Renal failure stage classification. Symptoms of chronic renal failure, stages, methods of treatment, drugs

Chronic renal failure (CRF) is a term that covers all degrees of reduced kidney function, from mild to moderate to severe. CKD is a global public health problem. Globally, there is an increase in morbidity with a poor outcome due to the high cost of treatment.

What is chronic renal failure

Chronic renal failure (CRF) or, according to the new terminology, chronic illness Kidney disease (CKD) is a type of disease in which there is a gradual loss of organ function over several months or years. On the early stages symptoms are often absent. They appear later, when the work of the organ is already significantly impaired. CKD is more common among older people. But while younger patients with chronic kidney disease typically experience progressive loss of kidney function, about a third of patients over 65 with CKD are stable.

The disease is associated with the death of the main functional units of the kidney - nephrons.. Their place is filled with connective tissue. As the scar tissue inside the organ becomes more than functioning, kidney failure progresses directly, which can, with a high degree of probability, lead to the extinction of kidney activity.

Chronic renal failure is a gradual decline in renal function due to the death of nephrons.

CKD is associated with an increased risk cardiovascular diseases and is the ninth leading cause of death in the United States.

In 2002, an organization called the National Kidney Foundation (USA) developed an international classification and definition of CKD. According to her, chronic renal failure is defined on the basis of:

• signs of kidney damage;
• decrease in glomerular filtration rate (GFR - the rate at which the kidneys filter blood) to a value of less than 60 ml / min / 1.73 m 2 for at least 3 months.

Whatever the underlying cause, when the loss of nephrons - the functional units of the kidney - reaches a certain point, the remaining ones also begin the process of irreversible sclerosis, leading to a gradual decline in GFR.

Classification and stages

The various stages of chronic renal failure reflect the five stages of the disease, which are classified as follows:

1. Stage 1: Kidney injury with normal or elevated GFR (> 90 ml/min/1.73 m2).
2. Stage 2: moderate decline in GFR (60–89 ml/min/1.73 m2).
3. Stage 3a: moderate decline in GFR (45–59 ml/min/1.73 m2).
4. Stage 3b: Moderate decline in GFR (30–44 mL/min/1.73 m2).
5. Stage 4: severe decrease in GFR (15–29 ml/min/1.73 m2).
6. Stage 5: kidney failure (GFR<15 мл/мин/1,73 м 2 или диализ).

At the stage of the first two stages of CKD, the glomerular filtration rate is not decisive for the diagnosis, because it can be normal or borderline. In such cases, the diagnosis is made when one or more of the following markers of kidney damage are present:

• albuminuria, or proteinuria, - excretion of protein in the urine (> 30 mg / 24 hours);
• abnormal urine sediment;
• electrolyte and other pathologies caused by disorders of the tubular system;
• kidney tissue damage;
• structural anomalies detected during imaging studies;
• history of kidney transplantation.

Hypertension is a common feature of CKD, but should not be considered in itself as an indicator of CKD, as high blood pressure is also common among people without CKD.

When determining the stage of the disease, it is necessary to consider the indicators of GFR and albuminuria together, and not separately. This is necessary to improve the predictive accuracy of CKD assessment, namely, when assessing risks:

• overall mortality;
• cardiovascular diseases;
• end-stage renal failure;
• acute renal failure;
• progression of CKD.

Clinical manifestations caused by poor kidney function usually appear in stages 4-5. 1-3 degrees of the disease are often asymptomatic.

Causes of Chronic Kidney Disease

Diseases and conditions that cause chronic kidney disease include:

• type 1 or type 2 diabetes;
• high blood pressure;
• glomerulonephritis - inflammation of the filtering units of the kidneys (glomeruli, or glomeruli);

  Chronic glomerulonephritis can develop into renal failure

• interstitial nephritis - inflammation of the tubules of the kidney and surrounding structures;
• polycystic kidney disease;
• long-term obstruction of the urinary tract due to an enlarged prostate, stones, and certain types of cancer;
• vesicoureteral reflux - the reverse flow of urine through the ureters to the kidneys;

  One of the complications of vesicoureteral reflux is the development of CKD.

• chronic kidney infection (pyelonephritis).

Additional factors that increase the risk of the disease include:

• cardiovascular diseases;
• obesity;
• smoking;
• hereditary predisposition to kidney disease;
• abnormal structure of the kidneys;
• old age.

Symptoms of the disease

Usually, before the onset of stage 4–5 CKD, the patient does not have clinical manifestations endocrine / metabolic disorders or disturbances in water and electrolyte balance. There are the following complaints of patients, allowing to suspect kidney disease and violation of their functions:

• pain and discomfort in the lumbar region;
• change in the type of urine (red, brown, cloudy, frothy, containing "flakes" and sediment);
• frequent urge to urinate, imperative urge (it is difficult to endure the urge, you must immediately run to the toilet), difficult urination (sluggish stream);
• decrease in the daily amount of urine (less than 500 ml);
• polyuria, violation of the process of concentrating urine by the kidneys at night (regular urge to urinate at night);
• constant feeling of thirst;
• poor appetite, aversion to meat food;
• general weakness, malaise;
• shortness of breath, decreased exercise tolerance;
• increased blood pressure, often accompanied by headaches, dizziness;
• pain behind the sternum, interruptions in the work of the heart;
• skin itching.

Symptoms of chronic kidney disease appear already in the last stages

The end stage is one of the last in chronic renal failure, it is characterized by total loss functionality of one or both kidneys. With it, uremia develops - poisoning of the body with its own metabolic products. Its manifestations include:

• pericarditis (inflammatory lesion of the lining of the heart) - can be complicated by cardiac tamponade (disturbance of heart contractions due to fluid accumulation), which can lead to death if not diagnosed and treated;
• encephalopathy (non-inflammatory brain damage) - can progress to coma and death;
• peripheral neuropathy (violation of the transmission of nerve impulses) - leads to the failure of certain organs, tissues, muscles;
• gastrointestinal symptoms - nausea, vomiting, diarrhea;
• skin manifestations - dry skin, itching, bruising;
• increased fatigue and drowsiness;
• weight loss;
• exhaustion;
• anuria - a decrease in the daily volume of urine to 50 ml;
• erectile dysfunction, decreased libido, lack of menstruation.

Studies also show that 45% of adult patients develop depression, which has somatic manifestations (trembling in the hands, dizziness, palpitations, etc.). Depression of this kind usually appears on the background of diseases internal organs.

Video: signs of impaired kidney function

Diagnostic methods

Diagnosis and treatment of chronic kidney disease is carried out by a nephrologist. Diagnosis is based on clinical history, physical examination, and urinalysis combined with measurement of serum creatinine.

It is important to differentiate CRF from acute renal failure (ARF) because AKI may be reversible. In CRF, there is a gradual increase in serum creatinine (over several months or years), in contrast to the sudden increase in this indicator in AKI (from several days to several weeks). Many patients with CKD have previously had some kind of kidney disease, although a significant number of patients develop the pathology for unknown reasons.

Laboratory methods

The following laboratory tests are used to make a diagnosis:

1. Rehberg's test - is designed to determine GFR using a special formula, which is substituted for the volume and time of urine collection in minutes, as well as the concentration of creatinine in the blood and urine. For analysis, blood is taken from a vein (in the morning on an empty stomach), as well as two hourly portions of urine. If the result is less than 20 ml/min per 1.73 m² of GFR, then this indicates the presence of CKD.
2. Biochemical analysis blood - taken from a vein, the following indicators indicate the disease:
   • serum creatinine more than 0.132 mmol/l;
   • urea more than 8.3 mmol/l.

With the death of less than 50% of nephrons, chronic renal failure can be detected only with a functional load. Additional laboratory tests used in the diagnosis of CKD may include:

• Analysis of urine;
• the main metabolic panel - a blood test that shows the body's water and electrolyte balance;
• checking the level of albumin (protein) in the blood serum - in patients with CKD, this indicator decreases due to malnutrition, loss of protein in the urine, or chronic inflammation;
• blood lipid analysis - patients with CKD have an increased risk of cardiovascular disease.

Imaging studies

Imaging tests that may be used in the diagnosis of chronic kidney disease include the following:

Patients with CKD should avoid x-ray studies that require intravenous contrast material, such as angiogram, intravenous pyelogram, and some CT scans, as these can cause more damage to the kidneys.

Ways to treat chronic kidney disease

Early diagnosis, treatment of the underlying cause, and introduction of secondary preventive measures are essential for patients with chronic kidney disease. These steps can delay or stop the progression of the pathological process. Extremely importance has an early referral to a nephrologist.

Depending on the underlying cause, some types of chronic kidney disease are partially treatable, but in general there is no specific cure for kidney failure. Health care for patients with CKD should focus on the following:

• delay or stop the progression of CKD;
• diagnosis and treatment of pathological manifestations;
• timely planning of long-term renal replacement therapy.

Treatment of chronic renal failure depends on the underlying cause and is aimed at controlling symptoms, reducing complications, and slowing progression.

Treatment options for CKD differ depending on the cause. But kidney damage can continue to worsen even if the underlying condition, such as high blood pressure, is controlled.

Medical treatment of the early stage of the disease

Treatment of complications includes the use of such groups of drugs:

1. Medicines for high blood pressure. Kidney disease is often associated with chronic hypertension. Blood pressure medications—usually angiotensin-converting enzyme (ACE) inhibitors or angiotensin II receptor blockers (ARBs)—are given to preserve kidney function. Keep in mind that these drugs can initially reduce organ function and alter electrolyte levels, so frequent blood tests will be needed to monitor the condition. The nephrologist prescribes a diuretic (diuretic) and a low-salt diet at the same time.
2. Medications to lower cholesterol. People with chronic kidney disease often suffer from high levels of bad cholesterol, which can increase their risk of heart disease. In this case, the doctor prescribes medications called statins.
3. Drugs for the treatment of anemia. In certain situations, the nephrologist recommends taking the hormone Erythropoietin, sometimes with the addition of iron. Erythropoietin increases the production of red blood cells, which reduces fatigue and weakness associated with anemia.
4. Medications to minimize swelling (diuretics). People with chronic kidney disease often suffer from excess fluid buildup in the body. This can lead to swelling in the legs and high blood pressure. Diuretics help maintain fluid balance in the body.
5. Medications to protect bones. Your doctor may prescribe calcium and vitamin D supplements to prevent brittle bones and reduce the risk of fracture. Phosphate binders are sometimes needed to lower the amount of phosphate in the blood and protect blood vessels from damage by calcium deposits (calcification).

Specific names of drugs for patients with chronic renal failure are prescribed by a nephrologist individually. At regular intervals, it is necessary to pass control tests that will show whether the kidney disease remains stable or progresses.

