic tubulointerstitial nephritis, alcoholic kidney damage, amyloidosis and diabetic nephropathy, as well as kidney damage in diffuse connective tissue diseases (primarily SLE) and systemic vasculitis.

84 Nephrotic syndrome: symptomatology, laboratory data. Proteinuria, types of proteinuria, diagnostic value of isolation of proteinuria. nephrotic syndrome- this is a clinical and laboratory symptom complex, which is characterized by edema (often massive), severe proteinuria exceeding 3.5 g per day, hypoalbuminemia, hyperlipidemia, lipiduria (fatty cylinders, oval fat bodies in the urinary sediment), increased blood clotting. appears in the same way regardless of the reason that caused it. It is characterized by massive proteinuria, hypo- and dysproteinemia, hyperlipidemia (in particular, hypercholesterolemia) and edema.

-proteinuria, exceeding 3.0-3.5 g per day and reaching 5.0-10.0-15.0 g. Up to 80-90% of the protein excreted in the urine consists of albumins. It is one of the main pathogenetic factors of hypo- and dysproteinemia. Hypoproteinemia - the level of total protein in the blood serum decreases to 60 g / l, and in severe cases - up to 50-40 and even 30-25 g / l. - edema. with nephrotic syndrome in patients with chronic glomerulonephritis. The most frequent complaints patients for general weakness, loss of appetite, thirst, dry mouth, decreased amount of urine, headache, discomfort or heaviness in the lumbar region, less often for nausea, vomiting, bloating and loose stools. Patients are inactive, sometimes adynamic, pale. The body temperature is normal or decreased, the skin is cold and dry to the touch. Peeling of the skin, brittle nails and hair are often noted. The boundaries of the heart are within the normal range, however, in the presence of transudate (fluid) in the pericardial cavity, they shift in all directions. The number of heart contractions and pulse are slowed down, and only with heart failure and anemia does tachycardia develop. Heart sounds are muffled, and with hydropericardium they are deaf. Blood pressure is often normal, but may be low. The ECG shows signs of myocardial dystrophy, low voltage of all teeth. In the lungs with large edema, a shortening of the percussion sound, weakening of breathing, and often moist fine bubbling rales over the lower sections are determined, which should be regarded as congestive. The tongue is often coated, the abdomen is enlarged, sometimes there is an increase in the size of the liver (for example, with amyloidosis or circulatory failure). In some patients, nephrotic syndrome may be accompanied by what is known as nephrotic diarrhea with loss through the gastrointestinal tract. a large number protein (protein diarrhea), which is believed to be due to an increase in the permeability of the intestinal mucosa. In patients with nephrotic syndrome, there is a decrease in basal metabolism, which is associated with a decrease in thyroid function. It is believed that the reduced function of the thyroid gland causes, to a certain extent, a violation of protein and fat metabolism and contributes to a decrease in urination (oliguria). Oliguria is one of the characteristic and permanent signs of nephrotic syndrome. Daily diuresis usually does not exceed 1000 ml, often amounting to no more than 400-600 ml. At the same time, in patients with preserved kidney function, the relative density of urine is normal or increased (up to 1030-1040) due to the high concentration of protein and other osmotically active substances in it. Hematuria (blood in the urine) is not typical for nephrotic syndrome, but it is possible, more often in the form of microhematuria, less often it can be moderate and even less often severe. The sediment also contains fat-transformed epithelium, cholesterol crystals, and sometimes drops of neutral fat. In some cases, there may be a small and unstable leukocyturia. On the part of the peripheral blood, the most constant sign of nephrotic syndrome is an increase in ESR, which can reach 60-85 mm / h. The number of leukocytes and the composition of the leukocyte formula usually does not undergo notable changes. . Sometimes there is a transient eosinophilia associated, apparently, with the intake of certain drugs and increased sensitivity of the body to them. It is possible to increase the number of platelets (up to 500-600 thousand) and a slight decrease in the level of red blood cells and hemoglobin. increased blood clotting, which can vary from a slight increase to the development of disseminated intravascular coagulation. This leads to disruption of microcirculation in the glomerular capillaries and contributes to the more rapid development of hyalinosis and sclerosis of the glomeruli with impaired renal function. Clinically, two forms of nephrotic syndrome are distinguished - pure and mixed. Pure nephrotic syndrome is said to occur when it occurs without hypertension and hematuria. The mixed form includes those cases of the disease when the signs characteristic of the nephrotic syndrome are combined with hypertension or hematuria. Some authors refer to such variants of nephrotic syndrome as nephrotic-hypertonic and nephrotic-hematuric forms, respectively.

Types of proteinuria. By the amount of protein in the urine and the types of protein structures: 1. Tamm-Khrsval protein 2. selective (toko albumins). 3. non-selective (albumins, globulins), 4. Massive (more than 3g per liter of urine). For reasons: tubular, overflow proteinuria, functional, orthostatic, febrile, extrarenal, proteinuria in obesity.

The diagnostic value of proteinuria lies in the fact that it can determine the type of renal and other pathologies, the degree of their development, the nature of the necessary treatment.

21. Topic of the lesson: Acute and chronic glomerulonephritis

21. Topic of the lesson: Acute and chronic glomerulonephritis

1. RELEVANCE OF THE THEME

Knowledge of the topic is necessary for solving professional problems in the diagnosis and treatment of patients with acute and chronic glomerulonephritis. The study of the topic is based on the knowledge of the course of normal anatomy and physiology of the kidneys, pathology of the urinary system, clinical radiology, propaedeutics of internal diseases, clinical pharmacology.

2. PURPOSE OF THE LESSON

Know the etiology, pathogenesis, clinical picture, complications and treatment of acute and chronic glomerulonephritis; be able to collect complaints and anamnesis, conduct a physical and laboratory-instrumental examination of a patient with acute and chronic glomerulonephritis, prescribe therapy.

3. QUESTIONS TO PREPARE FOR THE LESSON

1. Etiology and pathogenesis of acute and chronic glomerulonephritis

that.

2. Clinical manifestations and pathogenesis of the main symptoms of acute and chronic glomerulonephritis.

3. Variants of the course, criteria for the chronicization of acute glomerulonephritis, clinical and morphogenetic classification of chronic glomerulonephritis.

4. Treatment of acute and chronic glomerulonephritis.

5. Primary and secondary prevention of acute glomerulone-frit.

4. EQUIPMENT OF THE LESSON

1. Patients with a clinical picture of acute glomerulonephritis and chronic glomerulonephritis: collection of complaints, anamnesis, physical examination, including the use of palpation, percussion and auscultation.

2.Study of the results of laboratory and instrumental examination of a patient with acute and chronic glomerulonephritis: clinical analysis of blood, urine, biochemical and serological blood tests, Reberg's test, urine tests according to Nechiporenko, Zimnitsky, daily proteinuria, ultrasound, dynamic scintigraphy, kidney biopsy.

5. BASELINE TESTS

Choose one correct answer.

1. Glomerulonephritis is an immunoinflammatory disease with the primary involvement of:

A. Klubochkov. B. Kanaltsev.

B.Calyxes.

G. Vas affect. D. Vas effect.

2. The etiological factor of glomerulonephritis can be:

A. Hard physical labor.

B. Strong emotional stress.

B.AG.

D. Stenosis of the renal artery. D. Infection.

3. Nephrotic syndrome is characterized by:

A. Hyperproteinemia. B. Macrohematuria.

B. Arterial hypertension. G. Proteinuria up to 3 g/day.

D. Hyperlipidemia.

4. Acute nephritic syndrome is characterized by:

A. Proteinuria up to 3 g/day.

B. Proteinuria more than 3.5 g/day.

B. Hyperlipidemia.

G. Hypoproteinemia. D. Hyperproteinemia.

5. With glomerulonephritis, edema is characteristic:

A. Calves and feet. B. Loins.

B. Anterior abdominal wall. G. Faces.

D. Shoulder girdle.

6. Select the clinical variant of chronic glomerulonephritis:

A.Latent. B. Fibrous.

B. Capillary.

G. Rapidly progressive. D. Recurrent.

7. The most common etiological cause of acute glomerulonephritis:

A. Hepatitis C virus. B. Hepatitis B virus.

B. Escherichia coli. G. Streptococcus.

D. Staphylococcus.

8. For acute glomerulonephritis the most typical:

A. Nephrotic syndrome. B. Nephritic syndrome.

B. Isolated urinary syndrome. G. HPN.

D. Dyspeptic syndrome.

9. In the analysis of urine in acute glomerulonephritis, the following are found:

A. Glucosuria. B. Oxalates.

B. Urates.

D. Erythrocytes and their casts. D. Leukocytes and their casts.

10.Choose the clinical variant of chronic glomerulonephritis:

A. Stenosing. B. Hematuric.

B. Nephritic. G. Sclerotic. D. Purulent.

11. Specify the glomerular filtration rate at which CRF develops:

A.More than 120ml/min. B. 100-120 ml/min.

B.80-100 ml/min.

D. 60-80 ml/min. D. Less than 60 ml/min.

12. Causes of anemia in chronic azotemia:

A. Vitamin D synthesis is reduced.

B. The synthesis of erythropoietin is reduced.

B. Decreased excretion of electrolytes and water. D. There is platelet dysfunction.

13. Diuretic, which can be taken with glomerulonephritis:

A. Spironolactone. B. Mannitol.

B. Furosemide.

D. Hydrochlorothiazide.

D. Acetazolamide (diacarb*).

14. Target blood pressure in glomerulonephritis:

A. Less than 100/60 mmHg B. Less than 120/70 mm Hg.

B. Less than 125/75 mmHg D. Less than 130/80 mmHg. D. Less than 140/90 mmHg.

15. The means of choice for the treatment of hypertension in chronic glomerulonephritis are:

A. R - Adrenoblockers. B. a - Adrenoblockers.

B. ACE inhibitors. G. Statins.

D. Blockers of slow calcium channels.

16. Select an indicator indicating the activity of jade:

A. Nephrotic syndrome. B. Hyperproteinemia.

B. Proteinuria up to 1 g/day. G. Increase in glucosuria. D. A sharp decrease in blood pressure.

17. Indications for immunosuppressive therapy are as follows:

A. Low level creatinine at admission. B. Stenosis of the renal artery.

B.AG.

G. Persistent nephrotic syndrome. D. Macrohematuria.

18. The following are used as immunosuppressive therapy for glomerulonephritis:

A. Antibiotics.

B. Glucocorticoids.

B. Immunomodulators. G. Diuretics.

D. ACE inhibitors.

19. On the 15th day after the onset of streptococcal infection, a patient developed gross hematuria and paraorbital edema. This episode can be seen as:

D. Urinary syndrome.

20. On the 5th day after the onset of streptococcal infection, a patient developed gross hematuria and paraorbital edema. This episode can be seen as:

A. Acute poststreptococcal glomerulonephritis. B. Exacerbation of chronic glomerulonephritis.

B. Rapidly progressive glomerulonephritis. G. Nephrotic syndrome.

D. Urinary syndrome.

6. MAIN QUESTIONS OF THE THEME

6.1. Definition

The term "nephritis" is currently fully consistent with the term "glomerulonephritis" and includes a group of morphologically heterogeneous immunoinflammatory diseases of the kidneys with a primary lesion of the glomeruli, as well as involving the tubules and interstitial (interstitial) tissue.

Glomerulonephritis is considered an independent nosological entity, but can also occur in many systemic diseases, such as systemic lupus erythematosus, hemorrhagic vasculitis, IE, etc.

6.2. Etiology

.Infections: bacterial (streptococcus, staphylococcus, etc.);

lead, mercury, drugs, etc.).

. Exogenous non-infectious antigens, acting with the involvement of immune mechanisms, including the type of atopy.

. endogenous antigens(rare): DNA, neoplastic, uric acid.

6.3 Pathogenesis

The progression of glomerulonephritis after exposure to various triggering factors is determined by fairly stereotypical processes that gradually lead to sclerosis. These include mesangial cell proliferation and mesangial matrix accumulation, as well as damage to the glomerular capillary wall. In the induction of glomerulonephritis, the leading place is given to immune damage factors, humoral and / or cellular immunity; in the future, mediators of inflammation and non-immune mechanisms - hemodynamic and metabolic - acquire an important role in the progression of the process. At all stages of development, the persistence of the etiological factor plays a leading role, which, unfortunately, is known only in 10% of patients.

Immune damage is seen in most glomerular kidney diseases. There are two mechanisms of such damage: the action of nephrotoxic antibodies and the deposition of immune complexes.

Two types of nephrotoxic antibodies are involved in the reaction of antibodies against antigens on the glomerular filtration membrane:

Anti-glomerular basement membrane antibodies;

Antibodies against antigens that do not belong to the glomerular basement membrane.

In cases where the body begins to produce IgG against antigenic glycoproteins of the glomerular basement membrane,

refers to "anti-membrane disease". These changes lead to the development of pronounced proliferative glomerulonephritis with hemorrhages and rapidly increasing renal failure.

There are two types of antigens that do not belong to the glomerular basement membrane:

1) internal (own) antigens;

2) external antigens (formed from drugs, plant lectins, aggregated proteins and infectious agents).

The kidneys are one of the pathways through which immune complexes are normally excreted from the body. The glomeruli are subject to the accumulation of immune complexes, as a large amount of blood is filtered through them. Large immune complexes, which are formed in the presence of antibodies with high affinity for the antigen, settle mainly in the mesangium. After the deposition of pathological immune complexes in the basement membrane, the complement system is activated and vasoactive substances are released. These substances are mediators acute inflammation-responsible for damage to the basement membrane.

6.4. Classification of glomerulonephritis

There are three parallel and complementary classifications: etiological, immunological and morphological.

Below is a comprehensive classification of glomerulonephritis based on clinical, morphological and immunological characteristics.

Classification of glomerulopathies.

1. Congenital and acquired glomerulopathies.

2. Clinical types of glomerulonephritis:

Spicy;

Chronic (according to Tareev, 1972): latent, hematuric, nephrotic, hypertonic, mixed, CRF;

Rapidly progressive.

3. Primary kidney diseases (histopathological classification according to Serov).

Diffuse proliferative (acute) glomerulonephritis:

Minimal change disease;

Focal segmental glomerulosclerosis;

Membranous glomerulonephritis (nephropathy);

Mesangioproliferative glomerulonephritis: IgA nephropathy;

Membranoproliferative glomerulonephritis;

Semilunar glomerulonephritis;

Fibroplastic glomerulonephritis (diffuse sclerosis).

4. Glomerulonephritis in systemic diseases:

Lupus jade;

IgA nephropathy, Shenlein-Genoch purpura;

Glomerular lesions in systemic infections: post-streptococcal glomerulonephritis, nephropathy in AIDS, nephropathy in hepatitis B and C.

5. Glomerular lesions in vascular diseases:

Nephrosclerosis benign and malignant;

Anti-neutrophil cytoplasmic antibody-associated nephritis (ANCA);

Thrombotic microangiopathy (hemolytic-uremic syndrome).

6. Hereditary nephropathies:

diabetic nephropathy;

Amyloidosis;

The disease of deferred deposits;

Delayed immunoglobulin disease.

7. Other kidney diseases.

6.5 Clinical syndromes

1.Nephritic Syndrome: recurrent painless hematuria, which can vary from gross hematuria to microhematuria, determined only by special studies; oliguria; proteinuria; cylindruria; AG.

2.Nephrotic Syndrome: swelling; proteinuria above 3.5 g/day; hypoalbuminemia; hyperlipidemia.

3.Asymptomatic kidney disease: proteinuria, hematuria.

4.HPN.

The correlation between the histological variants of glomerulonephritis and the clinical picture of the disease is presented in Table. 48.

6.6 Clinical types of glomerulonephritis

Main clinical types glomerulonephritis - acute, chronic and rapidly progressive.

6.6.1. Acute glomerulonephritis

6.6.1.1. Definition

Acute glomerulonephritis is an acute diffuse immune-mediated inflammation that develops after sensitization by an antigen (usually bacterial or viral) and is manifested by acute nephritic syndrome.

The ratio of men and women is 2/1. Children 5-15 years old are more often ill. In 10% of cases, adults older than 40 years are affected.

6.6.1.2. Etiology

The most common post-streptococcal glomerulonephritis, Bright's disease. Group A p-hemolytic streptococcus is the most nephritogenic, especially strains 12 and 49.

Other bacterial causes of acute post-infectious glomerulonephritis can be diplococci, streptococci, staphylococci, mycobacteria, Salmonella typhosa, Brucella suis, Treponema pallidum, Corynebacterium bovis, Actinobacilli, Rickettsia rickettsiae, Mycoplasma species, Meningococcus species, Leptospira species.

Among the viruses that can cause acute glomerulonephritis, marked (with exclusion of streptococcal etiology) cytomegalovirus,

viruses Coxsackie, Epstein-Barr, hepatitis B and C, HIV, Rubella mumps virus.

Systemic diseases accompanied by the development of acute glomerulonephritis include Wegener's granulomatosis, cryoglobulinemia, systemic lupus erythematosus, polyarteritis nodosa, Henoch-Schonlein purpura, Goodpasture's syndrome.

In addition, abscesses can lead to the development of glomerulonephritis. internal organs, endocarditis, infected shunts, pneumonia, and medications such as sulfonamides, penicillin.

6.6.1.3. Pathophysiology

Glomerular damage results from the deposition or formation of immune complexes, complement activation, and inflammatory mediators. Macroscopically, the kidneys can be enlarged by 50%. Under a light microscope, changes in the glomeruli are diffuse generalized, with proliferation of mesangial and epithelial cells. Most often, streptococcus acts as a trigger for the formation of immune complexes. An increase in antibody titers against antistreptolysin-O, antihyaluronidase, and streptokinase also indicates a recent streptococcal infection. Morphological examination most often reveals IgA nephropathy.

6.6.1.4. Clinical picture

The latent period can last up to 3 weeks. If a disease occurs after pharyngitis, the latent period can last up to 2 weeks, after pyoderma - up to 2-4 weeks. The onset of symptoms within the first 4 days of a streptococcal infection is indicative of pre-existing kidney disease.