Photo gallery: drugs prescribed for kidney failure

Captopril - effective remedy to normalize blood pressure and reduce proteinuria Losartan normalizes blood pressure and improves kidney function in their chronic insufficiency.
Renagel binds phosphates in the digestive tract, reducing their concentration in blood serum and protecting blood vessels from calcification. Erythropoietin stimulates the production of red blood cells, helping to treat anemia

Treatment of advanced chronic kidney disease

When the kidneys can no longer cope with the excretion of waste and fluid on their own, this means the transition of the disease to the final (terminal) stage of chronic renal failure. At this point, dialysis or organ transplantation becomes vital.

Dialysis

Dialysis is a lifelong non-renal procedure to remove toxins and excess fluid from the blood. There are two options for doing it:

1. Hemodialysis. The medical device "artificial kidney" is used on an outpatient basis for 4 hours 3 times a week.

   The device for hemodialysis removes toxic compounds, uric acid salts from the bloodstream, normalizes water-salt metabolism, prevents the occurrence of arterial hypertension

2. peritoneal dialysis. The procedure can be carried out at home in a sterile room (the room must be regularly quartzed). To do this, a thin tube (catheter) is implanted into the patient's stomach, which is constantly there. Every 4-5 hours, the patient independently pours about 2 liters of dialysis solution into the abdominal cavity. It absorbs waste and excess liquid, then the spent solution is drained (drained). The drainage process takes 20-30 minutes, after which it is necessary to repeat the entire cycle again. This procedure is associated with a significant amount of inconvenience, taking a lot of time from the patient. The second option for peritoneal dialysis is blood purification at night using an apparatus that works automatically according to a set program and performs several sessions of filling and pumping out dialysis fluid during the night. As a result, the patient leads a relatively independent daytime lifestyle.

   Peritoneal dialysis is a method of artificial purification of blood from toxins, based on the filtration properties of the patient's peritoneum.

Video: hemodialysis and peritoneal dialysis

kidney transplant

Kidney transplantation - method replacement therapy in patients in the terminal stage of CKD, which consists in replacing the damaged recipient kidney with a healthy donor organ. A donor kidney is obtained from a living or recently deceased person.

Various approaches to kidney transplantation have been developed:

As with any organ transplant, a kidney recipient will have to take drugs throughout his life that suppress the body's immune response in order to prevent rejection of the transplant.

It has been proven that kidney transplantation not only significantly improves the quality of life of a patient with CRF, but also increases its duration (compared to chronic hemodialysis).

Video: Treatment of Stages 4-5 Chronic Kidney Disease

Folk methods

People suffering from kidney failure should not take any supplements on their own without consulting a doctor. Herbs and nutrients are metabolized differently, and for kidney disease, some of the home remedies can actually make things worse. But if the attending nephrologist approves of the use of alternative methods, then some of them may be useful for maintaining health and preventing diseases of the kidneys and other digestive organs (for example, the liver).

So, a decoction of parsley is considered an ideal remedy for cleansing the kidneys and is used for home treatment of diseases of the urinary system. Parsley is a rich source of vitamins A, B and C, as well as thiamine, riboflavin, potassium and copper. Her decoction improves general state health and reduces the level of toxins in the blood, whether as a preventive measure or as a treatment to slow the progression of the disease. Parsley is also an excellent diuretic, flushing out harmful substances from the body.

Decoction preparation:

1. Grind 2-3 tbsp. spoons of parsley leaves.
2. Add 0.5 l of water and bring to a boil.
3. Cool and strain the decoction.

There are many herbal teas that are often prescribed to treat kidney problems. The most common and recommended are:

• green;
• bilberry;
• from marshmallow officinalis;
• from a purple vine;
• from dandelion.

These are one of the most effective herbal varieties. They are rich in antioxidants and detoxifying compounds that are beneficial to kidney function. Tea is prepared in the classical way at the rate of 1 teaspoon of a dry plant per 250 ml of boiling water.

Cranberry juice - the most famous home remedy to treat kidney problems. This product is widely available and palatable. Organic compounds found in cranberries are very effective in reducing the severity of infections in the kidneys. It is recommended to drink 2-3 glasses of cranberry juice during periods of inflammation. It is also a good prevention method. How to prepare a healing drink:

1. Mash 250 g of cranberries in a bowl.
2. Strain the resulting juice through cheesecloth.
3. Pour the squeezed berries with 1 liter of water and boil for 5 minutes.
4. Strain the broth and mix with juice, you can add honey to taste.

Photo gallery: folk methods of treating kidney failure

Parsley decoction is a popular kidney cleanser. Blueberry tea removes excess fluid from the body Dandelion has a strong diuretic effect
Grapevine purple helps to get rid of edema and high blood pressure Cranberry juice is effective against kidney infections

Diet food

Principles of dietary nutrition in chronic kidney disease:

• Selecting and preparing foods with less salt to control blood pressure. In the daily diet, it should not exceed 3-5 g, which is approximately equal to 1 teaspoon. It should be borne in mind that salt is added to many finished products or semi-finished products. Therefore, fresh products should prevail in the diet.
• Eating the right amounts and types of protein. In the process of protein processing, toxins are formed, which are excreted from the body by the kidneys. If a person eats more protein food than he needs, this greatly burdens these organs. Therefore, protein foods should be consumed in small portions, preferring mainly plant sources, such as beans, nuts, cereals. It is recommended to minimize animal protein, namely:
  • red meat and poultry;
  • fish;
  • eggs;
  • dairy.

Features of treatment in pregnant women

Chronic kidney disease during pregnancy is rare. This is because many women with kidney failure are either past childbearing age or are secondarily infertile due to uremia. Most pregnant women with mild kidney dysfunction do not feel the negative impact of pregnancy on their own health.

But according to studies, approximately 1-7% of women of childbearing age who undergo dialysis treatment still manage to become pregnant. The survival rate of infants in this case is about 30-50%. The frequency of spontaneous abortions varies in the range of 12-46%. An increase in survival has been observed in the children of women who received dialysis ≥ 20 hours per week. The study authors concluded that increasing dialysis time may improve outcome, but prematurity remains the leading cause of neonatal mortality and likely contributes to the high incidence of long-term medical problems in the surviving infant.

As for pregnancy after a kidney transplant, women have such chances if the transplant is successful (there are no signs of kidney failure and transplant rejection) after at least two years. The entire pregnancy takes place under strict medical supervision and the development of a treatment regimen that will be correctly combined with immunosuppressants in order to avoid possible complications:

• anemia;
• exacerbation of urinary tract infections;
• late toxicosis of pregnant women;
• transplant rejection;
• fetal growth retardation.

Prognosis and complications

The life prognosis of patients with chronic renal failure depends on many individual factors. The cause of kidney failure has a great influence on the outcome of the disease. The rate at which kidney function declines directly depends on the underlying disorder causing CKD and how well it is controlled. People with CKD have a higher risk of dying from a stroke or heart attack.

Unfortunately, in most cases, chronic renal failure will continue to develop regardless of treatment.

The life expectancy of a patient who refuses dialysis or kidney transplantation in favor of conservative treatment is no more than a few months.

If a few years ago, the life expectancy of a patient on dialysis was limited to 5–7 years, today the world's leading developers of artificial kidney devices say that modern technologies allow a patient to live on hemodialysis for more than 20 years, while feeling good. This, of course, subject to diet, daily routine, healthy lifestyle life.

But only a successful organ transplant makes it possible to live a more fulfilling life and not be dependent on dialysis. A transplanted kidney functions on average for 15–20 years, then a second operation is required. In practice, one person can perform 4 kidney transplant operations.

Prospects for the treatment of chronic kidney disease

Regenerative medicine has the potential to completely heal damaged tissues and organs, offering solutions and hope for people in conditions that are beyond repair today. In particular, new therapeutic strategies for tissue repair have recently emerged, and one of the most promising approaches is the use of stem cells to reduce injuries in chronic kidney disease.

Treatment of chronic renal failure with stem cells - a promising method of regenerative medicine

Although there is currently no cure for kidney failure and progressive kidney disease, there are already promising results that have been seen with stem cell therapy for kidney injury.

Stem cells are immature cells of the body that can self-renew, divide and, if properly activated, transform (differentiate) into functional cells of any organ, including the kidney. Most of them are found in the bone marrow, as well as in adipose and other tissues with a good blood supply.

This means that a group of stem cells taken from body fat can be activated and used to repair kidney cells and tissues damaged by chronic or acute illness. After transplantation of so-called mesenchymal stem cells, there is a significantly slower progression of CKD, which reduces the need for dialysis and kidney transplantation.

Need more a large number of studies, but it is already clear that stem cells can help stop the progression of pathology and improve healing. In the future, stem cells are planned to be used to reverse the damage done to the kidneys.

Prevention

To reduce the risk of developing chronic kidney disease, you must first follow the rules of a healthy lifestyle, in particular:

• Follow instructions for use of over-the-counter medications. Overdose of pain relievers such as Aspirin, Ibuprofen and Paracetamol can lead to kidney damage. Reception these drugs even more so if you already have kidney disease. To be sure of the safe long-term use of a drug freely sold in a pharmacy, it is recommended that you first consult with your doctor.
• Maintain a healthy weight. The absence of excess body weight is the key to optimal load on all organs, including the kidneys. Physical activity and reduced calorie intake are factors that directly affect the maintenance of optimal weight.
• Quit smoking. This habit can lead to new kidney damage and worsening the existing condition. The smoker should consult a doctor to develop a strategy for quitting tobacco. Support groups, counseling, and medication will help such a person stop in time.
• Control blood pressure. Hypertension is the most common cause of kidney damage.
• Get treated by a qualified doctor. In the presence of a disease or condition that potentially affects the kidneys, it is necessary to contact a professional in a timely manner for detailed diagnosis and therapy.
• Control blood sugar levels. Approximately half of people with diabetes develop chronic kidney disease, so these patients should have their kidneys checked regularly, at least once a year.

Chronic renal failure is a serious disease that inevitably reduces the quality of life over time. But today there are treatment options that can slow the progression of this pathology and significantly improve prognosis.

CHRONIC RENAL FAILURE

Until recently, chronic renal failure (CRF) was defined as a clinical and biochemical syndrome that occurs with kidney damage of any etiology, caused by a gradually progressive loss of excretory and endocrine functions of the organ due to the irreversible loss of functioning nephrons.
In this case, unlike acute renal failure, there is an irreversibility of pathophysiological processes that lead to these disorders. Their development only partially depends on the etiology of the underlying renal disease, since the leading pathogenetic mechanisms of damage to functioning nephrons in such a situation are intraglomerular hypertension, hyperfiltration in the glomerulus, and the nephrotoxic effect of proteinuria (more precisely, impaired renal protein transport).
The discovery of the unity of the mechanisms of the pathogenesis of damage to the kidney tissue in chronic diseases of this organ was one of the important factors that led to the creation of a fundamentally new concept - chronic kidney disease (CKD).
Reasons for the emergence of the concept of CKD.
Currently, there is a dramatic increase in the number of patients with chronic renal pathology.
This is primarily determined by the increase in the incidence of diabetes mellitus, the aging of the population and, accordingly, the increase in the number of patients with kidney damage of a vascular nature.