Acute glomerulonephritis is characterized by acute nephritic syndrome, which includes three main clinical symptoms:

swelling;

macrohematuria; .AG.

Approximately 95% of patients have at least two of the three symptoms.

Edema is observed in 80-90% of patients. Facial edema usually develops, especially periorbital, but may be systemic, accompanied by a decrease in the amount of dark, tea-colored or rusty urine. Severe oliguria indicates the development of rapidly progressive glomerulonephritis.

AH also occurs in 80% of patients.

Nonspecific symptoms are weakness, malaise, lethargy, fever, abdominal pain. Other symptoms may include pharyngitis, respiratory infection, scarlet fever, weight gain, back pain, anorexia, pallor, impetigo. If acute glomerulonephritis develops as part of a systemic disease, then the symptoms of this disease are revealed: for example, rash, arthritis, arthralgia, etc.

With poststreptococcal glomerulonephritis, the oligoanuric phase lasts 3-5 days, after which diuresis increases, and the relative density of urine falls. Urine takes on the color of meat slops. In cases of microhematuria, the color of the urine may not change.

6.6.1.5. Laboratory methods of examination

AT general analysis blood, normochromic normocytic anemia is noted due to an increase in circulating blood volume. Creatinine and urea reflect the degree of damage to kidney tissue. In 5% of patients, nephrotic syndrome develops, accompanied by hypoproteinemia and hyperlipidemia. The concentration of the third complement fraction increases. With streptococcal etiology of glomerulonephritis, the titer of antistrepto-lysin-O increases in the first 3 weeks, reaching a maximum after 3-5 weeks and returning to normal after six months. In addition, it is necessary to examine the patient's blood for antibodies to DNA, cryoglobulins, hepatitis B and C viruses, HIV, anti-neutrophil cytoplasmic antibodies (ANCA), antibodies to the basement membrane of the renal glomeruli. If infective endocarditis is suspected, blood cultures and echocardiography are required.

Analysis of urine. Dark urine due to erythrocyte hemolysis, specific gravity over 1020, proteinuria, acidosis. At the microscopy of the sediment at the beginning of the disease, fresh erythrocytes predominate, in the future, mainly leached ones are isolated. Hyaline and cellular casts are almost always found. Proteinuria (albuminuria) is usually moderate (up to 3-6 g / l), may disappear in the first

2-3 months, or slowly decline over 6 months. In some patients, proteinuria may recur intermittently for another 1-2 years. Microhematuria disappears after six months. Very rarely, it can persist for 1-3 years. You can think about the transition to a chronic form if proteinuria and hematuria together persist for more than 12 months.

On ultrasound, the kidneys are of normal size or slightly enlarged with increased echogenicity.

When radiography chest pulmonary venous congestion is usually noted, occasionally - an increase in the shadow of the heart.

Renal biopsy is indicated to clarify the diagnosis, especially in primary kidney disease. Patients with a history of kidney disease, including those of relatives, and in the case of atypical clinical and laboratory findings, including massive proteinuria, nephrotic syndrome, and a rapid increase in creatinine, are considered candidates for biopsy.

After 2-3 weeks, edema disappears, blood pressure returns to normal, and a polyuric crisis occurs. Usually recovery occurs in 2-2.5 months.

6.6.1.5. Treatment

By the time a patient with acute glomerulonephritis develops symptoms, the damage to the glomeruli has already taken place and the healing process has already begun. Therefore, it is too late to act on the cause of the disease. Symptomatic therapy is carried out, aimed at preventing possible complications.

Hospitalization is indicated if there is significant hypertension, massive proteinuria, or a combination of oliguria, generalized pulmonary edema, and elevated serum creatinine or potassium.

In the acute phase, when edema and hypertension are observed, a diet is indicated with salt restriction to 2 g per day and liquid to 1 liter per day (diuresis volume - 400 ml). Longer restrictions are not required.

Limitation of physical activity is indicated in the acute period of the disease, especially in the presence of hypertension. Bed rest can reduce the degree and duration of gross hematuria. Longer bed rest does not affect the course and prognosis of the disease.

With significant edema and / or severe hypertension, loop diuretics are indicated. If hypertension cannot be controlled, then

calcium channel blockers or ACE inhibitors. For mild or moderate hypertension, bed rest and fluid restriction are most effective.

The swelling is usually minor and causes little discomfort. It is enough to limit fluid intake. With significant edema, furosemide is indicated. Osmotic diuretics are contraindicated as they may increase blood volume. Potassium-sparing diuretics are contraindicated due to the risk of hyperkalemia.

If a connection with streptococcal infection is proven, titers of antistreptococcal antibodies are elevated and sowing from the pharynx is positive, antibiotic treatment is indicated for 8-12 days. It is necessary to examine family members and the immediate environment of the patient for infection with nephritogenic streptococcus and treat those infected. This event will prevent the spread of nephritogenic strains.

For other infections, appropriate therapy is indicated.

Glucocorticoids and immunosuppressants are indicated for severe proteinuria and a rapid decrease in glomerular filtration rate, which occurs with a non-infectious nature of the disease, in particular, with diffuse diseases connective tissue (systemic lupus erythematosus, vasculitis).

In patients with low physical activity, with prolonged bed rest, heparin and antiaggregants are indicated to prevent venous thrombosis.

Forecast depends on histological examination. An excellent prognosis is in minimal change disease and focal segmental glomerulosclerosis. With mesangial and membranous variants of glomerulonephritis, 25% of patients develop chronic renal failure, with mesangiocapillary - in 70%.

Medical examination. Treatment and observation by a nephrologist. Control of blood pressure, urinalysis and blood creatinine.

Prevention. Streptococcal infection should be aggressively treated.

In most epidemic cases, there is a complete recovery (100%). Sporadic cases in adults in 30% progress to chronic glomerulonephritis.

With non-streptococcal etiology of the disease, the outcome depends on the etiology of glomerulonephritis and may be different. When bacterial

In endocarditis, kidney function returns after successful antibiotic treatment. With AIDS, the process leads to the development of CRF.

6.6.2. Chronic glomerulonephritis

6.6.2.1. Definition

Chronic glomerulonephritis is a chronic immune-mediated inflammation of the glomeruli of the kidneys with persistent changes in urine tests (proteinuria and/or hematuria). It is characterized by irreversible and progressive hyalinization of the glomeruli, fibrosis of the tubulointerstitial apparatus, interstitial fibrosis, leads to a decrease in the glomerular filtration rate and chronic renal failure. Pathological examination reveals membranous glomerulonephritis in 50% of cases, proliferative glomerulonephritis in 20%, and IgA nephropathy (Berger's disease) in 30% with unknown etiology. The course of the disease is a slowly progressive decline in kidney function, usually over 20 years.

6.6.2.2. Pathophysiology

Reducing the mass of nephrons reduces the glomerular filtration rate. Compensatory hypertrophy and hyperfiltration of the remaining nephrons occur, and intraglomerular hypertension is triggered. These changes lead to further progression of glomerulosclerosis and loss of nephron mass.

In the initial stages of the disease, a significant decrease in glomerular filtration rate may lead to a slight increase in serum creatinine. Azotemia develops when the glomerular filtration rate decreases to less than 60-70 ml/min. Along with an increase in urea and creatinine levels with a decrease in glomerular filtration rate:

The synthesis of erythropoietin decreases, which leads to anemia;

The synthesis of vitamin D decreases, which leads to hypocalcemia, hyperparathyroidism, hyperphosphatemia and renal osteodystrophy;

The excretion of acids, potassium, salt and water decreases, which leads to acidosis, hyperkalemia, hypertension and edema;

Platelet dysfunction is observed, which leads to increased bleeding.

Uremic toxins affect all organs and systems. Uremia develops at a glomerular filtration rate of about 10 ml/min.

Clinical symptoms of uremia: weakness, fatigue, loss of appetite, weight loss, itching, nausea and vomiting in the morning, taste disturbance, insomnia at night and drowsiness during the day, peripheral neuropathy, seizures, tremors, edema and hypertension, shortness of breath or chest pain cell, depending on the position of the body, suggest the presence of stagnation or pericarditis. Leg cramps may indicate an electrolyte imbalance.

6.6.2.3. Clinical picture

On examination: Hypertension, jugular venous distention (in severe heart failure), crackles in the lungs (in pulmonary edema), pericardial friction rub in pericarditis, epigastric tenderness, or blood in the stool suggest uremic gastritis or enteropathy.

6.6.2.4. Laboratory diagnostics

Urinalysis: the presence of altered erythrocytes, erythrocyte casts, albumin, low specific gravity. Proteinuria more than 1 g/day is considered a predictor of the rapid development of CRF.

Blood test: anemia as a result of a violation of the synthesis of erythropoietin, an increase in the levels of urea and creatinine, retention of potassium, fluid and acids leads to hyperkalemia, hyponatremia, and a decrease in bicarbonate levels. Violation of the synthesis of vitamin D 3 leads to hypocalcemia, hyperphosphatemia, increased levels of parathyroid hormone. The low level of albumin is due to the diet or increased excretion in nephrotic syndrome.

6.6.2.5. Instrumental research methods

Ultrasound: a decrease in the size of the kidneys indicates the irreversibility of the process.

Morphological examination reveals the following variants.

.Minimal glomerular change disease It is more common in children, but it also occurs in adults. The expressed nephrotic syndrome with massive hypostases is characteristic; erythrocyturia and hypertension are rare. It is with this form that glucocorticoids are most effective.

cocorticoids, which sometimes allow stopping edema in 1 week. The prognosis is quite favorable, CRF rarely develops.

.Focal segmental glomerulosclerosis: 80% of patients develop chronic renal failure within 10 years. The course is progressive, the prognosis is serious, it is one of the most unfavorable morphological variants, rarely responding to active immunosuppressive therapy.

.Membranous glomerulonephritis(membranous nephropathy). Within 10 years, chronic renal failure develops only in 20-30% of patients. In a third of patients, it is possible to establish a connection with known antigens: hepatitis B or E viruses, tumor, drugs (captopril, gold, lithium, mercury, penicillamide). In addition, the reasons for the development of this form of chronic glomerulonephritis can be systemic diseases of the connective tissue, infectious agents.

.Membranoproliferative glomerulonephritis- the most common morphological type of glomerulonephritis. There is a familial form that is inherited in an autosomal dominant manner. In addition, this variant of chronic glomerulonephritis can occur with systemic lupus erythematosus, Sjogren's syndrome, rheumatoid arthritis, hereditary complement deficiency, scleroderma, chronic infections: hepatitis B and C, cryoglobulinemia, malaria, schistosomiasis, mycoplasmosis, endocarditis, multiple abscesses of internal organs; with cirrhosis of the liver, hemolytic-uremic syndrome, thrombotic thrombocytopenic purpura, antiphospholipid syndrome, radiation nephritis, etc. Within 10 years, 40% of patients develop chronic renal failure.

. IgA nephritis or Berger's disease- a separate variant of membrane-proliferative glomerulonephritis with deposition of immunoglobulin A in the glomeruli. The disease develops at a young age, more often in men, the leading symptom is hematuria. In 50% of patients, there is recurrent macrohematuria that occurs in the first days or even hours of febrile respiratory diseases. The prognosis is favorable, but worsens significantly with the addition of nephrotic syndrome and / or hypertension. Within 10 years, CRF develops in 10% of patients.

. Mesangiocapillary glomerulonephritis may be associated with hepatitis C virus, as well as with cryoglobulinemia. This is unfavorable

ny variant of glomerulonephritis with a progressive course and the development of CRF, poorly responding to therapy.

Renal biopsy is not indicated for reduced kidney size. A small number of patients who have experienced a sharp exacerbation of the disease need a biopsy. In the early stages, it is still possible to evaluate the primary process. In the later stages, hyalinosis and glomerular degeneration, tubular atrophy, significant interstitial fibrosis, and arteriolosclerosis are detected.

Depending on the clinical manifestations and course, the following are distinguished clinical options chronic glomerulonephritis (according to Tareev, 1972):

Latent;

Hematuric;

Nephrotic;

Hypertensive;

Mixed; .HPN.

Latent glomerulonephritis- the most common form of chronic glomerulonephritis, manifested only by changes in urine (proteinuria up to 2-3 g / day, slight erythrocyturia), sometimes AH I degree. The course is usually slowly progressive.

Hypertensive glomerulonephritis- this is a latent glomerulonephritis with more pronounced hypertension and minimal urinary syndrome.

Hematuric glomerulonephritis manifested by constant hematuria, often with episodes of gross hematuria, proteinuria does not exceed 1 g / day, the course is quite favorable.

Nephrotic glomerulonephritis characterized primarily by nephrotic syndrome, usually relapsing in nature. In the absence of erythrocyturia and hypertension (which is commonly seen in children), the prognosis is relatively good. In adults, isolated nephrotic syndrome is rare, the combination with erythrocyturia and / or hypertension significantly worsens the prognosis; when combined with hypertension, they speak of mixed glomerulonephritis.

6.6.2.6. Treatment

Progression to CKD can be slowed by various interventions, including aggressive control of diabetes, hypertension, proteinuria, dietary protein, phosphate, lipid control.

blood. Specific therapy is indicated for systemic diseases (eg, systemic lupus erythematosus). Anemia and renal osteodystrophy should be aggressively controlled. Target BP less than 130/80 mm Hg.

ACE inhibitors are considered the treatment of choice for hypertension. They have a renoprotective effect, reduce proteinuria by reducing the tone of the descending arteriole and reducing intraglomerular pressure. An alternative may be the use of angiotensin receptor blockers. Perhaps the combined use of drugs of these groups.

Furosemide has been shown to control edema and blood pressure. This drug may reduce hyperkalemia caused by ACE inhibitors. To achieve the target blood pressure, other antihypertensive agents (slow calcium channel blockers, β-blockers) may also be prescribed.

Correction of renal osteodystrophy is carried out by prescribing vitamin D.

Before prescribing erythropoietin drugs, other possible causes of anemia should be excluded.

All potentially nephrotoxic drugs should be avoided. NSAIDs, aminoglycosides, intravenous contrast agents can lead to the development of acute kidney failure.

6.6.3. Rapidly progressive glomerulonephritis

In addition to acute and chronic glomerulonephritis, there are rapidly progressive (subacute) glomerulonephritis, characterized by a decrease in glomerular filtration rate of about 50% in a short period - from several days to 3 months - and rapidly progressive renal failure without episodes of latent course or remission. Microscopy reveals fibrinoid necrosis, 50% of the glomeruli show "crescents". These patients have anti-basement membrane antibodies. Rapidly progressive glomerulonephritis can develop after infections, contact with organic solvents, but more often it is caused by systemic vasculitis and systemic lupus erythematosus. In the mid 70s. 20th century a group of patients with rapidly progressive glomerulonephritis was identified, in which deposits in the glomeruli were not found. 80% of them had circulating A1HSA.

6.6.3.1. Classification

1. Diseases associated with antibodies against the basement membrane of the renal glomeruli: Goodpasture's syndrome and disease with antibodies against the basement glomerular membrane (involving only the kidneys).

2. Diseases associated with immune complexes: post-infectious, post-streptococcal, visceral abscesses, systemic lupus erythematosus, Henoch-Schonlein purpura, mixed cryoglobulinemia, IgA nephropathy, membranoproliferative glomerulonephritis.

3. Diseases associated with A1HSA: Wegener's granulomatosis, microscopic polyangiitis, necrotizing glomerulonephritis with crescents, Churg-Strauss syndrome. The most common cause of death in these patients is massive pulmonary hemorrhage. If immunosuppressive therapy is started, they are more likely to die from infectious complications.

Men and women of all ages are equally affected.

6.6.3.2. Clinical picture

Some patients come with manifestations of kidney disease: anemia, hematuria, edema, oliguria, uremia. Most often, nephritic syndrome develops (rarely nephrotic), there is a rapid progression to CRF. Symptoms of weakness, nausea, vomiting usually dominate the clinical picture.

In other patients, the signs and symptoms of the underlying disease come first.

In still others, the prodromal period is characterized by flu-like symptoms: malaise, fever, arthralgia, myalgia, anorexia, and weight loss. This is followed by abdominal pain, painful skin nodules or ulcerations, migratory polyarthropathy. AG is not typical. Further, vasculitis progresses with the defeat of all organs and systems.

In 15% of patients, the onset of the disease may be asymptomatic.

Symptoms of CRF develop over several weeks or months: weakness, fatigue, nausea, vomiting, anorexia, malignant hypertension, retinopathy with retinal detachment, joint and abdominal pain, hemoptysis in Goodpasture's syndrome, oliguria, proteinuria, hematuria.

6.6.3.3. Examination methods

In terms of examination, in addition to routine tests, it is necessary to identify diseases that led to the development of rapidly progressive glomerulonephritis, as well as the study of A1HSA and kidney biopsy.

6.6.3.4. Treatment

The start of therapy should not be delayed until the results of the biopsy are available.

Most forms of rapidly progressive glomerulonephritis are more or less progressive diseases; the most reliable way to stop progression is to identify and eliminate the etiological factor. If it is impossible to establish the etiology, efforts should be aimed at suppressing the activity and stopping the exacerbation, which makes it possible to stabilize the course of the disease.

The prognosis is very serious, only massive immunosuppressive therapy can stop the progression. Glucocorticoids and cytostatics are used to suppress activity.

Glucocorticoids, which have immunosuppressive and anti-inflammatory effects, have been the main means of pathogenetic therapy for nephritis for several decades. Renal failure requiring dialysis is not considered a contraindication to initiating therapy.

Cytostatics in the treatment of nephritis are used somewhat less frequently due to the greater severity of side effects. As a rule, alkylating compounds are used - cyclophosphamide and chlorambucil; the antimetabolite azathioprine is less effective, although less toxic.

The presence of the following complications remains an indication for urgent dialysis: metabolic acidosis, pulmonary edema, pericarditis, uremic encephalopathy, uremic gastrointestinal bleeding, uremic neuropathy, severe anemia and hypocalcemia, hyperkalemia.