The progressive increase in the number of such patients is regarded as a pandemic. The above factors have led to a catastrophic increase in the number of people requiring kidney replacement therapy (RRT) - different kinds dialysis or kidney transplant.
The long-standing approach to secondary prevention of end-stage renal disease (ESRD) has also contributed to the increase in the number of patients on RRT.

When a certain degree of decline in kidney function was reached, it was not considered necessary to resort to any special methods slowing down the progression of the pathological process in the renal tissue.
In addition, over the past decades, the quality of RRT technologies has continuously improved, which has caused a sharp increase in the life expectancy of patients receiving such treatments.

All this has led to an increase in the need for dialysis places, organs for transplantation and rising costs.
Already in the sixties of the last century, it became clear that many mechanisms of the progression of chronic kidney diseases are quite universal and largely act regardless of etiology. Equally important was the identification of risk factors for the development and progression of a chronic pathological process in the renal tissue.
Like the mechanisms of progression, they were found to be largely the same in various chronic kidney diseases and quite similar to cardiovascular risk factors.

Clarification pathogenetic mechanisms the progression of chronic kidney disease, the identification of risk factors for their occurrence and development has made it possible to develop well-founded treatment regimens that can actually delay the onset of RRT or reduce the number of fatal complications.
Approaches to renoprotection various diseases kidneys were mostly identical (angiotensin-converting enzyme inhibitors, angiotensin II AT1 receptor antagonists, non-dihydropyridine calcium channel blockers, low-protein diet).
All of the above required rethinking, primarily in order to develop effective measures to further improve medical and social care for patients with chronic diseases kidneys.
One of the prerequisites for this should be the unity or at least the similarity of the criteria for identifying, describing, assessing the severity and rate of progression of renal pathology.
However, there was no such unity among nephrologists. For example, in the English-language literature, one could find about a dozen terms used to refer to conditions associated with the appearance of chronic renal dysfunction.

It should be noted that in domestic nephrology the terminological problem was less acute. The phrase "chronic renal failure" (CRF) or, in appropriate cases, "terminal renal failure", "terminal stage of chronic renal failure", etc., was usually used.
However, there was no common understanding of the criteria for chronic renal failure and assessment of its severity.

Obviously, the adoption of the concept of CKD should drastically limit the use of the term "chronic renal failure".

In the NKF classification, the phrase "renal failure" remained only as a synonym for Art. V. CKD.
At the same time, in the English-language nephrological literature, the term “end-stage renal disease” became widespread.
The developers at NKF felt it appropriate to retain the use of this term as it is widely used in the US and refers to patients who are receiving therapy. various methods dialysis or transplant, regardless of the level of kidney function.
Apparently, in the domestic nephrological practice it is worth keeping the concept of "terminal renal failure". It is advisable to include in it patients who are already receiving RRT, as well as patients with stage V CKD, who have not yet started substitution treatment or who are not provided with it due to organizational problems.
Definition and classification of CKD.
A number of issues briefly mentioned above have been taken over by the US National Kidney Foundation (NKF). The Foundation created a group of experts who, as a result of analyzing many publications on diagnostics and treatment, assessing the significance of a number of indicators in determining the rate of progression of kidney diseases, terminological concepts and agreements with representatives of the administration, proposed the concept of chronic kidney disease (CKD - ​​chronic kidney disease - CKD ).

Developing the concept of CKD, the experts of the NKF working group pursued several goals: Definition of the concept of CKD and its stages, regardless of the cause (etiology) of renal failure (disease).
Choice of laboratory indicators (research methods) that adequately characterize the course of CKD.
Determination (study) of the relationship between the degree of impaired renal function and complications of CKD.
Stratification of risk factors for progression of CKD and occurrence of cardiovascular diseases.

NKF experts proposed a definition of CKD, which is based on a number of criteria:
Kidney damage lasting > 3 months that manifests as structural or functional disorders activity of the body with or without a decrease in GFR.
These lesions manifest either pathological changes in the renal tissue, or changes in the composition of the blood or urine, as well as changes in the use of methods for imaging the structure of the kidneys GFR< 60 мл/мин/1,73 м2 в течение трех и более месяцев, при наличии или отсутствии других признаков повреждения почек.
In other words, chronic kidney disease can be defined as "the presence of kidney damage or decreased levels of kidney function for three months or more, regardless of diagnosis."

NKF experts identified five stages of CKD depending on the severity of GFR decline

Let us again pay attention to a very important point.
In the classification, risk factors for the development and progression of CKD are singled out as a separate line.
One of the most important among them is the systemic arterial hypertension or proteinuria.
At the same time, it should be borne in mind that, according to the conclusion of NKF experts, the presence of risk factors alone does not give grounds for making a diagnosis of CKD, but requires a certain set of preventive measures).

The concept of CKD, which is not directly related to a nosological diagnosis, does not cancel the nosological approach to the diagnosis of a specific kidney disease.
However, it is not a purely mechanical association of chronic kidney damage of various nature.
As noted earlier, the development of this concept is based on the unity of the leading pathogenetic mechanisms of the progression of the pathological process in the renal tissue, the commonality of many risk factors for the development and progression of kidney diseases, and the resulting similarity in the methods of therapy, primary and secondary prevention.

In this sense, CKD is close to such a concept as ischemic disease heart (CHD).
The term CKD, having barely appeared, won the rights of citizenship not only in the United States, but also in many other countries.
The VI Congress of the Scientific Society of Nephrologists of Russia, held on November 14-17, 2005 in Moscow, unequivocally supported the need for a wide introduction of the concept of CKD into the practice of national health care.

General clinical manifestations of late stages of CKD.
Signs associated with the development of renal dysfunction and little dependent on the underlying pathological process in the kidneys usually begin to be detected at the third stage of CKD and reach their maximum severity by the fifth. At first, moderate polyuria, nocturia, decreased appetite, and a tendency to anemization are usually recorded.

A drop in GFR below 30% of the normal level leads to the appearance of symptoms of uremic intoxication, to an increase in hyporegenerative anemia (due to a decrease in the production of erythropoietin), to disturbances in phosphorus-calcium metabolism, and to the formation of symptoms of secondary hyperparathyroidism (due to a decrease in intrarenal synthesis of the active metabolite of vitamin D-1, 25 (OH) 2D3; synonyms: 1,25-dihydroxy-cholecalciferol, calcitriol, D-hormone, etc.), metabolic acidosis (due to a decrease in renal excretion of hydrogen ions and suppression of bicarbonate ion reabsorption).

Compensation for metabolic acidosis is carried out by the lungs due to increased alveolar ventilation, which leads to the appearance of deep, noisy breathing. Secondary hyperparathyroidism, along with acidosis, leads to the development of osteodystrophy, which can manifest as pathological fractures. In addition, disturbances in calcium-phosphorus homeostasis often cause the appearance of extraosseous calcifications, including vascular calcification. Secondary hyperparathyroidism, skeletal damage, and soft tissue calcification reach their maximum severity in patients receiving RRT and represent a very serious clinical problem in them.
As CKD progresses, patients develop hemocoagulation disorders, which is accompanied by mild subcutaneous hematomas and an increased risk of bleeding, including gastrointestinal bleeding.

Characterized by dryness skin("Braitics don't sweat"), many patients experience excruciating itching, leading to scratching.
Initially present, polyuria can be replaced by oliguria, leading to hyperhydration and edema of internal organs, including pulmonary and brain edema.
In the late stages of CKD, uremic polyserositis, in particular uremic pericarditis, can form, which is a poor prognostic sign and requires the immediate start of RRT.

Sometimes there is a so-called. terminal nephrotic syndrome.
Cerebral symptoms gradually increase: lethargy, drowsiness, apathy, and sometimes sleep rhythm disturbances.
Almost all patients are characterized by uremic dyslipoproteinemia, leading to an acceleration of atherogenesis processes and an increase in cardiovascular risks.

Diagnostics. On condition early detection the main renal pathological process (GN, secondary nephropathy, diabetic nephropathy, etc.) and dispensary observation for patients, diagnosis is usually not difficult. As a monitoring function of the kidneys in practical work, the level of blood plasma creatinine and GFR are monitored in dynamics.
Some diagnostic difficulties may arise in the management of patients in whom azotemia is detected for the first time. In these cases, the issue of distinguishing between acute and chronic renal failure may become relevant.

Now a little mathematics, without which, unfortunately, this section cannot be dispensed with.
The problem of assessing the glomerular filtration rate in practical medicine. Glomerular ultrafiltration is the initial and main mechanism of urinary formation.
The performance by the kidneys of all their diverse functions decisively depends on its condition.
Not surprisingly, the members of the NKF working group chose the glomerular filtration rate (GFR) not only as the main criterion for distinguishing between specific stages of CKD, but also as one of the most important bases for making a diagnosis of chronic kidney disease. The developers of the National Kidney Foundation have convincingly shown that the degree of decrease in GFR is very closely associated with other clinical or metabolic changes that occur as chronic nephropathy progresses.

Clearly, the introduction of the concept of CKD requires a reliable, simple, and inexpensive way to measure GFR in clinical practice.

To date, a very large number of methods and their modifications have been developed, which make it possible to estimate GFR with varying degrees of accuracy. However, their use in wide clinical practice is limited by complexity and high cost.
Therefore, they are usually used for specific research purposes.

Throughout the world in practical medicine, the main estimates of GFR until recently remained the concentration of creatinine in blood serum (Cgr) or endogenous creatinine clearance (Ccr).
Both of these methods have a number of significant shortcomings. Serum creatinine concentration as an index of GFR.

Creatinine is a low molecular weight product of nitrogen metabolism.
It is mainly excreted by the kidneys by glomerular filtration, although some of it is secreted in the proximal tubules. In streets with undisturbed filtration capacity, the proportion of creatinine released by the tubules is small. However, the contribution of tubular secretion to the distortion of the glomerular filtration rate estimate can increase sharply with a decrease in kidney function.

The process of formation of creatinine in healthy people is almost constant speed.
This determines the relative stability of Cgr.
Despite the relative stability of creatinine production, there are a significant number of reasons, including those not directly related to the functional state of the kidneys, that can affect the Cgr level. The main determinant of serum creatinine levels.
apparently, is the volume of muscle mass, since the production of this metabolite is proportional to this volume.
Age is an important factor influencing serum creatinine levels.
GFR in adults declines progressively after age 40.
The decrease in creatinine generation caused by age naturally raises the level of GFR. Cgr in women is usually slightly lower than in men. The main significance in the appearance of these differences, apparently, is also associated with less muscle mass in females.
Thus, a clinical assessment of GFR based on serum creatinine cannot be carried out without taking into account the anthropometric, sex, and age characteristics of the patient.

In conditions of pathology, including pathology of the kidneys, all factors that determine the level of serum creatinine can be modified to one degree or another.
The available data do not allow a definitive conclusion to be drawn as to whether creatinine production is elevated, unchanged, or reduced in patients with chronic kidney disease.

However, when GFR drops to 25-50 ml/min, patients usually spontaneously reduce their protein intake (nausea, vomiting, anorexia).
Serum creatinine levels may be affected by various medicines.
Some of them (amnoglycosides, cyclosporine A, platinum preparations, x-ray contrast agents, etc.) are nephrotoxic drugs, when prescribed, an increase in Cgr reflects a real decrease in GFR.
Others are capable of entering into a Jaffe reaction.
Finally, some drugs selectively block proximal tubular creatinine secretion without any significant effect on GFR.
Cimetidine, trimethoprim, and possibly to some extent phenacetamide, salicylates, and vitamin D3 derivatives have this property.

The determined value of the concentration of creatinine in the blood serum depends quite significantly on the analytical methods used to measure this indicator. Until now, the level of creatinine in biological fluids is most often assessed by the Jaffe reaction.
The main disadvantage of this reaction is its low specificity.
This reaction can involve, for example, ketones and keto acids, ascorbic and uric acids, some proteins, bilirubin, etc. (“non-creatinine chromogens”). The same applies to some cephalosporins, diuretics, if they are prescribed in high doses, phenacetamide, acetohexamide and methyldopa (for parenteral administration). At normal values of serum creatinine, the contribution of non-creatinine chromogens to its total concentration can be from 5 to 20%.

As kidney function declines, serum creatinine concentration naturally rises.
But this increase is not accompanied by a proportional increase in the level of non-creatinine chromogens.
Therefore, their relative contribution to the concentration of total chromogen (creatinine) in serum decreases and usually does not exceed 5% in this situation. In any case, it is clear that the level of creatinine, measured using the Jaffe reaction, will underestimate the true values ​​of GFR.
Rapid changes in the latter parameter also lead to violations of the clarity of the inverse relationship between the concentration of serum creatinine and GFR.
In relation to them, the increase or decrease in Cgr may be delayed by several days.
Therefore, special care must be taken when using Cgr as a measure of the functional state of the kidneys in the development and resolution of acute renal failure.
Use of creatinine clearance as a quantitative measure of GFR. The use of Ccr over Cgr offers one significant advantage.
It allows you to get an estimate of the glomerular filtration rate, expressed as a numerical value with a dimension corresponding to the nature of the process (usually ml/min).

However, this method of assessing GFR does not solve many issues.
It is obvious that the accuracy of Ccr measurement largely depends on the correctness of urine collection.
Unfortunately, in practice, the conditions for determining the volume of diuresis are often violated, which can lead either to an overestimation or an underestimation of Csh values.
There are also categories of patients in whom quantitative urine collection is practically impossible.
Finally, when assessing the value of GFR, the value of tubular creatinine secretion is of great importance.
As noted above, in healthy people, the proportion of this compound secreted by the tubules is relatively small. Nevertheless, in conditions of kidney pathology, the secretory activity of the epithelial cells of the proximal tubules in relation to creatinine can increase sharply.

However, in a number of individuals, including those with a significant decrease in GFR, creatinine secretion may even have negative values. This suggests that they actually have tubular reabsorption of this metabolite.
Unfortunately, it is impossible to predict the contribution of tubular creatinine secretion/reabsorption to the error in determining GFR based on Cs in a particular patient without measuring GFR using reference methods. "Calculated" methods for determining GFR.

The very fact of the presence of an inverse, although not direct, relationship between Cgr and GFR suggests the possibility of obtaining an estimate of the glomerular filtration rate in quantitative terms based only on the concentration of serum creatinine.

Many equations have been developed to predict GFR values ​​based on Cgr.
Nevertheless, in the real practice of "adult" nephrology, the Cockcroft-Gault and MDRD formulas are most widely used.

Based on the results of the MDRD (Modified of Diet in Renal Disease) multicenter study, a series of empirical formulas have been developed to predict GFR values ​​based on a number of simple indicators. The best correspondence between the calculated values ​​of GFR and the true values ​​of this parameter, measured by the clearance of 125I-iothalamate, was shown by the seventh version of the equations:

It should, however, be borne in mind that there are situations where "estimated" methods for determining GFR are unacceptable.

In such cases, at least the standard measurement of creatinine clearance should be used.
Situations in which clearance methods for determining GFR should be used: Very elderly age. Non-standard body sizes (patients with amputation of limbs). Marked emaciation and obesity. Diseases of the skeletal muscles. Paraplegia and quadriplegia. Vegetarian diet. Rapid decline in kidney function.
Before prescribing nephrotoxic drugs.
When deciding whether to start renal replacement therapy.
It must also be remembered that the Cockcroft-Gault and MDRD formulas are not applicable in children.

Special attention should be paid to cases of acute deterioration of kidney function in patients with pre-existing chronic kidney disease, the so-called "ARF on CRF", or, according to the terminology of foreign authors, "acute on chronic renal failure".
From a practical point of view, it is important to emphasize that the timely elimination or prevention of factors leading to acute renal dysfunction in patients with CKD can slow down the progression of organ function deterioration.

Causes of acute renal dysfunction in patients with CKD may include: dehydration (liquid restriction, uncontrolled use of diuretics); CH; uncontrolled hypertension; the use of ACE inhibitors in patients with bilateral renal artery stenosis; obstruction and/or urinary tract infection; systemic infections (sepsis, bacterial endocarditis, etc.); nephrotoxic drugs: NSAIDs, antibiotics (aminoglycosides, rifampicin, etc.), thiazides, radiopaque agents.
It should also be mentioned that patients with CKD are especially sensitive to any potentially nephrotoxic factors, and therefore the problems of iatrogenesis and self-treatment (herbs, sauna, etc.) in these cases should be given Special attention.

Another important indicator of the rate of progression of CKD is proteinuria.
In an outpatient setting, to evaluate it, it is recommended to calculate the protein / creatinine ratio in the morning portion of urine, which is almost equivalent to measuring daily protein excretion.
An increase in daily proteinuria always means an acceleration in the rate of progression of CKD.

Treatment. Dietary recommendations.
The basic principles of the CKD diet are as follows:
1. Moderate restriction of NaCl intake depending on the level of blood pressure, diuresis and fluid retention in the body.
2. The maximum possible fluid intake depending on diuresis, under the control of body weight.
3. Restriction of protein intake (low-protein diet).
4. Restriction of foods rich in phosphorus and / or potassium.
5. Maintaining the energy value of the diet at the level of 35 kcal/kg of body weight/day.
Given the fact that as tubulointerstinial sclerosis develops, the ability of the kidneys to reabsorb Na may decrease, in some cases the salt regimen must be increased to 8 or even 10 g of salt per day. This is especially true for patients with the so-called "salt-wasting kidney".
In all situations, it is necessary to take into account the concomitant use of diuretics and their dose.
In a number of patients taking loop diuretics in high doses (more than 80-100 mg / day of furosemide), restrictions on the intake of table salt with food are not required.
The most adequate method of controlling NaCl intake is the daily excretion of Na in the urine.
In a healthy person, at least 600 milliosmoles (mosm) are excreted per day osmotically active substances(OAV).
Intact kidneys are able to significantly concentrate urine, and the total concentration of OAB (osmolality) in the urine can be more than four times the osmolality of blood plasma (1200 or more and 285-295 mosm / kg H2O, respectively).
The kidneys cannot excrete OABs (mainly urea and salts) without excretion of water.
Therefore, a healthy individual is theoretically able to excrete 600 mines in 0.5 liters of urine.

With the progression of CKD, the concentration ability of the kidneys steadily decreases, the urine osmolality approaches the blood plasma osmolality and is 300-400 mosm/kg H20 (isostenuria).

Since the total excretion of OAV does not change in the advanced stages of CKD, it is easy to calculate that in order to excrete the same 600 my OAV, the volume of diuresis should be 1.5-2 l / day.
From here it becomes clear the appearance of polyuria and nocturia, and ultimately the restriction of fluid intake in such patients accelerates the progression of CKD.

However, it should also be taken into account that in CKD III-V st. the ability to excrete osmotically free water is gradually impaired, especially if the patient is taking diuretics.
Therefore, fluid overload is fraught with the development of symptomatic hyponatremia.

Guided by the above principles, it is permissible to allow patients a free water regime, taking into account the implementation of self-monitoring of daily diuresis, adjusted for extrarenal fluid loss (300-500 ml / day). It is also necessary to regularly monitor body weight, blood pressure, clinical signs hyperhydration, determination of daily excretion of Na in the urine and periodic examination of the level of Na in the blood (hyponatremia!).

For many decades in practical nephrology there has been a recommendation to limit the intake of proteins with food, which has a number of theoretical premises.
However, it is only recently that a low-protein diet (LPD) has been shown to slow down the rate of progression of CKD.

Adaptive mechanisms of MBD in patients with CKD include: improvement of intraglomerular hemodynamics; limitation of hypertrophy of the kidneys and glomeruli; positive influence dyslipoproteinemia, effects on renal metabolism, restriction of 02 consumption by renal tissue; decrease in the production of oxidants; impact on T-cell function; suppression of AN and transforming growth factor b, limiting the development of acidosis.
MBD is usually prescribed to patients, starting from the III century. CKD.
On the II Art. a diet with a protein content in food of 0.8 g / kg body weight / day is advisable.

Standard MBD implies limiting protein intake to 0.6 g/kg/day.
In order to enrich the diet with essential amino acids, a low-protein diet can be prescribed with supplements.
Low protein diet options:
- standard MBD - protein 0.6 g/kg/day (on the basis of conventional food);
- MBD supplemented with a mixture of essential amino acids and their keto analogs (Ketosteril preparation, Fresenius Kabi, Germany); food protein 0.4 g/kg/day + 0.2 g/kg/day ketosteril;
- MBD supplemented with soy proteins, protein 0.4 g/kg/day + 0.2 g/kg/day of soy isolate, for example Supro-760 (USA).

As mentioned above, when using MBD, it is very important to maintain the normal energy value of the diet at the expense of carbohydrates and fats at the level of 35 kcal/kg/day, since otherwise the body's own proteins will be used by the body as an energy material.
In practical work, the issue of monitoring compliance with MBD by patients is essential.