6.7. Prevention

There is no specific prophylaxis for most cases of glomerulonephritis. In some cases, it is likely that stopping or limiting contact with organic solvents, mercury, and non-steroidal anti-inflammatory analgesics can help.

6.8. Clinical examination

A patient with suspected kidney disease should be seen by a nephrologist. Early referral to a nephrologist improves prognosis and outcome.

7. CURATION OF PATIENTS

1. Under the supervision of a teacher, collect complaints, anamnesis and examine a patient with a clinical picture of acute and chronic glomerulonephritis, you should pay attention to:

Non-specific nature of complaints: weakness, decreased ability to work, dyspeptic complaints, etc.;

Risk factors for nephrological pathology: severe hypothermia, especially in conditions of high humidity, infectious diseases, allergic reactions, intoxication, occupational hazards, etc.;

Characteristic symptoms: pallor with an icteric tint and dryness of the skin, rarely erythema, swelling of the face, limbs, rarely ascites and anasarca, urinary disorders with a decrease in the amount of urine (oliguria, anuria), increased urination, especially at night, and a change in transparency and urine color, fever, subfebrile condition, shortness of breath, palpitations, hypertension.

2. Development of methods of physical examination of patients: palpation, percussion, auscultation (including renal arteries).

3. Drawing up a plan for examining a nephrological patient.

4. Evaluation of the results of laboratory and instrumental examination of a patient with acute and chronic glomerulonephritis with the determination of the leading nephrological syndrome: nephritic, nephrotic, urinary, hypertonic, tubular disorders (tubulopathy syndrome), acute or chronic renal failure.

5. Discussion of the basic principles of treatment of the examined patient.

8. CLINICAL ANALYSIS OF THE PATIENT

Clinical analysis is carried out by a teacher or students under the direct supervision of a teacher.

Tasks of clinical analysis.

Demonstration of the methodology for questioning and examining patients with acute and chronic glomerulonephritis.

Control of the skills of examination and questioning by students of patients with acute and chronic glomerulonephritis.

Demonstration of a method for diagnosing acute and chronic glomerulonephritis based on the data of a survey, examination and examination of a patient.

Demonstration of the method of drawing up a plan of examination and treatment.

During the lesson, the most typical and / or complex cases of acute and chronic glomerulonephritis from a diagnostic and / or therapeutic point of view are analyzed. At the conclusion of the clinical review, a structured final or preliminary diagnosis should be formulated and a plan for the examination and treatment of the patient should be drawn up. The results of the work are recorded in the curation diary.

9. SITUATIONAL TASKS

Clinical challenge? one

Patient D., 32 years old, turned to the local doctor with complaints of general malaise, feeling of weakness, decreased efficiency, swelling of the eyelids, face, dull, aching, prolonged pain of low intensity in the lumbar region, change in the color of urine (the color of "meat slops") .

The patient suffered a sore throat and two weeks after it began to notice a decrease in efficiency, a change in the color of urine, swelling of the eyelids. Sick for 2 days.

Past diseases: childhood infections, tonsillitis, acute respiratory viral infections, pneumonia. The patient works as a controller, he does not notice any occupational hazards. Bad habits denies. Family history: mother has hypertension, father peptic ulcer stomach, the daughter is healthy. Allergological anamnesis is not burdened.

On examination: a state of moderate severity. Body temperature 36.8 °C. The face is pale, puffy, the eyelids are swollen, the eyes are narrowed. The skin and mucous membranes are pale, clean, moist. Respiratory rate - 20 per minute. On auscultation of the lungs: hard breathing.

The heart sounds are muffled, there are no noises, the rhythm is correct, 78 beats per minute. BP - 130/80 mm Hg.

General blood test: hemoglobin - 120 g/l, erythrocytes - 4.1 x 10 9 /l. Color indicator - 0.9, leukocytes - 6.8x 10 9 /l, segmented - 76%, stab - 1%, eosinophils - 2%, monocytes - 2%, lymphocytes - 15%. ESR - 25 mm/h.

Urinalysis: relative density - 1018, protein - 1.066 g/l, erythrocytes - 10-12 in the field of view, leukocytes - 2-4 in the field of view.

Urinalysis according to Nechiporenko: erythrocytes - 6000 in 1 ml, leukocytes - 3000 in 1 ml, no cylinders were found. Daily proteinuria - 1.8 g.

Biochemical blood test: total protein - 70 g/l, albumin - 33 g/l, urea - 7.9 mmol/l, creatinine - 102 µmol/l, potassium - 4 mmol/l.

Bacteriological examination of a throat swab: no pathological microflora was detected.

1. What symptoms and syndromes are determined in the patient?

4.Prescribe a treatment.

Clinical challenge? 2

In patient S., 47 years old, during a dispensary examination, an increase in blood pressure up to 200/110 mm Hg was revealed. With a more thorough questioning, it was possible to establish that the patient has been worried about headaches, dizziness, flies before his eyes for 4-5 years. Deterioration in the last six months. Due to busyness, I did not go to the doctor. Continued to work.

Past diseases: childhood infections, SARS, tonsillitis, appendectomy 10 years ago. The patient works as an economist, he does not notice any professional hazards. Bad habits are denied. Family history: mother is healthy, father has gastric ulcer, son is healthy. Allergological anamnesis is not burdened.

On examination: the condition is relatively satisfactory. Body temperature 36.5 °C. Skin and mucous membranes of normal color, clean, moist. There are no edema.

Respiratory rate - 19 per minute. On auscultation of the lungs: vesicular breathing, no wheezing.

The left border of the relative dullness of the heart is 2 cm outward from the midclavicular line in the fifth intercostal space. Auscultation of the heart: clear heart sounds, accent II tone over the aorta, no noise. The rhythm of the heart is correct. Pulse - 68 per minute, satisfactory filling, tense. BP - 200/110 mm Hg.

The abdomen is soft and painless. Liver at the edge of the costal arch.

The area of ​​the kidneys is not changed, the kidneys are not palpated, the symptom of effleurage is negative on both sides.

Clinical blood test: hemoglobin - 118 g / l, erythrocytes - 4.2x 10 9 / l, leukocytes - 5.8x 10 9 / l, stab - 4%, segmented - 56%, lymphocytes - 33%, monocytes - 7%. ESR - 16 m m / h.

Urinalysis: relative density - 1016, protein - 4.3 g/l. leukocytes - 1-2 in the field of view, erythrocytes - 6-8 in the field of view. Daily proteinuria - 2.2 g.

Zimnitsky's test: daytime diuresis - 1060 ml, nighttime - 1400 ml, fluctuations in the relative density of urine from 1006 to 1018.

Reberg's test: glomerular filtration - 60 ml / min, tubular reabsorption - 98%.

Biochemical blood test: creatinine - 138 µmol/l.

2. Formulate a clinical diagnosis.

3. What additional investigations should be performed for the patient to confirm the diagnosis?

4.Prescribe a treatment.

Clinical challenge? 3

Patient M., 35 years old, turned to the local doctor with complaints of general malaise, weakness, fatigue, decreased performance, nausea, vomiting, lack of appetite, swelling of the eyelids, face, dull, aching, prolonged pain of low intensity in the lumbar region, discoloration urine (“meat slops”), a decrease in the amount of urine, swelling of the face, legs and feet, an almost constant headache in the occipital region, flies before the eyes.

The patient had a sore throat and two weeks after suffering a sore throat began to notice a decrease in efficiency, a change in the color of urine, swelling of the eyelids. Sick for a week.

Past diseases: childhood infections, tonsillitis, SARS. The patient works as an official, does not note any occupational hazards. Bad habits are denied. Family history: parents are healthy, daughter is healthy. Allergological anamnesis is not burdened.

On examination: a serious condition. Body temperature 37.8 °C. The face is pale, puffy, the eyelids are swollen, the eyes are narrowed, the legs and feet are swollen. The skin and mucous membranes are pale, clean, moist. Respiratory rate - 22 per minute. On auscultation of the lungs: hard breathing.

Heart sounds are muffled, there are no noises, the heart rhythm is correct. Heart rate - 78 per minute. BP - 200/120 mm Hg. Art.

The abdomen is soft and painless. The lower edge of the liver is palpable at the edge of the costal arch, painless.

The area of ​​the kidneys is not changed, the kidneys are not palpable, the symptom of effleurage is weakly positive on both sides.

Complete blood count: hemoglobin - 102 g / l, erythrocytes - 3.1x 10 9 / l, leukocytes - 7.6x 10 9 / l, segmented - 70%, rod-nuclear - 2%, eosinophils - 2%, monocytes - 4%, lymphocytes -

22%. ESR - 32 mm/h.

Urinalysis: relative density - 1018, protein - 2.066 g/l, erythrocytes - 10-12 per field of view, leukocytes - 2-3 per field of view.

Urinalysis according to Nechiporenko: erythrocytes - 6000 in 1 ml, leukocytes - 3000 in 1 ml, no cylinders were found. Daily proteinuria - 2.8 g.

The glomerular filtration rate is 50 ml/min, tubular reabsorption is 80%.

Biochemical blood test: total protein - 68 g/l, albumin - 30 g/l, cholesterol - 5.2 mmol/l, urea - 10.9 mmol/l, creatinine - 402 µmol/l, potassium - 4 mmol / l.

1. What symptoms and syndromes are observed in the patient?

2. Formulate a clinical diagnosis.

3. What additional investigations should be performed for the patient to confirm the diagnosis?

4.Prescribe a treatment.

10. STANDARDS OF ANSWERS

10.1. Answers to test tasks of the initial level

1.A.

2.D.

3.D.

4.A.

5.G.

6.A.

7.G.

8.B.

9.G.

10.B.

11.G.

12.B.

13.B.

14.G.

15.B.

16.A.

17.G.

18.B.

19.A.

20.B.

10.2. Answers to situational tasks

Clinical challenge? one

1. A patient has nephritic syndrome: macrohematuria, proteinuria 1.8 g/day.

2. Diagnosis: acute post-streptococcal glomerulonephritis with nephritic syndrome.

3. Ultrasound of the kidneys, kidney scintigraphy.

4. Treatment.

Bed rest.

ACE inhibitor with nephroprotective purpose.

Clinical challenge? 2

1. The patient has a urinary syndrome: proteinuria 2.2 g/day, hematuria, arterial hypertension - 200/110 mm Hg, CRF: decrease in glomerular filtration rate to 60 ml/min, increase in serum creatinine to 138 µmol/l.

2. Chronic glomerulonephritis, hypertonic form. HPN.

3. Additional studies: fundus examination, ECG, echocardiography, renal ultrasound, kidney scintigraphy.

4. At this stage, symptomatic therapy is carried out.

Table? 7 (restriction of salt consumption to 3-5 g.

Antihypertensive therapy: ACE inhibitors, slow calcium channel blockers, β-blockers, angiotensin receptor antagonists.

During therapy, it is necessary to reduce the pressure to a level of less than 130/80 mm Hg.

Clinical challenge? 3

1. The patient has a nephritic syndrome: gross hematuria, proteinuria 2.8 g/day, arterial hypertension up to 200/120 mm Hg; CRF: increase in urea - 10.9 mmol / l, creatinine - 402 μmol / l, decrease in glomerular filtration to 50 ml / min and tubular reabsorption up to 80%, anemia - 102 g / l,

2. Diagnosis: post-streptococcal glomerulonephritis with nephritic syndrome, rapidly progressive. CRF, mild anemia.

3.Ultrasound of the kidneys, scintigraphy of the kidneys, biopsy of the kidneys, examination of the fundus, blood test for serum iron, total iron-binding capacity of blood serum, ferritin, erythropoietin.

4. Treatment.

Table? 7. Reducing the intake of fluids, salt, protein foods.

Bed rest.

Diuresis control (accounting for drunk and excreted fluid).

Furosemide to reduce edema and lower blood pressure.

Nephroprotective therapy: ACE inhibitor and angiotensin receptor blocker (and to lower blood pressure), heparin.

Blockers of slow calcium channels, p-blockers to reduce blood pressure.

Erythropoietin in the exclusion of iron deficiency.

Immunosuppressive therapy: glucocorticoids, cytostatics.

Internal diseases: a guide to practice. classes in faculty therapy: textbook. allowance A. A. Abramov; ed. Professor V. I. Podzolkov. - 2010. - 640 p.: ill.

Timely and correct diagnosis is half of successful treatment. If the classical course of glomerulonephritis - glomerular inflammation of the kidneys - has its own bright characteristic features, then the latent forms of the disease can mimic a variety of pathologies. In order for the doctor to be able to make a correct diagnosis, the patient must undergo a comprehensive clinical, laboratory and instrumental examination.

Why is early diagnosis so important?

Glomerulonephritis is an acute or chronic infectious-allergic disease with a primary lesion of the main functional apparatus of the kidneys - the glomeruli. The main role in its development is played by the action of bacteria or viruses, as well as autoimmune processes.

According to statistics, acute form glomerulonephritis develops more often in children (3-7 years old) or young people (20-30 years old). Males are more susceptible to the disease. Chronic inflammation of the renal glomeruli occurs among all age groups. This pathology accounts for up to 1% of all therapeutic patients.

In the acute course of glomerulonephritis, clinical diagnosis is usually not difficult. In more than 70% of cases, the pathology responds well to therapy, and patients are completely cured. Without timely delivery medical uniform the disease becomes chronic, which can cause:

• progressive renal failure;
• heart failure;
• purulent-inflammatory lesions of the skin and internal organs;
• atherosclerosis at a young age.

The sooner a patient with glomerulonephritis turns to a doctor with his complaints, will be examined and begins treatment, the higher his chances of recovery with a complete restoration of the functional activity of the kidneys.

Stage one: interview and clinical examination

The first thing the examination of the patient begins with is the collection of complaints and anamnesis. Most often, the patient is concerned about:

• unstable increase in blood pressure (mainly due to the diastolic component);
• headaches, bouts of dizziness;
• flashing flies before the eyes;
• noise, ringing in the ears;
• decrease in the number and volume of urination (oliguria, anuria);
• change in the color of urine: it becomes a dirty brown, rusty shade (the color of "meat slops");
• constant feeling of thirst;
• the appearance of edema, first on the face and upper body, then spreading to the chest, abdominal cavity (hydrothorax, anasarca);
• dull aching pain, discomfort in the lumbar region;
• increase in body temperature up to 38.5-39°C;
• signs of intoxication - fatigue, weakness, loss of appetite.

A possible glomerulonephritis is also indicated by a recent bacterial (tonsillitis, acute rheumatic fever) or viral infection, vaccination, interaction with toxic substances.

Then the doctor conducts a clinical examination, including an assessment of habitus (the appearance of the patient), palpation and percussion of the kidneys, auscultation of the heart, lungs, and measurement of blood pressure. Objective signs of glomerulonephritis can be considered edema (favorite localization - eyelids), pain on palpation of the kidneys, a weakly positive symptom of Pasternatsky, hypertension.

Based on the data obtained, the specialist makes a preliminary diagnosis and draws up a plan for further examination. Differential diagnosis of glomerular inflammation is carried out with pyelonephritis, amyloidosis, urolithiasis, tuberculous changes and tumors in the kidneys.

Second stage: laboratory tests

If glomerulonephritis is suspected, the following laboratory methods are prescribed:

• general blood analysis;
• blood chemistry;
• clinical analysis of urine;
• samples according to Nechiporenko, Zimnitsky, Reberg - according to indications;
• allergy tests;
• immunological blood test.

In the results of the KLA of patients with glomerulonephritis, there are signs of acute inflammation - leukocytosis and accelerated ESR. Also noteworthy are the manifestations of anemia - a decrease in the level of red blood cells (erythrocytes) and hemoglobin.

Biochemistry is accompanied by hypoproteinemia (decrease in the level of total protein and albumin against the background of an increase in globulins). With the development of renal failure, the level of urea and creatinine progressively increases.

Urinalysis is the most important laboratory method in the diagnosis of exacerbations of glomerulonephritis. The following pathological changes are observed in it:

• an increase in the relative density of urine;
• color change;
• proteinuria - from microalbuminuria to massive excretion of protein in the urine (3 g / day or more);
• hematuria, erythrocyturia.

Immunological examination and allergy tests can reveal various disorders in the functioning of the body's defense system and confirm the autoimmune nature of the disease.

The third stage: instrumental methods of examination

Instrumental tests allow you to confirm the doctor's assumptions, determine the morphological form, the characteristics of the course of glomerular inflammation and make a clinical diagnosis.

Ultrasound of the kidneys is an effective, safe and non-invasive method for diagnosing diseases of internal organs. Acute or chronic glomerulonephritis has the following signs on ultrasound:

• the kidneys acquire vague, fuzzy contours;
• bilateral thickening of the parenchyma (functional layer);
• increased echogenicity, heterogeneity of the structure of the renal tissues: both hypo- and hyperechoic foci (“pyramids”) appear.

An ultrasound examination of blood flow (Dopplerography) shows a decrease in vascular resistance in the arcuate (arc) arteries. At the same time, blood flow can remain normal in the segmental and interlobar vessels.

It is possible to confirm the diagnosis and determine the nature of changes in tissues only with the help of a morphological study. The role of kidney biopsy in chronic glomerulonephritis is especially great.

The diagnostic procedure belongs to minimally invasive surgical interventions and is carried out only in stationary conditions. Under local anesthesia, the surgeon inserts a thin hollow needle through the skin of the lower back, capturing a small piece of kidney tissue. Then micropreparations are prepared from the obtained biomaterial, which the cytologist carefully examines under a microscope. The obtained data of histological examination reflect the morphological features of inflammation, allow you to determine the type of glomerulonephritis (for example, membranous, mesangioproliferative, mesangial, etc.) and even make a prognosis of the disease.

With the development of complications, the diagnostic plan may include additional laboratory and instrumental tests.

With the help of a timely comprehensive examination, it is possible to diagnose glomerulonephritis at an early stage, and begin treatment of the disease before irreversible changes occur in the tissues of the kidneys. This will quickly get rid of unpleasant symptoms, avoid the development of complications and achieve a full recovery.

The patient's condition depends on the stage and form of the disease. In the stage of compensation, it can be satisfactory (latent form), moderate and heavy. In the stage of renal decompensation, the condition is always severe.