The amount of protein consumed per day can be determined based on the concentration of urea in the urine and knowing the amount of daily diuresis according to the modified Maroni formula:
PB \u003d 6.25 x EMM + (0.031 x BMI) + *SP x 1.25
where PB is protein intake, g/day,
EMM - urea excretion with urine, g / day,
BMI - ideal body weight (height, cm - 100),
*SP - daily proteinuria, g/day (this term is entered into the equation if the SP exceeds 5.0 g/day).
In this case, the daily excretion of urea can be calculated based on the volume of daily urine and the concentration of urea in the urine, which in Russian clinical practice laboratory diagnostics usually defined in mmol/l:
EMM = Uur x D/2.14
where Uur is the concentration of urea in daily urine, mmol/l;
D - daily diuresis, l.

Renoprotection.
In modern nephrology, the principle of renoprotection has been clearly formed, which consists in carrying out a complex of therapeutic measures in patients with kidney disease, aimed at slowing down the progression of CKD.

The complex of therapeutic measures is carried out in three stages, depending on the degree of impaired renal function:
Stage I - the nitrogen excretion function of the kidneys is preserved (CKD stage I-II), there may be a decrease in the functional reserve (no increase in GFR by 20-30% in response to protein load).
Stage II - kidney function is moderately reduced (CKD stage III).
Stage III - kidney function is significantly reduced (CKD stage IV - the beginning of stage V CKD).

Stage 1:
1. Adequate therapy of the underlying renal disease in accordance with the principles of evidence-based medicine (estimated indicator is a decrease in daily proteinuria below 2 g / day).
2. With diabetes, intensive control of glycemia and the level of glycated hemoglobin (estimated indicator - control of microalbuminuria).
3. Adequate control of blood pressure and proteinuria using ACE inhibitors, ATj receptor antagonists to AII, or a combination thereof.
4. Timely and adequate treatment of complications: heart failure, infections, urinary tract obstruction.
5. Exclusion of iatrogenic causes: drugs, Rg-contrast studies, nephrotoxins.
6. Normalization of body weight with a mass index>27kg/m2.
Successful pathogenetic therapy of the underlying renal disease is of paramount importance in preventing the formation of glomerulo- and tubulointerstitial sclerosis, and, consequently, in slowing down the progression of CKD.
In this case, we are talking not only about the treatment of newly diagnosed pathology, but also about the elimination of exacerbations.
Main activity inflammatory process(or its relapses) involves the activation of humoral and tissue immune reactions, naturally leading to the development of sclerosis.
In other words, the more pronounced the activity of the inflammatory process and the more often its exacerbations are noted, the faster sclerosis is formed.
This statement is in full agreement with the traditional logic of the clinician and has been repeatedly confirmed by clinical studies.
In glomerular diseases, arterial hypertension is formed, as a rule, long before the decline in kidney function and contributes to their progression.
In parenchymal diseases, the tone of the preglomerular arterioles is reduced and the system of their autonomous autoregulation is disrupted.
As a result, systemic hypertension leads to an increase in intraglomerular pressure and contributes to the defeat of the capillary bed.

When choosing antihypertensive drugs, it is necessary to proceed from the main three pathogenetic mechanisms of parenchymal renal hypertension; Na retention in the body with a tendency to hypervolemia; increased activity of the RAS; increased sympathetic activity nervous system due to increased afferent impulses from the affected kidney.

In any renal pathology, including diabetic nephropathy, if the creatinine level is normal and the GFR is more than 90 ml / min, it is necessary to achieve a blood pressure level of 130/85 mm Hg. Art.
If daily proteinuria exceeds 1 g/day, it is recommended to maintain blood pressure at 125/75 mm Hg. Art.
Taking into account current data that nocturnal hypertension is the most unfavorable in terms of kidney damage, it is advisable to prescribe antihypertensive drugs taking into account the data of daily monitoring of blood pressure and, if necessary, transfer their intake to the evening hours.

The main groups of antihypertensive drugs used in nephrogenic hypertension:
1. Diuretics (for GFR< 70мл/мин - преимущественно петлевые диуретики). 2. Ингибиторы АПФ и антагонисты АТ1 рецепторов к АII.
3. Non-dihydropyridine calcium channel blockers (diltiazem, verapamil).
4. Dihydropyridine CCBs of exceptionally prolonged action.
5. b-blockers.
Medications are listed in descending order of recommended frequency of use.
Any antihypertensive therapy for parenchymal renal disease should begin with the normalization of Na metabolism in the body.
In diseases of the kidneys, there is a tendency to retain Na, which is the higher, the higher the proteinuria.
At least in experimental studies, the direct damaging effect of sodium contained in the diet on glomeruli, regardless of the level of blood pressure, has been proven.
In addition, sodium ions increase the sensitivity of smooth muscles to the action of AII.

The average dietary salt intake in a healthy person is approximately 15 g/day, so the first recommendation for patients with kidney disease is to limit salt intake to 3-5 g/day (an exception may be tubulointerstitial kidney damage - see above).
In an outpatient setting, a measure of monitoring patient compliance with prescribed recommendations is monitoring sodium excretion in the urine per day.
In cases where hypervolemia is noted or the patient is not able to follow a hyposodium diet, diuretics are the first-line (priority) drugs.
With preserved kidney function (GFR > 90 ml/min), thiazides can be used, with a decrease in GFR< 70мл/мин назначаются петлевые диуретики (допустима комбинация петлевых диуретиков с тиазидами).
Potassium-sparing diuretics are absolutely contraindicated.

During treatment with diuretics, careful dose control is necessary to prevent the development of hypovolemia. Otherwise, kidney function may deteriorate sharply - "ARF on CRF."

Medical renoprotection.
Currently, many prospective placebo-controlled studies have proven the renoprotective effect of ACE inhibitors and AT1 receptor antagonists, which is associated with both hemodynamic and non-hemodynamic mechanisms of action of AN.

Strategy for the use of ACE inhibitors and / or AT1 antagonists for the purpose of nephroprotection:
- ACE inhibitors should be prescribed to all patients in the early stages of the development of any nephropathy with SPB> 0.5-1 g / day, regardless of the level of blood pressure.
ACE inhibitors have renoprotective properties even at low plasma renin levels;
- a clinical predictor of the effectiveness of the renoprotective action of drugs is a partial (SPB< 2,5 г/сут) или полная (СПБ < 0,5 г/сут) ремиссия протеинурии через несколько недель или месяцев после начала приема медикаментов.
When treating with ACE inhibitors, a dose-dependence phenomenon is noted: the higher the dose, the more pronounced the antiproteinuric effect;
- ACE inhibitors and AT1 receptor antagonists have a renoprotective effect, regardless of the systemic hypotensive effect.
However, if the level of blood pressure against the background of their use does not reach the optimum, it is necessary to add antihypertensive drugs of other pharmacological groups. In the presence of excess weight (body mass index> 27 kg/m2), it is necessary to achieve a decrease in body weight, which enhances the antiproteinuric effect of the drugs;
- in case of insufficient antiproteinuric effect of the use of any drug of one of the groups (ACE inhibitors or AT1 antagonists), their combination can be used.

Third line drugs are non-dihydropyridine CCBs (diltiazem, verapamil). Their antiproteinuric and renoprotective effects have been proven in diabetic and non-diabetic nephropathies.
However, they can only be considered as an addition to the basic therapy with ACE inhibitors or AT1 antagonists.

Less effective, in terms of nephroprotection, is the use of dihydropyridine CCBs.
This is associated with the ability of these drugs to dilate the adductor arterioles of the glomeruli.
Therefore, even with a satisfactory systemic hypotensive effect, conditions are created that contribute to intraglomerular hypertension, and, consequently, the progression of CKD.
In addition, short-acting dihydropyridine CCBs activate the sympathetic nervous system, which in itself has a damaging effect on the kidney.
The negative effect of non-prolonged dosage forms nifedipine on the course of diabetic nephropathy.
Therefore, the use of this drug in DN is contraindicated.
On the other hand, in last years data have appeared indicating the effectiveness of the renoprotective properties of a combination of ACE inhibitors and prolonged dihydropyridine CCBs.

To date, b-blockers as renoprotective drugs occupy the last place.
However, due to recent experimental studies that proved the role of activation of the sympathetic nervous system in the progression of chronic nephropathy, the view on the validity of their use in nephrogenic hypertension should be revised.

II stage(patient with any renal pathology and GFR 59-25 ml/min).
The treatment plan at this stage includes:
1. Dietary activities.
2. Use of loop diuretics to control hypertension and hypervolemia.
3. Antihypertensive therapy, taking into account possible side effects of ACE inhibitors. With a plasma creatinine level of 0.45-0.5 mmol / l, ACE inhibitors should not be used in high doses.
4. Correction of violations of phosphorus-calcium metabolism.
5. Early correction of anemia using erythropoietin.
6. Correction of dyslipoproteinemia.
7. Correction of metabolic acidosis. With a decrease in GFR below 60 ml/min (CKD stage III), all drug therapy carried out on the background of a low-protein diet.
A more stringent sodium and fluid intake regimen is needed to avoid hypo- or hypervolemia.
Loop diuretics are used exclusively as diuretics. Sometimes their combination with thiazides is acceptable, but the use of thiazide diuretics alone is not recommended.
It is necessary to take into account the possibility of side effects from the use of ACE inhibitors with GFR 59-30 ml / min, namely: deterioration in the excretory function of the kidneys, which is explained by a decrease in intraglomerular pressure; hyperkalemia, anemia.
With a plasma creatinine level of 0.45-0.5 mmol / l, ACE inhibitors are not first-line drugs and are used with caution.
A combination of long-acting dihydropyridine CCBs and loop diuretics is preferred.
When GFR is below 60 ml/min, treatment of phosphorus-calcium metabolism disorders, anemia, dyslipoproteinemia, and acidosis is started. A low-protein diet with restriction of dairy products helps to reduce the total amount of inorganic calcium entering the body. In addition, in CKD, the adaptive capacity of the intestine to increase calcium absorption is impaired (due to a deficiency of 1,25(OH)2D3).
All these factors predispose patients to the development of hypocalcemia.
If a patient with CKD has hypocalcemia normal level total protein in blood plasma, to correct the level of calcium in the blood, it is recommended to use 1 g of pure kalysh per day exclusively in the form of calcium carbonate.
This type therapy requires monitoring of calcium levels in the blood and urine. Hyperphosphatemia in patients with chronic renal failure contributes to the occurrence of calcifications of soft tissues, blood vessels (aorta, aortic valve) and internal organs. It is usually registered when GFR falls below 30 ml/min.

A low-protein diet usually involves a restriction in the intake of dairy products, and therefore the intake of inorganic phosphorus in the patient's body is reduced.
However, it should be borne in mind that prolonged and significant restriction of protein intake can lead to negative protein catabolism and malnutrition.
In these cases, it is recommended to add complete proteins to the diet with the simultaneous administration of drugs that disrupt the absorption of phosphates in the intestine.

The best known and widely used in practice at present are calcium carbonate and calcium acetate, which form insoluble phosphate salts in the intestine.
The advantage of these drugs is the additional enrichment of the body with calcium, which is especially important with concomitant hypocalcemia. Calcium acetate is distinguished by a large phosphate-binding capacity and a lower release of calcium ions.

Calcium preparations (acetate and carbonate) should be taken with food, the vines are selected individually and on average range from 2 to 6 g / day.
Currently, aluminum hydroxides are not used as phosphate binders due to the potential toxicity of the latter in patients with CKD.

A few years ago, phosphate-binding agents that do not contain aluminum or calcium ions appeared abroad - the drug Renagel (sevelamer hydrochloride 400-500 mg).
The drug has a high phosphate-binding activity, with its use no side effects are observed, but it is not registered in the Russian Federation.

In patients with CKD, due to impaired endocrine function of the kidneys, there is a deficiency active form vitamin D.
The substrate for the active form of vitamin D3 is 25(OH)D3 - 25-hydroxycholecalciferol, which is formed in the liver.
Kidney disease itself usually does not affect 25(OH)D3 levels, but in cases with high proteinuria, cholecalciferol levels may be reduced due to its loss from vitamin D-carrying proteins.
We should not ignore such reasons as insufficient insolation and protein-energy deficiency.
If the level of 25(OH)D3 in the blood plasma of patients with chronic renal failure is below 50 nmol/l, then patients require replacement therapy with cholecalciferol.
In cases where high concentrations of parathyroid hormone (more than 200 pg / ml) are noted with a normal concentration of cholecalciferol, it is necessary to use drugs 1,25 (OH) 2D3 (calcitriol) or 1a (OH) D3 (alpha-calicidiol).
The last group of drugs is metabolized in the liver to 1.25(OH)203. Usually low doses are used - 0.125-0.25 micrograms per 1,25-dihydroxycholecalciferol. This treatment regimen prevents the rise in the level of parathyroid hormone in the blood, but how much it can prevent the development of parathyroid hyperplasia has not yet been clarified.

Anemia correction
Anemia is one of the most characteristic features CKD.
It usually forms when GFR drops to 30 ml/min.
The leading pathogenetic factor of anemia in this situation is an absolute or more often a relative deficiency of erythropoietin.
However, if anemia develops in the early stages of CKD, factors such as iron deficiency should be taken into account in its genesis ( low level plasma ferritin), blood loss in the gastrointestinal tract due to the development of erosive uremic gastroenteropathy (the most common cause), protein-energy malnutrition (as a result of an inadequate low-protein diet or due to the patient's dietary self-restrictions in the presence of severe dyspeptic disorders), folic acid deficiency (rare cause), manifestations of the underlying pathology (SLE, myeloma, etc.).

Secondary Causes anemia in CKD must be ruled out whenever low hemoglobin values ​​(7-8 g/dl) are recorded in patients with GFR above 40 ml/min. In any case, basic therapy with iron preparations (orally or intravenously) is recommended.
Currently, among nephrologists, a unified point of view has been formed regarding the early initiation of erythropoietin therapy for anemia.
First, experimental and some clinical studies have shown that the correction of anemia in CKD with erythropoietin slows down the rate of progression of PI.
Secondly, early use of erythropoietin inhibits the progression of LVH, which is an independent risk factor for sudden death in chronic renal failure (especially later in patients on RRT).

Treatment of anemia begins with a dose of erythropoietin 1000 units s / c 1 time per week; it is first recommended to restore iron stores in the body (see).
The effect should be expected after 6-8 weeks from the start of treatment.
The hemoglobin level must be maintained within 10-11 g/dl. Failure to respond to treatment usually indicates iron deficiency or an intercurrent infection.
Even with a slight improvement in the indicators of red blood in patients, as a rule, the general state of health improves significantly: appetite, physical and mental work capacity increase.
During this period, some caution should be observed in the management of patients, since patients independently expand the diet, are less serious about compliance with the water and electrolyte regimen (hyperhydration, hyperkalemia).

Side effects of erythropoietin treatment include: possible increase blood pressure, which requires increased antihypertensive therapy.
Currently, when using low doses of erythropoietin s/c, hypertension rarely acquires a malignant course.

Correction of dyslipoproteinemia
Uremic dyslipoproteinemia (DLP) begins to form when GFR falls below 50 ml/min.
Its main cause is a violation of the processes of catabolism of VLDL. As a result, the concentration of VLDL and intermediate density lipoproteins increases in the blood, the concentration of the antiatherogenic fraction of lipolroteids - high density lipoproteins (HDL) decreases.
In practical work, to diagnose uremic DLP, it is enough to determine the levels of cholesterol, triglycerides, and α-cholesterol in the blood. characteristic features lipid metabolism disorders in CKD will be: normo- or moderate hypercholesterolemia, hypertriglyceridemia and hypo-a-cholesterolemia.

Currently, there is a growing trend towards lipid-lowering therapy in patients with CKD.
This is explained by two reasons.
Firstly, lipid metabolism disorders in CRF are potentially atherogenic. And if we take into account that other risk factors for accelerated development of atherosclerosis (AH, carbohydrate intolerance, LVH, endothelial dysfunction) are also present in CKD, the high mortality of patients with HF from cardiovascular diseases (including patients on hemodialysis) becomes understandable.
Secondly, DLP accelerates the rate of progression of PI in any renal pathology. Given the nature of lipid disorders (hypertriglyceridemia, hypo-a-cholesterolemia), fibrates (gemfibrozil) should theoretically be the drugs of choice.
However, their use in PN is fraught with the development of serious side effects in the form of rhabdomyolysis, since the drugs are excreted by the kidneys. Therefore, it is recommended to take small doses (no more than 20 mt / day) of 3-hydroxy-3-methylglutaryl reductase inhibitors - coenzyme A - statins, which are metabolized exclusively in the liver.
Moreover, statins also have a moderate hypotriglyceridemic effect.
The question of how lipid-lowering therapy can prevent the accelerated formation (development) of atherosclerosis in chronic renal failure remains open to this day.

Correction of metabolic acidosis
In CKD, the renal excretion of hydrogen ions, which are formed in the body as a result of the metabolism of proteins and partly phospholipids, is impaired, and the excretion of the bicarbonate ion is increased.
A low-protein diet contributes to the maintenance of acid-base balance, therefore, with pronounced phenomena of metabolic acidosis, it is necessary to meet in the late stages of CKD or in cases of non-compliance with the diet.
Patients usually tolerate metabolic acidosis well as long as the bicarbonate level does not fall below 15-17 mmol/L.
In these cases, it is recommended to restore the bicarbonate capacity of the blood by prescribing sodium bicarbonate orally (1-3 g / day), and in case of severe acidosis, administer a 4% solution of sodium bicarbonate IV.

Patients subjectively endure light degrees of acidosis easily, therefore, it is optimal to manage patients at the level of base deficiency (BE - 6-8).
With prolonged intake of sodium bicarbonate inside, strict control over the exchange of sodium in the body is necessary (hypertension, hypervolemia, increased daily excretion of sodium in the urine are possible).
With acidosis, the mineral composition of bone tissue (bone buffer) is disturbed, and renal synthesis of 1,25 (OH) 2D3 is suppressed.
These factors may play a role in the origin of renal osteodystrophy.

Stage III carrying out a complex of therapeutic measures in patients with CKD marks the direct preparation of the patient for the start of renal replacement therapy.
The NKF guidelines recommend starting RRT at GFR less than 15 ml/min, and in patients with DM, it is reasonable to start this treatment at higher levels of GFR, although the issue of its optimal value in this situation is still a matter of debate.

Preparing patients for the start of RRT includes:
1. Psychological training, training, information for relatives of patients, solving employment issues.
2. Formation of vascular access (in the treatment of hemodialysis) - arteriovenous fistula at GFR 20 ml/min, and in patients with diabetes and/or poorly developed venous network - at GFR about 25 ml/min.
3. Vaccination against hepatitis B.

Naturally, the start of hemodialysis or peritoneal dialysis therapy is always a drama for patients and their families.
In this regard, psychological preparation is of great importance for subsequent treatment outcomes.
Clarifications are needed regarding the principles of the forthcoming treatment, its effectiveness in comparison with methods of treatment in other areas of medicine (for example, in oncology), the possibility of kidney transplantation in the future, and so on.

From the standpoint of psychological preparation, group therapy and patient schools are rational.
The issue of employment of patients is essential, since many patients are able and willing to continue working.
Early creation of vascular access is preferable, since the formation of an arteriovenous fistula with adequate blood flow requires 3 to 6 months.

According to modern requirements, vaccination against hepatitis B should be carried out before the start of hemodialysis treatment.
Vaccines against the hepatitis B virus are usually administered three times, intramuscularly, with an interval of one month after the first injection, then six months after the start of vaccination (scheme 0-1-6 months).
A faster immune response is achieved by administering the vaccine according to the 0-1-2 month schedule. The dose of HBsAg for an adult is 10-20 mcg per injection.
Post-vaccination antibodies persist for 5-7 years, but their concentration gradually decreases.
With a decrease in the AT titer to the surface antigen of the hepatitis B virus to a level of less than 10 IU / l, revaccination is necessary.

kidney transplant
The most promising method of treatment.
Kidney transplantation is a dramatic treatment.
In perspective, the patient is healthy man if everything goes smoothly, if the kidney is transplanted according to all the rules.
In 1952 in Boston, at the transplant center, J. Murray and E. Thomas successfully transplanted a kidney from a twin, and 2 years later - from a corpse.
This success made surgeons laureates Nobel Prize.
The same prize was awarded to A. Carrel for his work on transplantation.
The introduction of modern immunosuppressants into the practice of transplantation has provided a cosmic increase in the number of transplanted kidneys.
Today, kidney transplantation is the most common and most successfully developing type of internal organ transplant.
If in the 50s It was about saving patients with GN, but now kidneys are successfully transplanted to patients with diabetic nephropathy, amyloidosis, etc.
To date, over 500,000 kidney transplants have been performed worldwide.

Transplant survival has reached an unprecedented level.
According to the United Organ Distribution Network (UNOS) kidney registry, the one-year and five-year survival rates for cadaveric kidney transplants are 89.4% and 64.7%, respectively.
Similar figures for transplants from living donors are 94.5% and 78.4%.
The survival rate of patients in the same terms with cadaveric transplants was 95% and 82% in 2000.
It is slightly higher in patients with kidneys transplanted from living donors - 98% and 91%.