Consciousness is preserved in the stage of compensation, in the stage of renal failure it can be clouded up to coma (uremic).

General examination data depend mainly on the form of the disease. In the nephrotic form, the main manifestations are widespread swelling of the ankles, face, trunk, genitals, then the patients show signs of accumulation of fluid in the cavities (ascites, hydrothorax, hydropericardium). There may be severe shortness of breath, convulsions due to cerebral edema, decreased vision up to blindness due to retinal edema. The skin is dry, inelastic, scaly, severe wasting of the muscles occurs due to hypoproteinemia.

The mechanism of edema in the first years of chronic glomerulonephritis is the same as in acute. In the future, hypoproteinemia develops due to large and constant proteinuria, which leads to a decrease in oncotic pressure and increased edema. Due to the drop in oncotic pressure and increased filtration in chronic glomerulonephritis, hypovolemia and hyponatremia develop, which stimulates excess production of aldosterone. A vicious circle emerges. An increase in capillary permeability is also important.

In the hypertensive form, signs of damage to the cardiovascular system are characteristic: pallor of the skin due to spasm of arterioles, visual impairment due to retinal hemorrhages, shortness of breath; after acute injury cerebral circulation- signs of hemiparesis with unilateral muscle atrophy.

The mixed form is characterized by a combination of features.

With a latent form, it is often possible to detect only a slight swelling of the eyelids.

With the development of renal decompensation, an ammonia smell from the mouth appears, lethargy increases, further deterioration of vision occurs, and hemorrhagic diathesis develops uremia.

Symptoms of chronic glomerulonephritis in the study of the cardiovascular system.

On examination, palpation, percussion and auscultation of the heart, the changes will be the same as in acute glomerulonephritis and are due to arterial hypertension. Therefore, they will be expressed in hypertonic and mixed forms.

Blood pressure rises: systolic up to 200 mm Hg, diastolic - up to 120 mm Hg, while the degree of increase in systolic pressure is greater than diastolic. The pulse pressure decreases. The increase in blood pressure is permanent. Arterial hypertension in chronic glomerulonephritis is based on a proliferative-sclerosing process, which leads to increased production of renin, that is, the main mechanism for increasing blood pressure is the activation of the renin-angiotensin-aldosterone system. Also, a decrease in the depressor function of the kidneys - a violation of the production of prostaglandins - plays a certain role.

Palpation of the kidneys.

The kidneys are not palpable, soreness is not typical.

6.3.7.6. Laboratory and instrumental diagnosis of chronic glomerulonephritis.

Clinical analysis of urine.

On physical examination:

- in the stage of compensation, the amount and density of urine are not changed in hypertonic, latent and mixed forms, in nephrotic due to severe proteinuria, urine density is more than 1020.

- in the stage of decompensation comes hypostenuria, polyuria, turning into oliguria.

In a biochemical study, proteinuria is determined, which is the main and obligatory symptom of chronic glomerulonephritis. Proteinuria is persistent, its magnitude depends on the form of the disease:

- in hypertonic and latent, the amount of protein is insignificant, less than 1 g/l.

- with nephrotic and mixed always more than 1 g / l - 1-20 g / l.

Microscopic examination of the urine sediment shows:

- hematuria - usually small, only microhematuria (up to 10-15 in the field of view), more often detected in the urine test according to Nechiporenko, more pronounced in hypertonic and mixed forms.

- leukocyturia - no more than 10-15 per field of view is possible, as an indicator of inflammation, but the number of erythrocytes always prevails over the number of leukocytes.

- cylindruria is a mandatory symptom of chronic glomerulonephritis, quite significant, there are hyaline, granular casts, with a nephrotic form - waxy, which serves as a poor prognostic sign, as it indicates large destructive changes in the renal tissue. In hypertonic and latent forms, cylindruria is less pronounced.

− renal epithelial cells- more sediment in nephrotic form.

Urinalysis according to Nechiporenko - an increased number of cylinders is determined, especially in the nephrotic form. The number of leukocytes and erythrocytes is increased moderately with a predominance of erythrocytes over leukocytes.

Bacteriological examination of urine - bacteria are absent.

Functional trials kidneys.

Test according to Zimnitsky: in the stage of decompensation, polyuria is detected, then oliguria, nocturia, isohyposthenuria.

Reberg's test - a decrease in filtration to 40-50 ml / min is determined, in the final stage of renal failure up to 1-5 ml / min, a decrease in reabsorption up to 60-80%.

Clinical and biochemical blood tests.

Clinical blood test: in patients with chronic glomerulonephritis, especially in the stage of renal decompensation, severe hyporegenerative anemia is detected. The number of erythrocytes can drop to 1.0x1012 in 1 liter of blood and below. Often found toxic leukocytosis, reaching 20/30x109 in 1 liter of blood, shift to the left, accelerated ESR, thrombocytopenia.

Biochemical analysis of blood: in the stage of renal compensation, the level of residual nitrogen and urea may remain within the normal range, an increase in creatinine levels is possible. Hyperlipidemia and hypercholesterolemia are characteristic, the content of a2- and g-globulins in the blood increases, hypoproteinemia, especially pronounced in patients with nephrotic and mixed forms. In the stage of renal failure in the blood, the level of creatinine, uric acid, residual nitrogen, urea increases, hypoproteinemia increases.

ECG. In the hypertensive form: signs of left ventricular hypertrophy, in the nephrotic form and the development of hydropericardium - a decrease in voltage, in hydrothorax - a load on the right heart.

Chest radiograph. Changes are identical to those in acute glomerulonephritis.

Data of ultrasonic and isotope research methods. In the stage of compensation, the changes will be the same as in acute glomerulonephritis. In the stage of decompensation, when wrinkling of the kidneys occurs, absolutely straight lines with a slight initial rise will be recorded on the renograms above both kidneys. Isotope and ultrasound studies reveal a significant reduction in the kidneys.

The diagnosis of glomerulonephritis in adult patients is a very threatening health condition. Glomerulonephritis is a complex of immunological diseases that affect the kidneys. Pathology affects the glomerular filter, further involving the interstitial tissue of the kidney in the pathological process, with further progression of the process, resulting in the development of sclerotic changes in the renal tissue and further renal failure.

Case history of glomerulonephritis (mcb 10)

This pathology was first identified and described by a doctor named Bright R. in 1827. Such a disease acquired the name of its "creator", after which a more detailed description and classification appeared in the twentieth century. As a result, the disease was divided into stages and type of course. And only after the biopsy entered medical practice, only then it became possible to study the disease from the point of view of pathogenesis.

At this time, according to modern classification kidney disease glomerulonephritis (ICB code N00 - N08) there are many clinical forms.

Glomerulonephritis clinical forms, classification

The classification provides for the division of pathology into forms, phases of the disease, according to the morphology of the process.

According to the classification of clinical forms, there are:

• Nephrotic form;
• latent form;
• Hypertensive;
• Hematuric;
• mixed;

Like most chronic diseases glomerulonephritis is subdivided according to the phases of the course into the phase of exacerbation, when kidney function decreases sharply, acute symptoms appear, and changes in the structure of the kidney parenchyma increase. And also - the stage of remission. During this period, the disease subsides, kidney function can recover, and symptoms subside.

According to their morphology, that is, the specific process occurring in the kidney tissue, multiple forms of glomerulonephritis are distinguished, for example, rapidly progressive renal glomerulonephritis. This principle of separation of the disease as a whole determines the further treatment of the patient.

Glomerulonephritis, pathogenesis

There are several theories in the development of the disease glomerulonephritis. One of them, more than others, has the right to life and it is immune. Some sources of literature consider the mechanism of development of such a pathology as a genetic anomaly of one of the links in the formation of the immune system. As a result, recovery processes in some parts of the nephron (the functional unit of the kidney) are disrupted. That is, to put it simply, a person's own immune system begins to consider kidney tissue as foreign (antigen) and, as a result, attacks it, as it destroys, for example, a virus that has entered the body.

Glomerulonephritis, clinic

The manifestations of this disease are several main symptoms:

• As a rule, the patient develops edema in the area of ​​the face, upper and lower limbs;
• The symptom of hypertension is manifested in the form of an uncontrolled increase in pressure. Such hypertension is not amenable to classical adjustment through drug therapy;
• The appearance in the urine of blood cells (erythrocytes), which can be seen with the naked eye in the form of blood impurities in the urine, while the urine has the color of "meat slops", for example, in the pathology of hematuric glomerulonephritis, (reviews). Also, a significant amount of protein appears in the urine. This condition is explained by a violation of the filtration process in the glomeruli of the kidney, as a result of a violation of their structure.

And also the most severe symptom of the manifestation of glomerulonephritis is cerebral. This condition is manifested by attacks of convulsions, similar to epilepsy, but are called eclampsia.

If the disease progresses rapidly, then the symptoms increase rapidly. At the same time, patients with glomerulonephritis should undergo a permanent medical examination and inpatient treatment.

Diagnostics

Diagnosis requires numerous laboratory studies and the availability of competent specialists. First, the patient's complaints are collected, then an objective examination is carried out. After that, a clinical and laboratory examination is carried out. In the urine, signs of hematuria are detected. Microhematuria - at the beginning of the process, or macrohematuria - in the acute form of the disease.

The excretion of protein in the urine is also a diagnostic sign of the development of the disease glomerulonephritis. Further, a clinical blood test is carried out and biochemical indicators kidney samples. An increase in ESR, leukocytes in the blood, a decrease in total protein, an increase in lipoproteins, nitrogen, creatinine and urea indicates the presence of kidney pathology. And an analysis for streptococcal antibodies will more accurately tilt the diagnosis towards glomerulonephritis.

After that, a series of instrumental studies is carried out using ultrasound, radiography of the kidneys (excretory urography), and computed tomography. If it is necessary to clarify the immediate cause of the development of the process, biopsy material is taken. To do this, under the control of ultrasound, a piece of kidney tissue is taken and sent to histological examination.

After the diagnosis is made, treatment begins.

Glomerulonephritis (ICB code 10), treatment

A patient with such a diagnosis should be hospitalized in a specialized department and be on bed rest. A dietstol according to Pevzner No. 7a is prescribed, with salt and protein restriction.

But the main direction in treatment is the use of drugs that depress the immune system. Apply hormonal preparations(prednisolone) and cytostatics (azathioprine). Also, for the purpose of auxiliary therapy, anticoagulants and anti-inflammatory drugs are used.

But before proceeding with treatment and making a diagnosis, it is necessary to understand in detail the causes of the disease. We will describe in more detail about the possible causes of glomerulonephritis in the next article.

The reasons

In most cases, diseases of a streptococcal nature lead to the development of glomerulonephritis. But there are other infections and their complications. Numerous factors that can provoke the onset of such a severe pathology as glomerulonephritis, the causes of occurrence, namely the pathogenesis of the development of the disease, have several theories.

Theories of development of glomerulonephritis (pathogenesis)

There are several theories of the occurrence of this disease, but the main cause of glomerulonephritis and the main theory is immunological. So, pathogenetically, according to this theory, the disease develops against the background of a focus of acute or chronic infection, which can be located in various organs, not only in the kidneys. Streptococcus is usually the source of infection. But it is also possible the presence of streptococcus pneumonia, and the causative agent of meningitis, and toxoplasma, malarial plasmodium, the appearance of some infections of viral etiology.

The essence of the immunological theory of the development of the process in the kidneys is the formation of immunological complexes in the bloodstream. These complexes appear as a result of exposure to the body of various bacteria and infectious processes, to which the immune system responds by producing antibodies to the emerging antigen. Moreover, the antigen can be both endogenous (inside the body) and exogenous (from outside). Both a microorganism and a first introduced drug, toxins, heavy metal salts can be perceived as an organism antigen. Also, one's own body, for some reason, can perceive its own kidney tissue as an antigen.

Further, the resulting immune complex circulates in the systemic circulation, passing through the glomerular filters, where they are retained and deposited, which leads to subsequent damage to the tissue of the glomerular filter and other parts of the kidney.

Or, when antibodies appear directly to the kidney tissue, they seem to attack and destroy the identified antigen (filtration glomeruli), causing inflammation and further damage and destruction. Such inflammation leads to the activation of hypercoagulation processes (increased coagulation) in the bloodstream of microvessels. Then the processes of reactive inflammation join. After that, the glomerular tissue is replaced by connective tissue, and actually dies. All this leads to the loss of the filtering function of the kidney and the further development of renal failure.

The second theory of the appearance of glomerulonephritis is hereditary, that is, there is a predisposition to this disease along the genetic line. It is also called Alport syndrome. This syndrome is characterized by a dominant type of inheritance, most often in the male line with manifestations of hematuric glomerulonephritis, a combination of this pathology with hereditary deafness.

Glomerulonephritis: causes of the disease

Modern medicine identifies the following possible causes and predisposing factors for the occurrence of glomerulonephritis:

• The presence in the body of a focus of acute or chronic infection, more often streptococcal, but the presence of the pathogen and staphylococci, gonococci, malarial plasmodium, toxoplasma, and others is possible. But only microorganisms can lead to such a disease. A wide variety of viruses and even fungal infections can provoke the onset of glomerulonephritis;
• The impact on the body of various highly toxic chemicals leads to sclerotic changes in the renal tissue, and even possibly to the development of acute renal failure with complex exposure and systemic damage;
• Allergization of the body through the use of new medicines that have not previously been introduced into the organism. And also this manifestation is typical in patients with aggravated allergic anamnesis;
• The introduction of vaccines - the causes of glomerulonephritis in children;
• Presence of systemic diseases such as systemic lupus erythematosus, rheumatoid arthritis and others in which a generalized lesion occurs;
• Errors in nutrition in the form of the use of large quantities of low-quality preservatives.

Glomerulonephritis: causes, symptoms, predisposing factors

Predisposing factors that can lead to the development of glomerulonephritis indirectly are:

• Prolonged exposure to low temperatures is a serious factor leading to the development of such a pathology in the future. This is due to the fact that as a result of hypothermia, a spasm of blood vessels occurs throughout the body reflexively, in order to save energy;
• It also contributes to the appearance of the disease glomerulonephritis, the presence in the patient diabetes the second and first type, due to systemic metabolic disorders;
• For women, a predisposing factor is childbirth, and / or curettage of the uterine cavity (as an open entrance gate for the infectious process and infection by the hematogenous route).

Cause of acute and chronic glomerulonephritis

Of course, in modern clinical practice the main cause of acute glomerulonephritis is streptococcal infection. Along with this, glomerulonephritis in children (symptoms, causes, treatment) appears as a result of vaccinations, since it is this contingent that is subject to routine vaccination.

But often, many believe that the causes of the development of an acute and chronic process should be radically different. But it's not. The dependence of the process is purely individual. In this case, the causes of chronic glomerulonephritis, as a rule, are a long, sluggish process in the body.

In any case, if there are predisposing factors, if the body is exposed to streptococcal or any other infection, as well as if there is a predisposition to allergic processes, the risk of glomerulonephritis increases. But no one is immune from the occurrence of an autoimmune process. Therefore, it is worth considering the etiology of the occurrence of the disease glomerulonephritis (causes, treatment) in the next article.

Etiology

In fact, the main etiological factor in the occurrence of glomerulonephritis is hemolytic streptococcus. So, the etiology, pathogenesis, clinic of glomerulonephritis depend on when and how severely the streptococcal infection was transferred.

A few weeks before the first signs of glomerulonephritis appear, the patient has angina, streptococcal tonsillitis, pharyngitis, and various skin lesions. Moreover, the development of the process in the kidneys may not be observed for some time. The defeat of streptococcus can also begin, for example, with the cardiovascular system, and then it will start glomerulonephritis.

In this case, glomerulonephritis, etiology, pathogenesis has a starting point in the form of the appearance of endostreptolysin A nephritogenic streptococci, which is the main antigen to which the immune system reacts, starting an irreversible process. As a result, immune complexes appear (antigen - antibody), which are deposited on the renal tubules of the filtration system, which causes a violation of the structure of the renal tissue and leads to the replacement of normal renal tissue with connective tissue.

Such an etiology, or rather the stages of development of the process, determine the clinical picture, which, depending on the degree of damage, differs in symptoms. Next, we consider all possible manifestations of glomerulonephritis, both typical and atypical.

Symptoms

We can suspect each disease if there are any symptoms, a clinical picture. Glomerulonephritis is no exception. As a rule, the manifestations of this disease are not long in coming and occur one to three weeks after the onset of a sore throat, for example, or tonsillitis involving streptococcal infection. In total, the symptoms are similar to each other, but depending on the form of the course and the nature of the process, they may differ. As a result, further treatment of the patient will depend.

The main symptoms of glomerulonephritis in women and men

The disease begins abruptly, immediately after suffering pharyngitis or tonsillitis. The patient has symptoms of intoxication of the whole organism in the form of constant feeling nausea, periodic vomiting, general significant weakness, decrease or lack of appetite, fever.

More specific manifestations for glomerulonephritis join the general intoxication:

• Pain in the lumbar region of a dull or aching nature, characteristic of kidney damage;
• Swelling of the upper half of the trunk (face) and lower limbs also swell;
• An increase in blood pressure that is not reduced is not controlled by classical therapy for hypertension;
• Paleness of the skin;
• Decreased daily diuresis by reducing filtration in the glomeruli of the kidneys;
• Urine acquires a characteristic red color, in the literature it is described as the color of "meat slops", due to damage to the microvessels of the filtration apparatus of the kidney.

Of the above symptoms, there are the most characteristic manifestations of glomerulonephritis, such as the classic triad. This is the presence of mandatory hypertensive manifestations, urinary and edematous syndrome in a patient. Each of them has a row distinctive features from other diseases with similar symptoms. Urinary syndrome manifests itself in the form of virtually absent urination. The patient complains of a significantly reduced amount of urine, which can reach about fifty milliliters per day (oliguria or anuria). Urine has a characteristic red color. This causes pain in the lumbar region.