The steady development of immunosuppression techniques has led to a significant increase in the "half-life" of grafts (almost 2 times).
This period is 14 and 22 years for cadaveric kidneys and kidneys from living donors, respectively.
According to the Freiburg University Hospital, which summarized the results of 1086 kidney transplantations, 20 years after the operation, the survival rate of recipients was 84%, the graft functioned in 55% of the operated patients.
The survival rate of grafts noticeably decreases mainly in the first 4-6 years after the operation, and especially significantly during the first year. After 6 years, the number of graft losses is negligible, so that in the next 15 years the number of transplanted kidneys that retain function remains almost unchanged.

The spread of this promising method of treating patients with end-stage CKD is constrained primarily by the shortage of donor kidneys.
A big problem of transplantation is the issue of providing donor organs.
The search for a donor is very difficult, as there are diseases that can prevent the taking of a kidney (tumors, infections, changes in the functional state of the kidneys).
It is obligatory to select a recipient by blood type and histocompatibility antigens.
This improves the results of the long-term functioning of the transplanted kidney.
This circumstance led to a significant increase in the waiting time for the operation.
Despite the high cost of immunosuppressive therapy in postoperative period, kidney transplantation is more cost-effective than other RRT methods.

In developed country settings, a successful operation can result in savings of about $100,000 over 5 years compared to a patient receiving dialysis treatment.
Despite the tremendous success of this method of treatment, many questions still need to be addressed.

A difficult problem is the indications and contraindications for kidney transplantation.
When establishing indications for surgery, it is assumed that the course of CRF has many individual features: the level of creatininemia, the rate of its increase, the effectiveness of other methods of treatment, as well as complications of CRF.

The generally accepted indication for kidney transplantation is the condition of patients when the developing complications of CRF are still reversible.
Contraindications for kidney transplantation are: age over 75 years, severe pathology of the heart, blood vessels, lungs, liver, malignant neoplasms, active infection, active current vasculitis or glomerulonephritis, severe obesity, primary oxalosis, uncorrected pathology of the lower urinary tract with urinary outflow obstruction, drug or alcohol addiction, severe psychosocial problems.

Without dwelling on the purely technical details of the operation, we will say right away that the postoperative period occupies a special place in the problem of kidney transplantation, since at this time the further fate of the patient is determined.

The most important are immunosuppressive therapy, as well as the prevention and treatment of complications.
In terms of immunosuppressive therapy, the leading place belongs to the "triple therapy" - GCS, cyclosporine-A (tacrolimus), mycophenolate mofetil (sirolimus).
To control the adequacy of immunosuppression when using cyclosporine-A and control complications of treatment, the concentration of this drug in the blood should be monitored.
Starting from the 2nd month after transplantation, it is necessary to maintain the level of CSA in the blood within the range of 100-200 µg/l.

In recent years in clinical practice included the antibiotic rapamycin, which prevents rejection of transplanted organs, including kidneys. Of interest is the fact that rapamycin reduces the likelihood of secondary vasoconstriction after balloon angioplasty. Moreover, this medicine prevents the metastasis of certain cancerous tumors and inhibits their growth.

Results of new animal experiments in American clinic Mayo suggests that rapamycin increases the effectiveness of radiation treatment malignant neoplasms brain.
These materials were presented by Dr. Sarcario and his colleagues in November 2002 to the participants of the oncology symposium in Frankfurt.
In the early postoperative period, in addition to rejection crises, patients are threatened by infection, as well as necrosis and fistula of the wall. Bladder, bleeding, development of steroid stomach ulcers.

In the late postoperative period, the risk of infectious complications, development of graft artery stenosis, recurrence of the underlying disease in the graft (GN) remains.
One of the urgent problems of modern transplantology is the preservation of the viability of the transplanted organ.
The chances of restoration of graft function are sharply reduced if the period of renal ischemia exceeds 1 hour.
Preservation of a cadaveric kidney is achieved by its non-perfusion conservation in a hypothermic solution resembling an intracellular fluid.

RCHD (Republican Center for Health Development of the Ministry of Health of the Republic of Kazakhstan)
Version: Clinical Protocols of the Ministry of Health of the Republic of Kazakhstan - 2013

Chronic renal failure, unspecified (N18.9)

Nephrology

general information

Short description

CRF- a syndrome of irreversible impairment of all kidney functions lasting for months or years, leading to a breakdown in water, electrolyte, nitrogen and other types of metabolism, due to the development of sclerosis of the renal tissue due to various kidney diseases.

CKD- kidney damage (microalbuminuria more than 30 mg / day, hematuria) or a decrease in their function for 3 months or more. The definition and classification of CKD was introduced by the National Kidney Foundation, the National Kidney Foundation (NKF) and the Kidney Disease Outcomes Quality Initiative (KDOQI) working group in 2002.

Further discussion of the protocol is carried out according to new classification CKD.

I. INTRODUCTION

Protocol name: Chronic renal failure (CRF)

Protocol code:

ICD codes:

N18 Chronic renal failure

N18.0 End-stage renal disease

N18.8 Other manifestations of chronic renal failure

N18.9 Chronic renal failure, unspecified

N19 Renal failure, unspecified

Abbreviations used in the protocol:

BP - blood pressure

BB - beta-adrenergic receptor blockers

CCB - calcium channel blockers

ARBs - angiotensin receptor blockers

PEM - protein-energy malnutrition

VARMS - congenital malformations of the urinary system

GP - doctor general practice

HD - hemodialysis

HDF - hemodiafiltration

GF - hemofiltration

RRT - renal replacement therapy

ACE inhibitors - angiotensin converting factor inhibitors

IP - artificial kidney

MI - myocardial infarction

MZPT - methods of renal replacement therapy

TIBC - total iron-binding capacity of serum

ONMK - acute violation cerebral circulation

AKI - acute renal failure

BCC - volume of circulating blood

PTH - parathyroid hormone

GFR - glomerular filtration rate

ESRD - end-stage renal disease

EPO - erythropoietin

CKD - ​​chronic kidney disease

CRF - chronic renal failure

CAPD - continuous ambulatory peritoneal dialysis
CRF - chronic renal failure

HB - hemoglobin

Ca-P - phosphorus-calcium metabolism

Kt/V - dialysis adequacy parameters

URR - residual proportion of urea

Patient category: Patients aged 18 years and older with chronic renal failure, as a result of diabetic nephropathy, hypertensive nephroangiosclerosis, primary and / or secondary kidney disease (glomerular, tubulointerstitial, kidney lesions in systemic diseases, cystic kidney disease), congenital anomalies in the development of the urinary system ( WARMS), and kidney transplant patients.

Protocol Users: nephrologists, specialists of the hemodialysis department, urologists, therapists, cardiologists, endocrinologists, rheumatologists, resuscitators, general practitioners.

Classification

Clinical classification

The modern classification is based on two indicators - glomerular filtration rate (GFR) and signs of kidney damage (proteinuria, albuminuria). Depending on their combination, five stages of CKD are distinguished.

International classification CKD versus GFR

CKD is defined in the presence of kidney damage and/or a decrease in GFR ≤ 60 ml/min/1.73 m2 for 3 months or more. Kidney damage is the structural and functional abnormalities of the kidneys detected in blood, urine, or imaging tests.

CKD stages 3-5 correspond to the definition of chronic renal failure (decrease in GFR of 60 ml/min or less).

Stage 5 corresponds to terminal chronic renal failure (uremia).

Calculation of GFR in patients with CKD stages 1-3 is carried out according to the Cockcroft-Gault formula, in stages 4-5 CKD is calculated using the MDRD and CKD-EPI formulas or is determined by the daily clearance of endogenous creatinine.

Diagnostics

II. METHODS, APPROACHES AND PROCEDURES FOR DIAGNOSIS AND TREATMENT

List of diagnostic measures

List of diagnostic measures for CKD stages 1-3

Biochemical research: creatinine, urea, blood electrolytes, glucose, total protein, albumin, protein fractions, serum iron, cholesterol

Parathormone, ferritin, transferrin iron saturation percentage

General analysis urine, urinalysis according to Nechiporenko

Protein/creatinine, protein/albumin ratios

Urinary protein electrophoresis (tubular, glomerular, selective proteinuria)

BP, height, weight, BMI

Calculation of GFR using the Cockcroft-Gault formula

Biochemical blood test: uric acid, glycemic profile, daily excretion of uric acid, alkaline phosphatase, GGTP, ALT, AST, lipid profile, complements (C3, C4), TIBC, transferrin, M-gradient, glycosylated hemoglobin, C-peptide, insulin , C-reactive protein

Immunological blood test for ANA, ENA, total nuclear antibodies, T3, T4, TSH, antibodies to TPO, c-ANCA, p-ANCA, anti-ds-DNA, anti-GBM, circulating immune complexes, ASLO, ASA, AFL- antibodies, antibodies to cardiolipin

Virological study: Wasserman reaction, ELISA and / or PCR for cytomegalovirus, herpes simplex virus types 1 and 2, viral hepatitis, HIV, Epstein-Barr virus, Poliomavirus, Parvovirus, Candida albicans

Procalcitonin, interleukin-18

Bence-Jones protein in urine

Ultrasound of organs abdominal cavity, kidneys (lying and standing), adrenal glands and bladder with the determination of residual urine

Ultrasound of the renal vessels

Dynamic nephroscintigraphy

ECG, echocardiography

Ophthalmoscopy

X-ray examination of bones

List of diagnostic measures for CKD stages 4-5

The main laboratory diagnostic measures:

Complete blood count (6 parameters), reticulocytes, percentage of hypochromic erythrocytes

Biochemical studies: creatinine (before and after HD session), urea (before and after HD session), potassium/sodium determination (before and after HD session), blood electrolytes, glucose, total protein, albumin, serum iron, cholesterol

Parathormone, ferritin, transferrin iron saturation percentage

Coagulogram 1 (prothrombin time, fibrinogen, thrombin time, APTT)

General urine analysis

BP, height, weight, BMI

Calculation of GFR using the MDRD and CKD-EPI formulas or is determined by the daily clearance of endogenous creatinine

Additional laboratory diagnostic Events:

Biochemical blood test: uric acid, ALT, AST, OZHSS, transferrin, glycemic profile. glycosylated hemoglobin, C-reactive protein,

Immunological blood test for ANA, ENA, total nuclear antibodies, T3, T4, TTE, antibodies to TPO, c-ANCA, p-ANCA, anti-ds-DNA, anti-GBM, circulating immune complexes, APL-antibodies, antibodies to cardiolipin

Virological study: Wasserman reaction, ELISA and / or PCR for cytomegalovirus, herpes simplex virus types 1 and 2, viral hepatitis, HIV, Epstein-Barr virus, Poliomavirus, Parvovirus, Candida albicans,

Sowing urine and other biomaterials on MT 3 times

Daily fluid balance (daily measurement of fluid intake and urine output)

Bacteriological examination and sensitivity to antibiotics of urine and other biomaterials

Instrumental Methods research:

Ultrasound of the abdominal organs, pleural cavities, kidneys, adrenal glands and bladder with the determination of residual urine

Ultrasound of the renal vessels

UDG AVF

X-ray of the chest organs

Excretory urography

ECG, echocardiography

Ophthalmoscopy

MRI, CT - according to indications (formation, cysts)

X-ray examination of bones, densitometry (for renal bone disease)

Outpatient diary of a patient with a record of blood pressure, fluid balance

Kidney biopsy (if indicated)

The list of diagnostic measures for patients with stage 4-5 CKD in a hospital may vary and depends on the severity of the patient's condition. In a hospital setting, all types of diagnostic and treatment measures can be carried out with reasonableness and indications, taking into account the existing underlying and concomitant diseases within the existing clinical protocols.