Glomerulonephritis is characterized by the presence of hypertensive syndrome, which manifests itself in the form of a persistent increase in blood pressure, which is not amenable to drug correction. The numbers in this case can range from 130/90 to 170/120 mm. rt. Art. Diastolic pressure rises to the same extent as systolic. The highest pressure figures are observed at the very beginning of the disease, after which they may decrease, but still remain elevated compared to normal indicators. Along with the rise in pressure, a rapid heartbeat appears, during an objective examination, the doctor listens to the accent of the second tone over the aorta. Pressure surges occur due to fluid retention in the body and sodium. Hypertension is followed by sleep disturbance, the presence of headaches, decreased vision, and a feeling of nausea. Edema develops.

Symptoms of acute and chronic glomerulonephritis

According to the clinical course, glomerulonephritis is divided into acute and chronic. Although in general terms their clinic is similar, there are some features and differences.

Acute glomerulonephritis symptoms and treatment in adults has its own, different from chronic. Such a clinical variant of the course manifests itself as a urinary, hypertensive, edematous and cerebral syndrome. Also, acute glomerulonephritis is divided into latent glomerulonephritis (symptoms and treatment in children and adults are generally similar). This form of acute course is common and often turns into a chronic course of the disease. Latent glomerulonephritis is characterized by a gradual onset and has no pronounced clinical signs, only slight shortness of breath and swelling of the lower extremities. It runs for two to six months.

There is also a cyclic form of acute glomerulonephritis, which is characterized by headache, pain in the lumbar region, swelling, shortness of breath and, of course, hematuria. There is an increase in pressure. This condition lasts up to three weeks, after which the volume of daily diuresis increases, as a result of which the pressure decreases and the swelling goes away. At the same time, the density of urine decreases sharply.

Every acute glomerulonephritis that has not been cured within one year is automatically considered chronic.

Chronic glomerulonephritis symptoms in adults are as follows, depending on the stage of the disease. There are two of them in the chronic course:

• The stage of compensation, during which there is a relatively intact ability of the kidneys to filter and excretory function. It can manifest itself only by the presence of protein in the urine and red blood cells.
• As well as the stage of renal decompensation, when the last possibilities of the urinary system are disrupted, resulting in hypertension, edema.
• Also, depending on which signs of chronic glomerulonephritis prevail, several forms are distinguished: nephrotic, hypertonic, latent, hematuric and mixed.

Glomerulonephritis in children: symptoms

In childhood, the onset of the disease is always violent and spontaneous a few weeks after suffering a sore throat or vaccination. Clinical manifestations in children are bright, and acute glomerulonephritis very often develops.

The characteristic signs of glomerulonephritis in children are as follows: pronounced swelling of the face and legs, increased pressure, not characteristic of childhood, tearfulness, lethargy, sleep and appetite disturbance, nausea, vomiting, fever, chills. With adequate therapy, complete recovery occurs after one and a half to two months.

Chronic glomerulonephritis in children often occurs in the form of a hematuric form.

About what is to be diagnosed with glomerulonephritis, symptoms and treatment with folk remedies, you can read in our next article.

Diagnostics

As a rule, in the presence of a pronounced clinical picture and the correct collection of anamnesis (data on a recent infection), they make it possible to suggest a diagnosis of glomerulonephritis. But not everything is always so simple in reality and far from “books”. Often, even acute glomerulonephritis, diagnosis, treatment, all the more difficult due to the erased clinical picture. Therefore, we will analyze all possible methods for making the correct diagnosis for this disease.

Complaints and history taking

Regardless of whether the clinical manifestations are erased or not, first of all, the path to the diagnosis is paved through the collection of complaints. Typical symptoms in this case are a sharp increase in blood pressure, swelling of the eyelids, face, and lower extremities. The patient may complain of pain in the lumbar region, shortness of breath, chills, fever. A clear sign indicating a pathological process in the kidneys is hematuria and urinary disorders. Often, the patient independently notices an unusual color of urine, as well as a decrease in the amount of urine excreted per day.

Analyzes for glomerulonephritis, indicators

Illustrative studies in the diagnosis of glomerulonephritis are laboratory studies. When the pathology of glomerulonephritis is suspected, the patient's blood counts are approximately as follows: there is an increase in ESR in a clinical blood test, leukocytosis with an increase in the number of eosinophils, and a decrease in hemoglobin.

A biochemical blood test gives the following indicators: the total protein in glomerulonephritis in the blood serum will be reduced, an increase in a-globulins, an increase in residual nitrogen, creatinine, urea, and cholesterol. An increase in the titer of antibodies to streptococcus (antistreptolysin O, antistreptokinase) is also detected.

Necessary and very informative is the analysis of urine for glomerulonephritis, the indicators of which will exceed the norm to a greater extent. There will be a significant amount of protein, a large number of red blood cells, due to which the urine becomes dark red. The presence of cylinders is also characteristic. The specific gravity of urine will be increased, but may be within the acceptable range.

You also need to find out what kind of urine with glomerulonephritis through special urine tests according to Nechiporenko and Zimnitsky.

Instrumental diagnostic methods

One of the most common methods today is the method of ultrasound diagnostics. Through ultrasound, it is possible to determine an increase in the size of the kidneys and structural changes in the renal tissue.

Radioisotope angiography allows you to evaluate the vasculature of the renal tissue, the functional ability of the kidneys and their viability. To do this, special substances are introduced into the patient's body that are capable of emitting radioactive rays and are a kind of labels by which the state of the kidneys is determined.

If glomerulonephritis is suspected, electrocardiography and examination of the fundus are mandatory. To exclude the manifestations of hypertension by the symptoms of hypertension.

For a more accurate diagnosis and determination of the specific form of the disease, a biopsy is used. Using a biopsy endoscope, a piece of kidney tissue is taken and sent for histological examination, where the final diagnosis is made. This procedure is a kind of differential diagnosis of glomerulonephritis according to their course and forms, in order to determine the tactics of further treatment.

Differential diagnosis of chronic glomerulonephritis

The most difficult is the correct diagnosis, especially if the clinic does not fully correspond to the pathology. Differential diagnosis of pyelonephritis and glomerulonephritis is aimed at identifying a particular disease. Also, differential diagnosis of glomerulonephritis is carried out between hypertension and amyloidosis of the kidneys, the tuberculous process of the kidney tissue.

Pyelonephritis is easier to distinguish from glomerulonephritis by the presence of significant hematuria and its features. With glomerulonephritis, altered erythrocytes are present in the urine and in larger quantities. Also, pyelonephritis will not have characteristic streptococcal antibodies in the blood serum, and bacteria will be present in the urine culture.

Hypertension is more difficult. But this is where the study of the fundus will help. With hypertension, there is a change in the vessels of the fundus, which will not happen with glomerulonephritis. There will also be less pronounced hypertrophy of the heart muscle, a lower tendency to hypertensive crises with glomerulonephritis. Characteristic changes in the urine with glomerulonephritis (hematuria) appear much earlier than the increase in pressure.

Glomerulonephritis differs from amyloidosis of the kidneys by the absence of a history of past or present tuberculosis, arthritis, chronic sepsis, purulent pathology of the lungs, and amyloidosis of other organs. The final confirmation of the diagnosis is the results of a biopsy of the renal tissue with a histological conclusion.

It should be remembered that edema in glomerulonephritis differs from those in other pathologies. But clinical manifestations are not reliable, and the most reliable diagnostic signs should be considered laboratory and instrumental diagnostics. Also, the differentiation of the diagnosis must be carried out not only with other pathologies, but also with a chronic process with an acute one. The management of these patients will differ. And depending on the clinical forms, treatment will be selected. To see what options are available clinical course, consider in the next article the classification of glomerulonephritis.

Classification

In order to carry out adequate treatment, it is necessary to understand what forms and degrees of glomerulonephritis are. For this purpose, many classifications of this pathology have been created.

Glomerulonephritis is subdivided according to the course, stages, clinical forms. Also, according to the causes of occurrence (bacterial infection, viral, the presence of protozoa in the body and unidentified), according to the nosological form, according to pathogenesis (immunologically determined and not determined). Let us consider in more detail all the above classifications.

Clinical classification of glomerulonephritis

The clinical classification is the most popular in medical practice, since it is by the manifestations of symptoms in a patient and their totality that the variant of the course of the pathology and further tactics of management are determined. This division of glomerulonephritis is an affordable method for determining the clinical course, due to the absence of the need for extensive and expensive diagnostics. And so, the following variants of glomerulonephritis are distinguished:

• A latent variant, when the disease does not have pronounced clinical manifestations, except for the presence of hematuria and minor jumps in blood pressure. Often this option is characteristic of the chronic course of glomerulonephritis.
• The hematuric variant of the course of glomerulonephritis is characterized by the presence of almost isolated hematuria (the presence of red blood cells in the urine, to a greater or lesser extent) without signs of proteinuria and other symptoms.
• There is also hypertensive glomerulonephritis, namely its variant of the course, when glomerulonephritis manifests itself to a greater extent by an increase in blood pressure. At the same time, the urinary syndrome is poorly expressed. The pressure can reach the limits of 180/100 and 200/120 mm Hg, and can also fluctuate significantly during the day. As a rule, the hypertensive variant of the course is already a consequence of the development of a latent form of acute glomerulonephritis. As a result, hypertrophic changes in the left ventricle develop, the doctor listens to the accent of the second tone over the aorta. Such hypertension often does not become malignant.
• Glomerulonephritis with nephrotic course is the most common. The characteristic signs for this variant of the course is the combination of this syndrome (increased excretion of protein in the urine) with signs of inflammation of the renal tissue.

The mixed variant of the course is characterized by a combination of nephrotic syndrome with hypertensive. Accordingly, the clinical manifestations will be characteristic of these two syndromes.

Classification according to the phases of the disease is also of great clinical importance. As in most pathologies with a chronic course, a phase of exacerbation and remission is distinguished.

Morphological variants of glomerulonephritis

Morphological classification provides for the division of glomerulonephritis according to the histological conclusion of histologists. Morphological forms of glomerulonephritis in children are similar to those in adults. The following forms of glomerulonephritis are classified according to morphology:

• The most common morphological form of chronic glomerulonephritis is mesangioproliferative glomerulonephritis, the clinical symptoms of which manifest themselves as follows. In this case, there will be persistent hematuria, and kidney damage of this kind is more common in males. In another way, one can also call such a form as the hematuric form of glomerulonephritis. An increase in blood pressure is quite rare. According to its morphological structure, this form is characterized by the deposition of immune complexes in the mesangium and endothelial structures of the glomerulus of the kidneys. Clinically, this form is comparable to the nephrotic form and less often hypertensive, as well as nephropathy, which occurs under the name Berger's disease.
• There is also membranous glomerulonephritis. Such glomerulonephritis is not widespread among the population, about five percent. In this case, an immunological study is carried out, through which fibrin threads and deposits of IgM and IgG are detected in the small vessels of the glomeruli. According to clinical manifestations, this variant proceeds rather slowly, and has proteinuria characteristic of it, or a possible manifestation of nephrotic syndrome. This form, although proceeding slowly, is predicted to be less optimistic compared to the previous form.
• Mesangiocapillary or membranoproliferative glomerulonephritis is observed in approximately twenty percent of cases, with damage to the basement membrane, namely mesangium. Immunologically, deposits of immunoglobulins A and G are detected in the capillaries of the glomeruli, as a result of which the epithelialization of the glomerular tubules changes. This form is more inherent in the female sex. According to the symptoms, the manifestations are characteristic of nephrotic syndrome, there is also significant hematuria and loss of protein in the urine. This form tends to progress.
• Due to the fact that this process begins after various kinds of infectious processes, it can be designated as post-streptococcal glomerulonephritis in adults.
• Morphological glomerulonephritis is also distinguished in the classification in the form of lipoid nephrosis. This pathology is typical for children. Lipids are detected in the tubules of the glomeruli. This form has a good prognosis in the treatment of glucocorticoids.

And there is fibroplastic glomerulonephritis according to morphological classification. This form manifests itself as diffuse processes of sclerosis and fibrosis in all glomerular structures of the kidneys. As a result, dystrophy processes predominate. Chronic renal failure develops rather quickly.

Morphological forms characterize chronic glomerulonephritis, the classification of which is described above. Other nuances of the course of chronic glomerulonephritis can be found in the following article.

Chronic glomerulonephritis

Chronic glomerulonephritis (microbial code N03) is a pathology that affects the glomerular apparatus of the kidneys through immunocomplex damage, leading to hematuria and hypertension.

Chronic glomerulonephritis (mcb 10) causes of development, pathogenesis

This variant of the course of glomerulonephritis can develop as a consequence of an acute one, or independently immediately in a chronic form. Chronic glomerulonephritis is more common than acute glomerulonephritis and mostly affects men around forty to forty-five years of age.

For reasons of occurrence, the chronic form of the course differs little from the acute one, but in chronic cases, viral infections, such as the hepatitis B virus, become important. herpetic infection and cytomegalovirus. Also, one of the reasons that cause xp glomerulonephritis (mcb 10 N03) is the ingestion of drugs and salts of heavy metals. And, of course, predisposing factors are of great importance - hypothermia, trauma, the systematic use of alcoholic beverages, excessively harmful working conditions.

In the pathogenesis, the leading role is played by immune disorders, which, with prolonged exposure, lead to inflammation in the glomerular apparatus of the renal tissue. Or, regardless of external factors, an autoimmune process of kidney damage can develop, this happens as a result of the perception by the body's immune system of glomerular membranes as a foreign body, that is, an antigen. Also has an impact on the formation of glomerulonephritis a number of processes that are formed as a result of running immune mechanisms. Thus, emerging proteinuria damages the tubules of the renal tissue, an increase in intraglomerular pressure in the vessels leads to an increase in their permeability and destruction.

The histological picture in the disease chronic glomerulonephritis (ICB code 10 N03) is characterized by total edema, the presence of fibrosis of the renal tissue, complete atrophy of the filtration link, which causes wrinkling of the kidney. As a result, they shrink and shrink in size. If there are glomeruli that have retained their function, then they are significantly enlarged.

Chronic glomerulonephritis, syndromes

There are a number of syndromes, according to the classification, characteristic of the clinical course of chronic glomerulonephritis:

• Hematuria syndrome manifests itself in the form of blood impurities in the urine, or urine completely stained with blood.
• Hypertensive syndrome affects the patient's condition through a sharp persistent increase in blood pressure, which is difficult to correct with medication, and its independent decrease. Pressure surges can be repeated up to several times a day.
• Nephrotic syndrome is characteristic of this disease and manifests itself as a large loss of protein in the urine.
• Also isolated is latent chronic glomerulonephritis of the kidneys, one of its most insidious manifestations. This type proceeds without typical clinical signs and often, imperceptibly for the patient, can lead to the development of chronic renal failure due to the absence of complaints, and as a result, the lack of treatment.
• Mixed syndrome combines the presence of hypertensive and nephrotic syndromes in conjunction with severe edema.

As a separate species, subacute glomerulonephritis is distinguished along its course. It has a malignant course. Prognostically, this pathology is unfavorable. Patients die from renal failure within six months to one and a half.

Diagnostics

The diagnosis of chronic glomerulonephritis is made on the basis of a thorough examination. In addition to the routine collection of complaints and anamnesis data, examination through laboratory tests and instrumental methods is the key to making a diagnosis.

It is necessary to carry out, in addition to many of the usual studies, the following main diagnostic measures:

• General analysis of urine, samples according to Nechiporenko and Zimnitsky, determination of daily proteinuria (protein excretion in urine per day).
• Biochemical analysis of blood with the determination of kidney samples (urea, creatinine, residual nitrogen, uric acid), as well as accounting for the total protein of blood serum and its fractions.
• Determine the immunogram.
• The ophthalmologist examines the fundus of the eye.
• Through radiological methods, excretory urography is performed to determine the safety of kidney function.
• A radionuclide examination of the urinary system is also carried out by introducing a special substance into the body, which seems to mark pathological areas.
• Of course, an ultrasound examination of the urinary system to examine the structure and size of the kidneys.
• Computed tomography or MRI may be used.

In conclusion, and in order to determine the morphological type of chronic glomerulonephritis, a kidney biopsy is performed under ultrasound control for histological examination.

Depending on which syndrome prevails, as well as on the degree of progression of the process and the morphological variant of the course, the appropriate therapy is selected. As a rule, therapy is symptomatic and is carried out in order to maintain the functional ability of the kidneys.

But with a malignant and rapidly progressive course, an aggressive four-component therapy is prescribed, consisting of glucocorticoids, cytostatics, plasmapheresis and anticoagulants. Such treatment is carried out in the case of an absolutely proven immune process in the kidneys.

Also, in case of chronic glomerulonephritis, recommendations are given on diet (table No. 7 a), on the daily regimen (during an exacerbation of the disease, he is in bed), on a further lifestyle.

Prognosis of chronic glomerulonephritis

The appearance of such a disease in a patient very often and quickly leads to disability at a relatively young age, the appearance of chronic renal failure, which worsens the quality of life, and even death.

Depending on the forms and stage of the disease, a more accurate prognosis for life can be made. In the next article, we will describe the possible existing stages and forms of glomerulonephritis.

Forms and stages

Any of existing species glomerulonephritis has its own division into forms and stages depending on the clinical course. Chronic glomerulonephritis has a greater division due to the duration of the disease and the variety of its course.

Forms of acute glomerulonephritis

Acute glomerulonephritis also has forms of the course of the pathological process, they are distinguished by two:

• The first can be attributed to the acute cyclic form. It is characterized by acute manifestations and rapid onset of the disease. Symptoms and complaints of the patient are expressed to a large extent. There is a sharp increase in temperature, pain in the lumbar region, impaired urination, urine becomes red, vomiting appears. In especially severe cases, urination disorders progress up to its absence for several days, followed by the development of acute renal failure. Although, usually, this variant of the clinical course is a favorable prognosis for recovery.
• The second form is latent or, in other words, protracted. Manifests itself as a long gradual onset of symptoms and lingering course the entire pathological period from six months to one year. The clinical manifestations are the same as those of the acute cyclic form, they only increase gradually, and for some time they can manifest themselves only as a couple of some symptoms.
• Any acute glomerulonephritis in the absence of positive dynamics and recovery during the year is automatically considered to have passed into chronic.

Chronic glomerulonephritis, stages

This disease in its chronic form has a larger subdivision according to the clinical course than acute. Depending on the “height” of the process, chronic glomerulonephritis is divided into the following stages, or phases:

• The active stage of the process, which is characterized by the rapid progression of the pathological process in the kidneys and vivid symptoms. This stage is divided into three more:
• The peak period of the disease;
• The period of attenuation of symptoms;
• And the stage of clinical remission;
• The inactive stage of chronic glomerulonephritis manifests itself in the form of clinical and laboratory subsidence of symptoms.

Also distinguish the terminal stage of the disease. This option is considered when signs of chronic renal failure appear.

There is a conditional division of chronic glomerulonephritis into two more stages according to the body's ability to resume kidney function:

• The stage of compensation, when the body is still coping with the pathology that has arisen and the kidney continues to function, albeit with significant disturbances in its structure.
• And the stage of decompensation of the process. It is characterized by the undermining of all compensatory mechanisms and manifests itself in the form of renal failure.

Clinical forms of chronic glomerulonephritis

Chronic glomerulonephritis can occur in several clinical directions, when, to one degree or another, certain symptoms predominate. The following clinical variants of chronic glomerulonephritis are distinguished:

• Latent glomerulonephritis;
• Nephrotic;
• Hematuric;
• Mixed;
• Hypertensive;
• Let's consider each of the flow options in more detail.

Chronic glomerulonephritis, the nephrotic form, is the most common variant of the course of this pathology. The nephrotic form manifests itself with significant indicators of proteinuria (more than 3.5 grams in the daily amount of urine). This symptom is often almost the only manifestation and occurs as a result of damage to the glomerular tissue. In the blood serum, a decrease in total protein can be detected, and an increase in globulins, lipids, as well as hypercholesterolemia.

Clinically, nephrotic syndrome can be assessed by appearance patient. The face is edematous, pale, dryness of the skin prevails. Patients are not active, inhibition processes appear in speech and actions. In case of development severe forms there may be accumulation of fluid in the pleural or abdominal cavity develops oliguria (little urine). Such phenomena are a provocative factor in the emergence and development of various infectious diseases.

Chronic glomerulonephritis hematuric form is characterized only by the presence of blood in the urine. It can be manifested by macro- and microhematuria. The excretion of protein in the urine is negligible. Other symptoms are usually absent. Hematuric chronic glomerulonephritis progresses slowly.

Chronic glomerulonephritis, a hypertensive variant of the course, manifests itself in the form of jumps in blood pressure, which appear periodically. In addition, the patient does not complain about anything, a small amount of protein is detected in the laboratory in the urine. The disease progresses imperceptibly and is detected by chance, already when there is hypertrophy of the left ventricle of the heart and altered vessels of the fundus. This course of the disease slowly leads the patient to chronic renal failure. Chronic glomerulonephritis, hypertensive form, the medical history of such patients is replete with examinations from cardiology and ophthalmology, as heart failure and retinal detachment may develop.

In the case when chronic glomerulonephritis develops, a latent form forms a latent course of the disease. This pathology has been asymptomatic for many years and can only be diagnosed after the development of chronic renal failure. The most insignificant manifestations may be the loss of protein in the urine, rarely hematuria, low numbers of arterial hypertension and edema, which the patient does not attach importance to.

The mixed form of the disease includes, based on the name, all possible manifestations. Progresses rapidly.

Chronic diffuse glomerulonephritis is also one of the forms of this disease, but belongs to a different classification, and more often occurs secondarily, that is, as a complication of another pathology (septic endocarditis).

All of the above forms exist in order to select the optimal treatment, the methods of which will be discussed later.

Treatment

For complex treatment chronic glomerulonephritis requires not only drug treatment, but also the use of diet therapy and spa treatment. In the stage of exacerbation of the disease, hospitalization is necessary. Let us consider in more detail the possible treatment and prognosis of chronic glomerulonephritis: can it be cured or not.

Treatment of chronic glomerulonephritis, symptomatic therapy drugs

For the correct selection of treatment, it is necessary to accurately establish the form of the clinical course of the disease. Different shapes require individual approach to therapy.

If a patient has chronic glomerulonephritis with a latent course, that is, if there is less than one gram of protein in the daily amount of urine and weak manifestations of hematuria (up to eight erythrocytes per field of view), curantyl, delagil and trental are used with preserved kidney function. The course of such drugs is up to three months.

In the hematuric form, which slowly progresses, membrane stabilizers are used for up to one month (dimephosphan solution), the same delagil and vitamin E. It is also possible to add indomethacin or voltaren to therapy for up to four months. Indispensable use are drugs trental and / or chimes.

With the hypertensive form of glomerulonephritis, treatment is more complex. Since this form is steadily progressing, and constantly elevated blood pressure is caused by impaired renal blood flow (“vicious circle”), it is necessary to use drugs that normalize hemodynamic processes in the kidneys (chimes, trental, long-term use for many years). Also used in therapy nicotinic acid, β-blockers, diuretics, calcium agonists.

In case of detection of chronic glomerulonephritis with a nephrotic form, even without the presence of hypertension and renal failure, active therapy must be applied. This type of therapy includes the use of glucocorticoids and cytostatics. The four-component treatment has a significant therapeutic effect. Also, this form is characterized by hypercoagulability, given this, anticoagulants are prescribed.

Pathogenetic methods of treatment of chronic glomerulonephritis

In order to prescribe treatment, which is aimed at eliminating the mechanisms of the development of the disease, the pathogenesis of chronic glomerulonephritis should be taken into account.

So, the leading drugs for the treatment of glomerulonephritis are glucocorticoids, cytostatic drugs, anticoagulants and plasmapheresis. This therapy is resorted to in cases where the process of disease progression is active and there are high risks of complications and a threat to the patient's life.

For this therapy, or a four-component treatment regimen, there are some indications: significant activity of the pathological process in the renal tissue, the presence of nephrotic syndrome even in the absence of hypertension, minor morphological changes in the glomerular apparatus of the kidneys. There are several treatment regimens. With nephritis with an active process in adults, prednisolone is used at a dosage of 0.5 to 1 milligram per kilogram of body weight for eight weeks, then the dosage is gradually reduced and therapy is continued for up to half a year. A similar treatment for chronic glomerulonephritis in children, but the scheme has its own nuances. In this case, prednisolone is prescribed for up to four days, and then a four-day break is taken.

Also, in the presence of the most active process in the kidneys with rapid progression of the pathology, "pulse therapy" is used.

But, like every therapy, this treatment has a number of side effects: the development of Itsenko-Cushing's syndrome, the development of osteoporosis, gastric ulcer with the possible development of bleeding.

Chronic glomerulonephritis must be treated along with glucocorticoids, drugs that suppress the immune system. These include cyclophosphamide, chlorambucil and others.

You should also take into account the entire pathogenetic process in order to treat glomerulonephritis and apply anticoagulants. Such a drug of choice is heparin in a daily dosage of up to fifteen thousand units, which are separated by more than four injections. The effectiveness of therapy is assessed by increasing the clotting time after several doses.

Indirectly, the process of producing an antiplatelet agent in the vascular wall of the glomerular filter is affected by chimes. Its clinical effects include an improvement in renal blood flow.

For the same purpose, acetylsalicylic acid is also prescribed.

Treatment of acute and chronic glomerulonephritis with NSAIDs

In order to reduce the inflammatory process and the analgesic effect, I use non-steroidal anti-inflammatory drugs (NSAIDs) in the treatment of glomerulonephritis - ibuprofen, indomethacin, voltaren.

With a weak activity of the process, NSAIDs can be prescribed as an alternative to glucocorticoids. For example, indomethacin is indicated for patients with urinary protein excretion and preserved kidney function. But even here there are contraindications. Also, in case of activation of the pathological process, they switch to corticosteroids.

Plasmapheresis is used as one of the components of therapy for glomerulonephritis. It is indicated for the treatment of a rapidly progressive disease, as well as in the case of the appearance of secondary glomerulonephritis against the background of other systemic pathology.

General principles for the treatment of chronic glomerulonephritis

Along with medication, diet should be followed. For this, table No. 7a is prescribed, and they give recommendations on reducing the amount of salt in food, and also reduce the protein load on the kidneys.

Sanatorium treatment is recommended for patients with a latent course of the process or in remission of the disease with mild nephrotic syndrome. It is possible to use in the complex treatment of chronic glomerulonephritis with folk remedies. But such treatment must be agreed with the doctor in accordance with the ongoing drug therapy so as not to aggravate the condition.

Is it possible to cure chronic glomerulonephritis forever

The prognosis of the disease of chronic glomerulonephritis is generally unfavorable and the treatment of the pathological process is carried out only in order to slow down the decline in kidney function, postpone disability and improve the patient's quality of life.

It all depends on the form of the disease and the therapy. But not infrequently, glomerulonephritis leads to disability or even death.

Therefore, the answer to the question of whether chronic glomerulonephritis can be cured is unequivocal.

Acute glomerulonephritis

This pathology in most cases affects young people and is characterized by inflammation of the glomerular apparatus of the kidneys of immune origin with further involvement of all kidney structures in the process.

Etiology and pathogenesis of acute glomerulonephritis

As a rule, glomerulonephritis develops after acute streptococcal infections, such as tonsillitis, tonsillitis, and others. It is also possible to establish that the patient has recently suffered pneumonia, diphtheria, viral infections. Possible development of glomerulonephritis as a result of exposure to malarial plasmodium and after the introduction of vaccines. But to a greater extent, the occurrence of such a pathology depends on beta-hemolytic streptococcus, namely group A. There are a number of provocative conditions, such as hypothermia, humid climate, prolonged exposure to harmful working conditions.

Other etiological factors may be various drugs that were introduced into the body for the first time, various chemical compounds and other allergens, in case of individual intolerance and activation of the immunological process.

The pathogenetic mechanism for the development of glomerulonephritis is an immune reaction in the formation of an antigen-antibody complex and their deposition on the vascular wall of the glomeruli of the kidneys. As a result, inflammatory processes occur in the capillary wall - vasculitis.

All manifestations of glomerulonephritis occur a few weeks after the disease.

Acute glomerulonephritis, clinic

Acute glomerulonephritis develops abruptly, with vivid clinical manifestations. Patients complain of pain in the lumbar region, which spread from both sides. Symptoms of general intoxication of the body appear: an increase in body temperature to high numbers, general weakness, nausea, and vomiting. Patients notice a sharp decrease in the amount of urine per day, oliguria develops. The color of urine also changes, it becomes red (“the color of meat slops”). With the progression of the disease, anuria (complete absence of urine) may develop. Usually such a symptom indicates the development of acute renal failure.

Edema is a typical manifestation. Patients develop swelling not only of the lower extremities, but also of the face. The eyelids swell, the skin acquires a pronounced pallor. With the development of severe conditions, the accumulation of fluid can occur in the natural cavities of the body: the chest cavity, abdominal, in the region of the heart. This type edema is characterized by their appearance in the morning, and in the evening the swelling decreases. A few weeks after the onset of the disease, the swelling disappears.

Another important manifestation of acute glomerulonephritis is an increase in blood pressure. It occurs abruptly at the onset of the disease and reaches numbers up to 180 systolic and up to 120 diastolic mm Hg. Such a symptom as hypertension can lead to the development of serious complications: pulmonary edema, left ventricular hypertrophy, the occurrence of epileptic seizures, but of a different nature (eclampsia). This concept, eclampsia, occurs due to swelling of the brain tissue, namely the motor centers. It is manifested by loss of consciousness, acrocyanosis (cyanosis of the limbs and face), seizures or increased tone of all muscles.

Acute glomerulonephritis, syndromes and forms

Acute glomerulonephritis can be divided into two forms according to the course of the disease:

• The first is the acute form of cyclic flow. It is characterized by a spontaneous rapid onset of the disease, vivid clinical manifestations. The prognosis for such a course is favorable, since it ends with a complete recovery of the patient.
• The second is a protracted form, which is accompanied by a slow progression of the pathological process and the gradual onset of symptoms. This form has a long course, from six months to one year.
• Acute glomerulonephritis is characterized by the presence of nephrotic syndrome. It manifests itself in the form of excretion of a large amount of protein in the urine, its corresponding decrease in blood serum, an increase in lipids, and swelling.
• There is a transition from acute glomerulonephritis to subacute glomerulonephritis, which tends to rapidly worsen the condition. And also, if the process is delayed, it can turn into a chronic process.
• Acute diffuse glomerulonephritis is also a form of acute, but it can also be chronic.

Complications of acute glomerulonephritis

The most frequent and severe complications of this disease are: acute renal failure, heart failure, cerebral edema with the development of eclampsia, hemorrhagic stroke, varying degrees retinopathy up to retinal detachment.

How is acute glomerulonephritis diagnosed (recommendations)

Diagnosis of glomerulonephritis is based on the collection of patient complaints, finding out the presence of infectious diseases a few weeks before the onset of symptoms, an objective examination by a doctor and clinical and laboratory diagnostics. As well as instrumental studies.

In the general analysis of urine, there is an increase in leukocytes, urine density, high protein excretion (from 1 to 20 grams per liter), hematuria. Urine analysis according to Zimnitsky is also carried out.

In the clinical analysis of blood, a decrease in hemoglobin, leukocytosis, and an increase in ESR are observed. A biochemical blood test reflects the presence of kidney damage: an increase in the level of urea, creatinine, uric acid. A proteinogram indicates a loss of protein by the body: a decrease in total protein in the blood serum and albumin.

When conducting an immunogram, it is possible to detect an increased amount of immunoglobulins, an increased titer of antibodies to streptococcus in the event of a disease - acute post-streptococcal glomerulonephritis in children and adults.

Diagnosis by means of instrumental methods begins with an ultrasound examination. It is also possible to carry out x-rays with a contrast agent. Examine the vessels of the fundus and carry out an ECG. In conclusion, for accurate diagnosis, a puncture biopsy of the kidneys is performed.

All recommendations for this disease are based on inpatient treatment and timely diagnosis. With the development of pathology, acute glomerulonephritis in children, clinical guidelines aimed at the timely appeal of parents for medical help in order to avoid the progression of the disease and the onset of the child's disability, or the chronicity of the process. Therefore, the disease needs urgent treatment, the methods of which will be discussed in the next article.

Treatment

The main therapy for acute glomerulonephritis is of course medication, but it is necessary to adhere to proper nutrition.

Diet for acute glomerulonephritis

There are special developed diets according to Pevzner. In acute glomerulonephritis, dietstol No. 7, 7a and 7b are used. The essence of these diets is a sharp restriction of salt in foods, restriction of protein foods, water and fluid intake.

At the beginning of the disease, foods with a high glucose content are recommended. Namely, five hundred grams of sugar per day, with five hundred milliliters of tea or fruit juice per day. Further, watermelons, oranges, pumpkins, potatoes are prescribed in the diet, which together represent the almost complete absence of sodium in the diet. It is also recommended that patients consider daily diuresis. With this diet, the amount of fluid consumed should be approximately equal to the amount of urine excreted.

The sequence of appointment of tables: at the beginning of the disease, table No. 7a is prescribed, it is adhered to for one week, then they switch to a month of table No. 7b, after which they eat according to table No. 7 for a year. But, given all of the above, nutrition in acute glomerulonephritis should be balanced.

Not only a diet, but you should also adhere to strict bed rest, as well as avoid hypothermia and drafts.

Acute glomerulonephritis, treatment, drugs

The main therapy for acute glomerulonephritis is medication. In the event that an exact connection of glomerulonephritis with a previously transferred disease with a streptococcal infection is established. As an antibacterial therapy, oxacillin is used in half a gram up to four times a day by intramuscular injection, or erythromycin in a quarter of a gram with the same frequency of use.

An important point in the treatment of acute glomerulonephritis is the use of immunosuppressive therapy. Such treatment is indicated in the absence of hypertensive syndrome, in the presence of a long course of pathology and signs of acute renal failure. Prescribe glucocorticoids such as prednisolone, or methylprednisolone in case of excessive activity and progression of the process. The course of admission is one and a half to two months at a dosage of one milligram per kilogram of the patient's body weight. After a period of admission, the dosage is gradually reduced and after which the drug is canceled.

There is another group of drugs that is superior in efficiency to glucocorticoids, but their use should be justified by the low therapeutic effect of prednisolone. Such drugs are cytostatics. These include cyclophosphamide and azathioprine. The first is taken one and a half - two milligrams per kilogram of body weight, azathioprine is administered at two to three milligrams per kilogram of the patient's body weight. The duration of the course is up to eight weeks, after which the effectiveness of the treatment is evaluated, and then the dosage is gradually reduced to the minimum maintenance. The above therapy is an etiotropic treatment for acute glomerulonephritis.

Each patient is treated individually. In rare cases, combination therapy with both glucocorticoids and cytostatics may be necessary. Acute glomerulonephritis in children, pathogenetic treatment and symptomatic therapy is almost the same as in adults, with the exception of dosages depending on the age of the child.

Acute glomerulonephritis, auxiliary therapy

But supportive therapy is also needed. In order to improve blood circulation and nutrition of the kidney parenchyma, namely the glomeruli, anticoagulants and antiaggregants are used. Such drugs are heparin, chimes and trental.

Additionally, if the patient has an increase in blood pressure, calcium agonists, such as verapamil, or ACE inhibitors, capoten, are prescribed.

Each syndrome is treated almost separately. In the presence of edema, fluid is naturally restricted and diuretics (saluretics) are prescribed:

• The most common is furosemide forty to eighty milligrams per day;
• Veroshpiron retains blood potassium and does not remove it. Take up to two hundred milligrams per day.
• Hypothiazide is prescribed up to one hundred mg per day.
• Also, symptomatic treatment is aimed at eliminating the phenomena of hematuria, the manifestations of which do not disappear after exposure to the main pathogenetic treatment. For this purpose, aminocaproic acid is prescribed in tablet form or intravenously by drip for seven days. Further, it is possible to use dicynone intramuscularly. The principles of treatment of the disease acute glomerulonephritis are described by faculty therapy in more detail, indicating the dosages of drugs and their diversity.

Complications such as acute heart failure and eclampsia due to cerebral edema require urgent resuscitation and should be treated in an intensive care unit with proper equipment.

Prevention of acute glomerulonephritis

Measures to prevent this condition are always aimed primarily at eliminating all predisposing factors, treating a chronic focus of infection, and avoiding hypothermia. In the case of a aggravated allergic anamnesis, especially this condition is typical for children, refuse vaccinations, administration of sera and administration of drugs into the body, for the first time, without a sensitivity test, in order to avoid acute drug-induced glomerulonephritis.

Acute glomerulonephritis is always more difficult to treat than to prevent. Especially when it comes to nephrotic glomerulonephritis, which will be described in the next article.

Therefore, any pathology that can provoke the appearance of glomerulonephritis should be diagnosed in a timely manner and treated so that it does not develop into such a complex disease.

Nephrotic glomerulonephritis

Glomerulonephritis is a disease that has many forms, stages, and phases of the course. There are two main types of the disease - acute and chronic. And it is chronic, due to its duration of the course of the disease and the variety of clinical forms, that has several classifications and divisions.

Forms of chronic glomerulonephritis

Chronic glomerulonephritis is divided into several forms of its clinical manifestations, which prevail in this particular case. Allocate:

• hematuric form, which manifests itself in the form of blood impurities in the urine;
• hypertensive, characterized by a predominant increase in blood pressure;
• latent form, clinically manifested by an isolated urinary syndrome;
• mixed, can combine several forms of clinical manifestations;
• and nephrotic form of glomerulonephritis.
• Let us examine in detail the nephrotic form, its clinical manifestations, diagnosis and treatment.

Nephrotic syndrome in glomerulonephritis, pathogenesis

The frequency of occurrence of this syndrome is about twenty percent. This form is a series of immunological reactions in the renal tissue, in which a factor appears in the urine, giving positive reaction on the lupus test, and symptomatically manifests itself polysyndromic.

The main clinical manifestation in this case is proteinuria. Loss of protein in the urine can occur to a significant extent, more than 3.5

grams in the daily amount of urine, this is inherent in the onset of the disease, and moderate, with a tendency to lower proteinuria in the later stages of glomerulonephritis, taking into account the decrease in kidney function.

Such a symptom as proteinuria directly reflects the nephrotic variant of glomerulonephritis. Its presence means a hidden lesion of the glomerular apparatus of the kidneys. Nephrotic glomerulonephritis, or the syndrome of this disease, develops as a result of prolonged exposure to the underlying pathological factor, as a result of which the permeability of the basement membrane of the glomerular filter increases. Then, blood protein and plasma begin to pass through the damaged membrane. This, in turn, causes even greater structural disturbances in the epithelium of the tubules of the kidneys, which aggravates the pathological process even more.

Nephrotic glomerulonephritis in children and adults, symptoms

The main symptom of the disease is the excretion of protein in the urine. As a result of changes in the interstitium of the tubules of the glomeruli of the kidneys and capillaries. In the general analysis of urine, a significant amount of protein is detected, an increase in leukocytes may be present, as a sign of a local inflammatory process, cylinders can be detected. A biochemical blood test proves protein loss, hypoproteinemia appears, a decrease in the amount of albumin and an increase in globulins. Hyperlipidemia, hypercholesterolemia, and triglyceride growth are also observed. In the coagulogram, there is evidence of an increase in fibrinogen, which can lead to complications in the form of thrombosis. The disease has both rapid and slow progression, but as a result it still leads to the development of chronic renal failure.

A patient with chronic glomerulonephritis with a nephrotic form complains of swelling of the face, eyelids, lower extremities in the area of ​​the legs and feet. On examination, you can notice the pallor of the skin and their dryness. The speech of such patients is inhibited, they are not active. The urinary function is disturbed, which manifests itself in the form of oliguria (significantly reduced amount of urine per day). In the case of the development of a severe course of the syndrome, fluid may accumulate in the pleural cavity, abdominal cavity with the development of ascites, and even in the pericardium.

The totality of all symptoms and pathogenetic factors lead to a significant decrease in overall immune reactions which provokes hypersensitivity to various kinds of infections that can complicate the course of the underlying disease.

Nephrotic and nephritic form of glomerulonephritis in children

Children are characterized by the manifestation of chronic glomerulonephritis in the form of nephrotic syndrome, which is similar to that in adults, and nephritic.

Glomerulonephritis with nephrotic syndrome in children has some similarities with nephrotic syndrome. But the main difference is the pathogenesis of the syndrome. It appears as a result of an inflammatory process in the renal tissue, which can be caused not only by glomerulonephritis, but also by other pathological conditions. It manifests itself not only with proteinuria, but also with hematuria, the presence of hypertension, and, in particular, peripheral edema.

The combination of these syndromes is typical for both children and adults, especially in the chronic course of the disease. But most often glomerulonephritis in children, the nephrotic form, is the main diagnosis.

Glomerulonephritis, nephrotic syndrome, treatment

Treatment of this form of the disease is aimed at reducing membrane permeability and protein loss. In this case, the general principles of managing patients with glomerulonephritis remain.

The diet for glomerulonephritis with nephrotic syndrome is shown seventh according to Pevzner, depending on the stage of the disease with various variations (7a, 7b or 7).

The same dietstol is prescribed for diffuse glomerulonephritis, which we will discuss later in the article.

Diffuse glomerulonephritis

Kidney disease diffuse glomerulonephritis is a collective and generic name and refers only to the extent of damage to the tissue of both kidneys.

Allocate acute and chronic diffuse glomerulonephritis.

Acute diffuse glomerulonephritis in children and adults

This pathology develops as a result of infectious diseases (tonsillitis, pneumonia, etc.), most often caused by group A streptococcal infection. There are options for the appearance of diffuse glomerulonephritis as a result of severe hypothermia, especially in conditions of high humidity, as well as after the introduction vaccines or sera.

The etiology of occurrence confirms the pathogenesis of the disease. That is, glomerulonephritis does not occur at the beginning of the infectious process, but after a couple of weeks, which is confirmed by the presence of blood antibodies to hemolytic streptococcus just at the onset of acute glomerulonephritis.

Chronic diffuse glomerulonephritis, pathophysiology, forms

This type of glomerulonephritis is a common pathology, and develops as a result of prolonged acute glomerulonephritis. It is also possible to have an independent onset of the disease, which is most often detected by chance during preventive examinations, since it often proceeds hidden, with minor changes in the general condition of the patient, or in the laboratory. A chronic course may occur as a result of untreated nephropathy of pregnancy. One of the most significant causes of chronic glomerulonephritis today is the autoimmune mechanism. As a result, antibodies are produced to the proteins of the kidney tissue and destroy it, causing local inflammation and destructive changes.

Such glomerulonephritis is a form of Bright's disease.

Also, chronic glomerulonephritis according to its morphological forms is divided into:

• membranous glomerulonephritis;
• Chronic diffuse mesangioproliferative glomerulonephritis;
• Membranoproliferative;
• fibroplastic;
• A form of focal glomerular sclerosis;
• Lipoid nephrosis.

The most common form is diffuse mesangial proliferative glomerulonephritis. Pathology is detected at a young age, more often in the male population. This form is characterized by hematuria and occurs as a result of the accumulation of immune complexes under the endothelium of small vessels of the glomerular filter of the kidneys, namely in the mesangium. This form is prognostically favorable and has a benign course.

Diffuse glomerulonephritis, treatment

The most interesting question of people who are faced with this form of pathology is treatment. There are certain subtleties in the treatment of acute and chronic diffuse glomerulonephritis, but the general principles of managing such patients remain.

Exists pathogenetic treatment, aimed directly at the impact and elimination of the causes of the disease, symptomatic, carried out when the patient has one or another manifestation of the disease, prevention of complications and relapses of the disease, and a therapeutic and protective regimen using diet and hospital stay.

The main drugs that are used for diffuse glomerulonephritis of any course (acute and chronic) are corticosteroids, non-steroidal anti-inflammatory drugs, cytostatics, antibacterial drugs, and means of symptomatic therapy. The same therapy will require diffuse proliferative glomerulonephritis, and any other form of chronic course.

It is also necessary to remember about the exclusion of the influence of predisposing factors, such as hypothermia and harmful working conditions. Conduct timely sanitation of foci of chronic infection and timely treatment acute processes in the body, including acute glomerulonephritis in order to avoid its transition to a chronic course. It is important to conduct preventive examinations for the timely detection of a latent form, which we will discuss in the next article.

Latent glomerulonephritis

Latent glomerulonephritis is one of the forms of the clinical course of chronic glomerulonephritis. This option is very insidious, since for a long time it can be almost asymptomatic for the patient, as a result of which, its timely diagnosis is difficult and, accordingly, treatment is delayed.

This clinical form is the most common among others. Clinically for the patient no visible reasons for anxiety, no swelling, hypertension, the patient is able to work. Only minor phenomena of microhematuria or loss of protein in the urine are suggestive of renal pathology. Rarely, patients may complain of short-term episodes of high blood pressure, minor edema, which may not bother, as well as general weakness and pain in the lumbar region.

Latent glomerulonephritis has a relatively favorable prognosis due to the fact that the disease has a chronic course, and almost always leads to chronic renal failure, but progresses poorly with adequate treatment. Therefore, with the pathology of latent glomerulonephritis, the forum of patients cites as an example many of their own case histories with fairly favorable prognosis for life. It is only necessary to adhere to the treatment regimen, in which, among other things, traditional medicine can be used. About how traditional medicine helps with glomerulonephritis, we will analyze further in the article.

Glomerulonephritis is a disease that needs constant monitoring and treatment. In the arsenal of specialists for the treatment of this pathology are numerous drugs with a powerful effect. But in addition to the main therapy, there is also an auxiliary one, which includes fees for glomerulonephritis according to traditional medicine prescriptions, diet, spa treatment, daily routine, and so on.

Alternative treatment of glomerulonephritis

This type of therapy is only an auxiliary part of the main treatment and can be prescribed or recommended by the attending physician after a detailed examination. On their own, herbs for glomerulonephritis will not cope with the disease, but can only worsen its prognosis.

But it should be noted that fees and decoctions have a positive effect on the course of the disease, reduce inflammatory processes in the kidneys and in the body in principle, and also contribute to the recovery processes, and the removal of fluid from the body and reduce the toxic effect of some drugs of the main drug therapy.

There are many recipes for fees and herbs separately that can help in the fight against glomerulonephritis. Let's consider some of them.

Quite common in urological practice is the kidney collection, which includes plantain, horsetail, rose hips, calendula, yarrow, string. This infusion is recommended to be taken three times a day for half a glass.

Also, folk medicine proposed a recipe for a decoction of flax seeds, harrow, birch leaves. The effect of the decoction will be observed when using one glass a day for a long course.

Well-established in matters of combating the pathology of the kidneys of celery. The juice of this plant must be applied fresh daily at fifteen milliliters. But it is possible to take not only celery juice. Recommend pumpkin juice, birch in an amount equal to the drinking regime. Such a drink is a good alternative to drinks such as tea for glomerulonephritis.

Corn silk always good helpers with kidney disease. To do this, make an infusion in the proportion of a teaspoon of raw materials per half liter of boiling water, you can also add cherry ponytails. After that, the broth is insisted for several hours and taken one dessert spoon up to four times a day. This remedy has a diuretic effect, reduces the severity of edema.

There are also delicious recipes. To do this, you need to take one glass of honey, one hundred grams of figs, a few lemons and walnuts, with glomerulonephritis, such a remedy will improve kidney function. It should be taken in the form of mixed ground raw materials, two tablespoons on an empty stomach once a day.

As a tea, a decoction of sea buckthorn branches is used. Its restorative properties are used in many branches of medicine.

The treatment of glomerulonephritis with folk remedies is widely used. For this, a decoction is prepared from one heaping spoonful of raw materials and a quarter liter of boiled hot water. The prepared broth must be divided into four doses.

In addition to folk remedies, you should remember about the daily routine and special nutrition.

Dietstol with glomerulonephritis

A doctor with glomerulonephritis prescribes a specialized diet, once developed by a nutritionist Pevzner. The main idea of ​​all subspecies of this food (7a, 7b) is the restriction of protein, salt, spices. Of course, alcohol is excluded. Table No. 7a is prescribed for acute glomerulonephritis or exacerbation of a chronic process. Table No. 7b is a continuation of the previous one, when the remission of the disease is achieved.

The method of cooking is mainly boiled and stewed, you can take lightly fried foods without breading. Meat and fish should be pre-boiled, and the broth should not be consumed, due to the accumulation of extractive substances in it.

• lean poultry, fish, preferably sea, beef;
• unleavened pastries, eggs, limited;
• low-fat sour-milk and dairy products;
• most vegetables, berries and fruits in any form;
• sugar, honey, cereals, pasta;
• up to twenty grams of butter per day when added to ready meals;
• vegetable refined oil for cooking;
• fruit and vegetable juices diluted with water in equal proportions.

It is forbidden to eat the following foods and dishes:

• smoked and pickled, even homemade;
• semi-finished products and sausage products of factory production;
• broths, margarine, spices and spicy foods;
• mushrooms, sorrel, peas, beans, radishes, onions and garlic;
• fatty meats (pork), fatty fish;
• carbonated drinks, strong black tea, coffee, hot chocolate;
• alcoholic beverages, regardless of strength.

It should be noted that the diet is designed in such a way as to take into account all the body's needs for nutrients, vitamins, and proteins, but at the same time minimize the burden on the kidneys.

Do not forget about the regime of the day and such health-improving institutions as a sanatorium, (glomerulonephritis), folk remedies are also helpful in the fight against disease. But, before going to the resort, you should achieve a stable remission of glomerulonephritis, as well as consult with a specialist.

The daily regimen should be gentle with this pathology. Sports with glomerulonephritis, especially acute and chronic exacerbation, are contraindicated. Otherwise, during the period of attenuation of symptoms in each case, depending on the sport, you should consult with your doctor.

In the event of the development of this disease, the patient should be given proper care, especially if there are complications and the process is rapidly progressive.

In order to find out what kind of care is needed for patients with glomerulonephritis, you should familiarize yourself with the material of the following article.

Care for glomerulonephritis

With glomerulonephritis, constant patient care is necessary, especially for situations with exacerbation of chronic and acute conditions of glomerulonephritis, as well as in case of complications of this disease. As a rule, such care is provided by medical personnel, since patients are in hospital.

Nursing care for glomerulonephritis

The duties of a nurse include not only fulfilling the doctor's prescriptions and performing manipulations, but also creating the proper conditions for patients for their speedy recovery. Comfort, treatment, nutrition and the effectiveness of treatment depend on the proper actions of a nurse. The work of nursing staff includes several points - this is to assist in recovery, improvement general condition patient, preventive actions and relief of the condition in the event of complications that bring suffering to the patient.

In addition to the fact that the nurse performs all the necessary doctor's orders for the collection of media for laboratory tests, preparing the patient for a particular diagnostic measure, as well as the direct administration of drugs, her duties include monitoring the frequency of taking tablet medicines and monitoring the general condition of the patient. At the same time, the nursing process for glomerulonephritis in adults and children is a series of measures to provide assistance and dynamic monitoring. The nurse is on duty next to the sick, and it is her responsibility to monitor the condition of the patients. At different times of the day, the patient may present certain complaints directly to the nurse, who, in turn, reports these data to the doctor. Also, its functions include the constant measurement of blood pressure, temperature and calculation of the daily diuresis of patients suffering from glomerulonephritis.

It is also necessary to take into account the fact that nursing care with glomerulonephritis, it also consists in assessing the quality of nutrition and meals. The sister monitors the implementation of the recommendations of the attending physician on dietstol. And in case of detection of errors in nutrition or its non-compliance, it conducts explanatory work with the patient or his relatives on compliance with the regimen.

Nursing interventions for glomerulonephritis

All the items indicated in the prescription list are performed by the nurse. The main interventions are intramuscular and intravenous drug injections. Also, if necessary, in the diagnosis, especially through radiography, and other methods, the nurse prepares the patient as follows:

• Explain the principle of preparation for the study to the patient;
• Monitor compliance with the fourth diet table on the eve of the study;
• Control the intake of a laxative before the procedure or perform an enema of the intestine;

Since with glomerulonephritis the patient's condition is constantly monitored through urine tests, the nurse explains:

• how to collect liquid;
• in what capacity and at what time of the day;
• how to label a container with collected urine;
• teach how the patient can independently collect data on daily urine output.

One of the main tasks of medical personnel is emergency care for glomerulonephritis. This disease is accompanied by severe edema, hypertension and other complications that can provoke the appearance of an emergency. But taking into account the fact that it is the nurse who is constantly with the patients, the further prognosis of the patient's condition will depend on her initial actions. And so, with the disease glomerulonephritis, the standard of medical care for the spontaneous occurrence of severe complications:

• In the case of the development of eclampsia, they try to prevent biting the tongue (put a handkerchief or a rubberized object between the teeth). Also administered intravenously or intramuscularly magnesium sulfate 25 percentage solution and 20-30 milliliters of 40 percent glucose;
• Convulsive syndrome is removed with sibazon;
• If excessively high blood pressure figures occur, it is reduced with sodium nitroprusside 10 mcg per kilogram of body weight per minute or labetalol. Furosemide may be used good effect administers nifedipine sublingually or intravenously;
• But always first of all, the nurse informs the doctor about the occurrence of acute conditions.

In cases where the patient is at home with a pathology of glomerulonephritis, the clinic, nursing care can be provided by agreement as a state aid, or privately in cooperation with commercial structures.

Of course, the disease glomerulonephritis, patient care requires constant, and not only during treatment, but also during prevention, the activities of which will be the next article.

Prevention

Any pathological condition in medicine, it is possible and costly to prevent, this also applies to glomerulonephritis. The basics of preventive methods for acute and chronic glomerulonephritis are the same.

Glomerulonephritis prevention primary and secondary

Prevention measures can be divided into primary and secondary.

Primary prevention of glomerulonephritis is a set of measures aimed at preventing the occurrence of this disease in people predisposed to it by the presence of certain factors. That is, in the presence of harmful working conditions, it is necessary to change them, avoid hypothermia and prolonged exposure to a humid cold climate. Also, do not inject drugs for the first time, without conducting an appropriate test for them in people with high allergization of the body. The same applies to vaccinations, and the introduction of various sera. When a focus of streptococcal infection appears, immediately begin treatment and dynamic monitoring of the state of all organs and systems, including the kidneys. Regularly carry out preventive examinations and conduct an ultrasound examination of the urinary system.

Secondary prevention of glomerulonephritis includes preventing the recurrence of the disease when it occurs even once (this applies to acute glomerulonephritis), or its progression (in the presence of a chronic course). To do this, the patient must adhere to a special diet, reduce physical activity, and exclude active sports. It is necessary to change working conditions to more favorable ones, you also need to regularly undergo prescribed treatment and observation by a nephrologist, if there are indications, be hospitalized in a hospital.

In the prevention of glomerulonephritis, the role of sanatorium treatment, timely rehabilitation after glomerulonephritis is important. This program is designed for the period after acute glomerulonephritis, as well as rehabilitation for chronic glomerulonephritis, with the attenuation of symptoms and the achievement of clinical and laboratory remission. It is a complex therapeutic gymnastics and exercises to stabilize the condition, reduce congestion, improve renal blood flow, the activity of the cardiovascular system, and normalize the emotional status of the patient. As well as adherence to dietstol and taking some herbal remedies or traditional medicine under the supervision of a specialist and only with his appointment and recommendations. Each set of exercises is assigned individually according to a specific program.

But any rehabilitation and prevention should be carried out competently and under the supervision and with the consent of a specialist, since non-compliance with certain rules of conduct can lead to a deterioration in the patient's condition and the development of complications. We will describe what complications may arise in the next article.

Complications of glomerulonephritis

Both acute and chronic glomerulonephritis can provoke the development of severe complications, as well as lead to undesirable consequences.

The main complications of glomerulonephritis in adults

As a rule, complications can develop in acute glomerulonephritis and the progressive course of chronic glomerulonephritis. For example, in the case of the development of uncontrolled hypertension, or anuria and other symptoms and syndromes that accompany this disease. What is dangerous glomerulonephritis:

• Acute renal failure may develop;
• The appearance of acute heart failure;
• Cerebral edema provokes the development of an eclamptic state;
• Due to a violation of blood clotting, thrombosis develops and the risk of developing pulmonary embolism;
• Hemorrhagic stroke of the brain is also observed as a complication of glomerulonephritis;
• Due to prolonged high blood pressure, retinopathy appears, turning into retinal detachment;

Consequences of glomerulonephritis

The adverse consequences of this disease include the development of disability in the patient, as a result of the complete loss of kidney function and forced permanent hemodialysis. The constant need for observation and inpatient treatment should be taken into account due to the appearance of a aggravated course of the disease and limitations in the patient's life. Also, with the development of some complications, in the absence of an adequate response of the body to ongoing emergency measures and therapy, the death of the patient may occur. Also, a fatal outcome is observed not only after the development of an attack of eclampsia, for example, or hemorrhage in the brain, but as a result of failures of all compensatory mechanisms and the onset of decompensation. For example, prolonged high blood pressure adversely affects the body as a whole and exacerbates the course of the disease. We will talk about this and much more in the next article.

pressure in glomerulonephritis

Arterial hypertension in glomerulonephritis is an integral symptom in its acute and chronic course.

Pressure in acute glomerulonephritis

Acute glomerulonephritis, in addition to all the variety of symptoms, is manifested by an increase in blood pressure. As a rule, the pressure does not reach high figures, while the systolic can be about 180, and the diastolic is about 120 mm Hg. At the same time, hypertension does not last long and responds quite well to medical correction. But, also in the presence of high blood pressure, acute left ventricular failure can develop with further pulmonary edema, and as a result, lead to myocardial hypertrophic processes. It is also possible that it affects the brain due to swelling of its tissue, which provokes an attack of eclampsia.

The mechanism of blood pressure increase in chronic glomerulonephritis

In chronic glomerulonephritis, there is also a symptom of increased blood pressure, and if this symptom is present, even one of the clinical forms of glomerulonephritis, hypertensive, is distinguished as the main one. At the beginning of the development of the disease, blood pressure with glomerulonephritis rises slightly, episodes of increased blood pressure are rare and patients rarely seek help with them. As the pathology progresses, hypertension becomes stable, diastolic pressure especially often rises, and reaches high numbers. Although the course of the disease is slow, it tends to progress. As a result, in the pathology of glomerulonephritis, renal failure occurs.

This symptom entails many disorders and complications. Chronic renal failure is associated with retinopathy, edema optic nerve retinal detachment may occur. Headaches, pains in the region of the heart, rhythm disturbances also appear.

The very mechanism of increasing blood pressure is based on the excess accumulation of fluid in the body, including in the bloodstream, as a result of which the volume of circulating blood increases, which causes the heart muscle to contract more actively in order to “drive” the resulting volume throughout the bloodstream. Following this, peripheral vascular resistance is formed, which further exacerbates the situation. As a result, the heart is forced to push through an already significant volume of blood, but in addition to this, it also has to overcome the increased resistance of the vascular wall. Also, at the same time, activation of coagulation and fibrin deposition in the renal tubules occurs, as a result of which the resistance of capillaries in the kidneys increases, blood thickens, which becomes more difficult to push through small vessels, and the circle closes.

These phenomena in the case of chronic glomerulonephritis are formed for a rather long time, but steadily lead to persistent hypertension. It should be noted that for any pathology of glomerulonephritis, the pulse is not an indicative symptom, only if heart failure has not formed.

Forecast of arterial hypertension

In the case of increased pressure in acute glomerulonephritis, the prognosis is quite favorable due to the high frequency of curability of this disease. As a result, the symptom of hypertension also disappears with the pathology.

With a chronic course, the pathology is more complicated. It is necessary to select a symptomatic therapy that corrects pressure and strictly observe it. Including there are many restrictions for such patients. And which ones, read on.

Restrictions

Glomerulonephritis serious illness requiring an integrated approach to treatment. Taking into account the pathogenesis, glomerulonephritis requires patients to comply with all the rules for lifestyle, nutrition, daily routine, in which there are many restrictions. We will analyze the main ones in the mode of answering a question.

Is it possible to play sports with glomerulonephritis?

The disease in the stage of attenuation of symptoms provides for rehabilitation in the form of physiotherapy exercises in order to increase the tone of the whole body, improve renal blood flow and urine outflow. But, if the patient was professionally engaged in sports before the illness, then increased physical activity is contraindicated in chronic, and is limited until the moment of recovery in acute glomerulonephritis. You can not participate in sports competitions and championships a year after the postponed acute illness, and throughout life in chronic course.

Of course, each case is unique and you need to approach it individually, and before physical activity, consult with a specialist.

Is it possible to eat seeds with glomerulonephritis?

According to the diet tables developed for this disease, namely No. 7, No. 7a, No. 7b, sunflower seeds are contraindicated in food. Since the product is fatty and also fried, which does not correspond to the basic concept of the entire diet for glomerulonephritis.

Can glomerulonephritis be cured on its own?

Glomerulonephritis is a disease in which an indispensable hospitalization is indicated, since it can result in various life-threatening conditions for the patient. In the case of self-treatment attempts, the patient's condition can worsen dramatically, which will lead to irreparable consequences, numerous severe complications, or even death. And in the case of an acute process - its transition to a chronic one. Therefore, it is best to entrust the treatment of glomerulonephritis to specialists.

When developed glomerulonephritis, is it possible to drink alcohol?

Alcohol is a terrible enemy in any kidney disease, as it carries a heavy load on the excretory function of the body. In the case of glomerulonephritis, in the presence of serious damage to the glomerular filter, as a result of which the process of filtering the waste products of the body is difficult. Therefore, if the kidneys are also loaded with alcohol breakdown products, many serious conditions can be provoked, including the development of acute renal or heart failure.

One of the most common questions is the question of the possibility of carrying a pregnancy with glomerulonephritis, which we will discuss in the next article.

Glomerulonephritis during pregnancy

In pregnant women, acute glomerulonephritis is quite rare, possibly due to increased production of glucocorticoids. There are also rare cases of exacerbation of chronic glomerulonephritis, but pathology during pregnancy takes place, and greatly aggravates the course of pregnancy.

How does glomerulonephritis occur during pregnancy

A number of scientists have conducted studies of patients who, during pregnancy, suffered preeclampsia on later dates. As a result of a puncture biopsy of the kidneys, signs of glomerulonephritis were morphologically revealed in all examined women. Therefore, it can be assumed that glomerulonephritis can be hidden under the mask of preeclampsia, and possibly even provoke its onset during pregnancy.

As a rule, glomerulonephritis in pregnant women occurs with signs of hypertensive, nephrotic and mixed syndromes.

The hypertensive form of glomerulonephritis in the event of pregnancy is the risk of many complications of both pregnancy and the woman's health. Against the background of constant hypertension, abortion can occur at short terms; at later gestation periods, such interruptions cause massive uterine bleeding. There is also a growing risk of intrauterine growth retardation due to constantly disturbed blood flow due to spasm of peripheral vessels. It should be noted the high risk of preeclampsia and eclampsia during pregnancy, compared with the usual state of women with this disease. The development of eclampsia is a risk to the fetus, and also endangers the health and even life of the mother.

Against the background of glomerulonephritis during pregnancy with nephrotic syndrome, there is also an unfavorable prognosis. This clinical form is accompanied by massive proteinuria, hypercholesterolemia, and the presence of edema, which can develop up to anasarca. In such a critical state of the body, premature detachment of the placenta with the development of bleeding may develop, and cases of antenatal death of the fetus are possible.

Also, in women with membranous nephropathy, severe complications can occur during pregnancy. This pathology is accompanied and complicated by thrombosis of small renal vessels, and subsequently of the renal veins, which can provoke acute renal failure, as well as lead to separation of a blood clot and pulmonary embolism.

Glomerulonephritis: can you give birth or not

The issue of carrying a pregnancy in the presence of glomerulonephritis in a woman is decided in each individual case purely individually based on all diagnostic data and only in a hospital setting. But, in total, we can say with confidence that the presence of glomerulonephritis is a high risk of obstetric complications, which a woman should be fully aware of before bearing.

Also, women suffering from glomerulonephritis are concerned about the method of delivery: is it possible to give birth with glomerulonephritis on their own or not. As in the case of gestation, such a decision is a combination of both nephrological and obstetric and general somatic factors. A woman must be hospitalized in advance in an obstetric hospital of the third level of accreditation, where the council decides on the conduct of childbirth. Generally speaking, it is always recommended to conduct childbirth conservatively, that is, naturally, and only according to strict indications to proceed with operative delivery.

You can also learn a lot of interesting information on the forums. About pregnancy with glomerulonephritis, the women's forum will tell you firsthand. But you should not completely trust everything that has been said, since each case is unique and needs an individual clinical analysis.

Forecast

The prognosis for the disease glomerulonephritis largely depends on the course of the disease (acute or chronic), on clinical form, progression, etc.

Prognosis of acute glomerulonephritis

The prognosis for the development of acute glomerulonephritis also largely depends on its clinical course, however, in terms of health and life, it is more favorable in comparison with its chronic course. But often, if acute glomerulonephritis has been started, or is poorly amenable to drug treatment, and lasts more than a year, then it can turn into chronic, and as a result, the prognosis for recovery changes. By itself, the acute process is quite productively cured, resulting in recovery. But even after that, the patient needs to continue observation and adherence to the regimen for another year in order to exclude the transition to a chronic course.

Prognosis for chronic pathology

In the case of the development of chronic glomerulonephritis, depending on the clinical and morphological form, the forecasts change. Thus, hematuric glomerulonephritis has a relatively favorable life prognosis, but in any case, chronic renal failure develops within ten to fifteen years if all recommendations and regular treatment are followed.

In the disease of autoimmune glomerulonephritis, the prognosis depends on the degree of damage to the renal tissue and the degree of progression of the process. The chronic course of pathology is most often caused by an autoimmune process in the body. To prolong the functioning of the kidneys and improve the quality of life, the patient needs to undergo ongoing treatment. Recovery in such a situation does not occur.

Priority problem in glomerulonephritis

To understand the possible chances of recovery or a long-term favorable course of the disease, the pathogenesis of glomerulonephritis should be taken into account. Indeed, as a result of the pathological process, immune destruction and inflammation of the glomerular tubules occurs. It is also necessary to take into account all risk factors and complications that have arisen during the course of the disease. In the presence of a hypertensive form, there are always risks of the appearance of pathological processes in cardiovascular system or pathology of the retina.

All forms of the chronic course of the disease can lead to disability, and this is the main problem of glomerulonephritis. It should also be remembered that kidney failure and complete shrinkage of the kidney can always develop, which entails a complete loss of its function. And, as you know, life is impossible without this organ, and such patients have to undergo hemodialysis regularly, and organ transplantation is not excluded - these are potential problems with glomerulonephritis.

The resulting glomerulonephritis brings the patient's problems mainly in the form of discomfort, which lies in the need for dynamic clinical observation, treatment and constant diagnosis. The usual rhythm of life is also changing, there are many restrictions on physical activity, food and so on.

It must be remembered that only acute glomerulonephritis has a chance for a complete recovery, and chronic, depending on the form of the course, always leads to the development of chronic renal failure, and even to the death of the patient. And what is most unpleasant about this disease is that the pathology most often affects a young age, especially small children, mostly males, can be affected. The occurrence of glomerulonephritis in a child worsens the further prognosis for his health and life. We will consider in more detail about the course of glomerulonephritis in childhood in the next article.

Glomerulonephritis in children

Glomerulonephritis is a polyetiological disease, with elements of immune inflammation of the renal tissue, mainly the glomeruli. Most often, this pathology is bilateral in nature, and occurs as a result of an infectious factor.

Glomerulonephritis in children, etiology

Do not write off predisposing factors, such as prolonged hypothermia, the influence of a cold, humid climate.

All of the above options are a trigger for the production of antibodies and the deposition of immune complexes on the vascular endothelium and membranes of the renal glomeruli. As a result, there is a process of local inflammation in the glomerular apparatus.

Syndromes of glomerulonephritis in children, pathogenesis, classification

Depending on the various manifestations of both clinical and morphological, as well as the course, the following types of glomerulonephritis in children are distinguished:

• By pathogenesis:
• The primary variant with the presence of an immune complex, which is characterized by an acute onset and recovery during treatment within one year.
• And secondary glomerulonephritis in children, the pathogenesis of which is an autoimmune variant with the development of inflammatory immune processes of one's own body against the endothelium of one's own renal vessels and glomerular membranes.
• They are also classified according to the course into an acute and chronic process;
• The stages are divided into the stage of exacerbation, remission, which in turn is divided into complete and incomplete;

From the forms of the clinical course, otherwise called syndromes, are presented:

• Nephrotic
• Hematuric
• mixed

According to the functional state of the kidneys:

• With stored function
• With impaired kidney function

And by morphological features divided into:

• Proliferative glomerulonephritis in children
• Non-proliferative.
• Let us examine in more detail the syndromes or forms of the clinical course in children.

Glomerulonephritis in children, clinical forms

The nephrotic form or syndrome affects children between the ages of one and seven. Pathology glomerulonephritis in the total mass covers the male sex more than the female. Clinically, this syndrome manifests itself in the form of significant edema, which can be aggravated and present in the chest cavity, pericardial cavity and abdominal cavity. There are also symptoms of general intoxication, nausea, weakness, lethargy, pallor of the skin. During an objective examination, the doctor notes an increase in the size of the liver, a significant proteinuria is detected in a laboratory study, and hematuria may appear. In a clinical blood test, high ESR, leukocytosis, in a biochemical study of blood serum - hyperlipidemia, hypoproteinemia.

The clinic of glomerulonephritis in children with hematuric syndrome manifests itself in the form of moderate edema, more often located on the face, weight loss, and most importantly, an increase in blood pressure. Hypertension can appear from a few hours and last up to several days. The child may have a headache, nausea, fever. An objective examination of the doctor notes the presence of tachycardia, muffled heart sounds. Also, in the hypertensive form, there is a urinary syndrome with the presence of blood in the urine and protein. In a laboratory examination of the patient, leukocytosis, an increase in ESR, and hypercoagulability are detected. This form is typical for the age group after five years.

If a child has a mixed form of the clinical course, the symptoms of the disease will be as follows: an increase in blood pressure with a tendency to progression, the spread of edema in the lower extremities, face, and more. The doctor notes an increase in the size of the child's liver, as well as symptoms of intoxication of the body (fever, nausea, vomiting, weakness, physical inactivity). Also, poststreptococcal glomerulonephritis in children is also manifested by urinary syndrome, which indicates severe damage to the glomerular apparatus.

Treatment and dispensary observation of children with glomerulonephritis

The approach to treatment, especially in childhood, is complex and is aimed at the impact of etiological and pathogenetic factors, as well as symptomatic treatment.

Inpatient treatment with strict bed rest.

Diet table number 7a (b).

Antibiotic therapy with penicillins or macrolides if tolerated.

The use of anticoagulants - chimes, heparin, as well as non-steroidal anti-inflammatory drugs.

Symptomatic therapy consists in lowering and stabilizing blood pressure, reducing swelling and increasing the amount of urine per day.

After achieving clinical and laboratory remission or complete recovery, the child is under the supervision of nephrologists for a long time and adheres to the necessary recommendations.

In the case of diseases such as pyelonephritis, glomerulonephritis in children, the prognosis for the future is often favorable. But in the event of an episode of recurrence of the disease glomerulonephritis within five years after its cure, the pathology is considered chronic. Long-term chronic glomerulonephritis, or rapidly progressive always sooner or later leads to the development of chronic renal failure.

Often, parents who are diagnosed with glomerulonephritis in children use the forum as a hint on what to do in this situation. It is only worth noting that with this pathology, it is necessary to seek specialized help in a hospital, since pediatrics considers pediatric glomerulonephritis as a rather severe pathology that cannot be dealt with at home alone.