Complaints and anamnesis

Patients with stage 1-3 CKD may have no complaints or complain about the disease that led to CKD (arterial hypertension, diabetes, glomerulonephritis, etc.). An integral part of the diagnosis is the active identification, specification of complaints and clarification of anamnestic data.

Patients with stage 4-5 CKD complain of weakness, fatigue, loss of appetite, nausea, vomiting, headaches, tinnitus, polyuria, polydipsia, decrease in urine output, edema, lag in physical development, pain in the bones, muscles, skin itching.

History: long-term diabetes mellitus and/or arterial hypertension, primary and/or secondary kidney diseases (glomerular, tubulointerstitial, HARMS), systemic diseases, corrective surgeries on the urinary system.

Physical examination

Pallor or pale earthy shade, dry skin, traces of scratching on the skin, edema, muscle wasting, asthenia, bone deformities, polyuria, oliguria, anuria, arterial hypertension, smell of ammonia from the mouth.

Instrumental Research

Ultrasound of the kidneys (reduction in the size of the kidneys, with the exception of diabetic nephropathy, kidney transplant and polycystic kidney disease), changes in Doppler ultrasound of the kidney vessels (reduction / absence of linear blood flow velocities, an increase in resistance indices of more than 0.7).
Ultrasound of the pleural cavities - fluid accumulation syndrome, ECG - signs of LV hypertrophy, electrolyte and metabolic disorders, myocardial dystrophy. Ophthalmoscopy - hypertensive, diabetic retinopathy, echocardiography - signs of heart failure (EF<60%), снижение сократимости, диастолическая дисфункция, перикардит, ФГДС - уремические гастропатии.
X-ray of the chest organs - uremic pleurisy, uremic and / or congestive pneumonia.
Densitometry - a decrease in bone mineral density. Kidney biopsy - morphological signs of renal pathology.

Indications for expert advice

Cardiologist - development of acute and chronic heart failure, cardiac arrhythmias, myocardial ischemia, pulmonary embolism

Ophthalmologist - changes in the fundus vessels with hypertension, diabetes, prolonged uremia or steroid use (angiopathy, cataract)

Neurologist - development of uremic encephalopathy, peripheral neuropathy, carpal tunnel syndrome

Psychologist - psychological disorders (depression, anorexia, etc.) associated with a long-term chronic illness, in preparation for transplantation

Anesthesiologist-resuscitator - if necessary, catheterization of the central vein for hemodialysis

Surgeon - for the formation of an arterio-venous fistula or implantation of a catheter for peritoneal dialysis, the presence of fluid in the pleural cavities, the presence of signs of acute surgical pathology

Rheumatologist - presence of signs of systemic pathology

Endocrinologist - the presence of diabetes mellitus, thyroid disease

Oncologist - the presence of signs of cancer

Phthisatr - for suspected tuberculosis

Urologist - presence of urinary tract obstruction

ENT - doctor - inflammation of the paranasal sinuses, decompensated tonsillitis, with suspected Wegener's syndrome, hearing loss with Alport's syndrome

Gastroenterologist - the presence of pronounced manifestations of uremic gastroenteropathy

Infectionist - the presence of hepatitis, acute and exacerbation of chronic infections

Gynecologist - detection of pathology in the small pelvis

Hematologist - severe DIC, regenerator anemia

Laboratory diagnostics

Laboratory research:

Anemia (hemoglobin<130г/л у мужчин, <120г/л у женщин),
- decrease in blood ferritin,
- uremia (increased levels of urea (above 8 mmol / l) and creatinine (in terms of GFR (see paragraph 10),
- hyperkalemia above 5.5 mmol / l,
- hypoproteinemia less than 60 g/l with hypoalbuminemia less than 35 g/l,
- violation of phosphorus-calcium metabolism (total calcium less than 2.1,

Hyperphosphatemia above 1.78 mmol / l,
- increase in CaxP value above 4.4 mmol2/l2,
- elevated parathyroid hormone levels above 300 pg/ml (see section 15.2.5 Bone disease in CKD)),
- violation of acid-base balance (metabolic acidosis Ph below 7.35),
- violation of the blood coagulation system (norm APTT -35-45 sec, INR-0.9 -1.1, PTI -90 -120%, fibrinogen 2-4 g / l, PTT - 16-17 sec),
- decrease in the specific gravity of urine below 1018,
- pathological urinary sediment (proteinuria above 150 mg / day, the presence of hematuria, cylindruria).

Differential Diagnosis

CKD must be differentiated from acute kidney injury.

Treatment abroad

Get treatment in Korea, Israel, Germany, USA

Get advice on medical tourism

Treatment

Purpose of treatment

For patients with CKD stages 1-3 - slowing down the progression of CKD by treating the underlying disease that led to CKD, treating complications of CKD.

For patients with stage 4-5 CKD, preparation for renal replacement therapy, adequate dialysis therapy: from the start of introductory dialysis to the achievement of target values ​​(see Hemodialysis protocol), treatment of complications of chronic renal failure and dialysis therapy.

Treatment tactics

Non-drug treatment

Mode: the mode of patients with CKD in a hospital depends on the severity of the condition.

Diet: correction of malnutrition, for patients with CKD stages 2-3 - a low-protein diet (15) in order to slow down the progression of CKD.

Malnutrition is the most common and most visible complication of CKD patients and leads to increased hospitalization and mortality rates

Principles of Diet Therapy in Patients with CKD

Replenishment of energy requirements in patients with CKD should be calculated depending on the age and stage of CKD (pre-dialysis, dialysis).

There is no need to restrict protein intake in pre-dialysis CKD patients as long as it does not exceed the daily requirement.

In case of poor nutrition, as well as in the treatment of dialysis, the possibility of additional administration of vitamins (folic acid, vitamins of group B, C, L-carnitine) should be taken into account.

Patient education involves the calculation of daily energy requirements using tables.

In case of failure of self-nutrition and a pronounced deficiency of BMI, take into account nutrition through a nasogastric tube.

Correction of sodium and fluid balance

Patients with CKD on the background of obstructive uropathy or renal dysplasia in polyuria (salt-wasting variant) often require additional provision of sodium chloride up to 4-7 meq/kg/day

Patients with CKD with primary glomerular disease or oliguria should limit salt and fluid intake to reduce the risk of edema and hypertension. It is recommended to limit the intake of table salt to 1.5 g / day.

Acidosis correction

According to the literature, chronic acidosis in patients with CKD is associated with accelerated progression of renal failure and high mortality.

The standard treatment for metabolic acidosis in patients with CKD is oral sodium bicarbonate (baking soda) at a rate of 1-3 mmol/kg/day.

Medical treatment

Correction of arterial hypertension

Arterial hypertension is one of the most important independent risk factors for the progression of CKD. It is necessary to pay great attention to the correct measurement of blood pressure. Target BP in CKD is ≤ 140/90 mmHg, in the presence of microalbuminuria/proteinuria ≤ 130/80 mmHg. In stages 4-5 of CKD, loop diuretics are applicable. Antihypertensive drugs are angiotensin II receptor blockers, beta blockers, calcium channel blockers. The selection of the dose of the drug should be carried out taking into account the GFR.

Correction of renal anemia:

Anemia is one of the earliest and most common complications of CKD. According to the latest revision of the KDIGO-2012 anemia guidelines, the diagnosis of anemia with CKD is based on the level of hemoglobin< 130г/л у мужчин и < 120 г/л у женщин.

Definition of anemia and target hemoglobin in patients with CKD

Key elements in the treatment of anemia in CKD are the use of erythropoietin stimulating agents such as recombinant human erythropoietin (epoetin-alpha, epoetin-beta, darbepoetin, epoetin-theta, methoxypolyethylene glycol-epoetin beta) and iron supplements. According to current literature data, early use of erythropoietin in patients with CKD improves appetite, exercise tolerance, oxygen uptake, and quality of life.

Initial dose of erythropoietin: 100-150 IU/kg per week subcutaneously, divided into 2-3 doses at intervals. Patients often require a 50% to 100% increase in starting dose (150 IU/kg subcutaneously per week). The goal of treatment is to achieve a monthly increase in hemoglobin levels of 10-20g/l until the target level (115g/l) is reached. The dose of EPO should be increased by 25% if anemia persists and hemoglobin levels have not increased by 10 g/l after 1 month of treatment. The dose of EPO should be reduced by 25% if the hemoglobin level exceeds the target level or the growth rate is greater than 20g/l per month. The condition in which the target level of hemoglobin is not achieved at a dose of EPO more than 500 IU / kg per week is called resistance to EPO treatment.

Initial doses of epoetins in patients with CKD

In patients with CKD, only parenteral iron preparations should be used, given the high level of hepcidin in CKD patients, which interferes with iron absorption from the intestinal lumen. Iron preparations used parenterally to correct iron in patients with stage 4-5 CKD:

Iron dextran hydroxide III, for parenteral administration

Iron III hydroxide sucrose complex for parenteral administration

Target values ​​for iron therapy in patients with CKD

In cases where there is no effect from the ongoing therapy with jelly and EPO preparations, the following reasons must be excluded:

Easily correctable:

Absolute iron deficiency

B12 deficiency, folate

L-carnitine deficiency

Hypothyroidism

Application of ACE inhibitors

hyperparathyroidism

Lack of adherence to treatment

Breaks in treatment

Potentially correctable:

infection/inflammation

Underdialysis

Hemolysis/bleeding

hyperparathyroidism

Partial red cell aplasia of the bone marrow

Tumors

Protein-energy malnutrition

Uncorrected:

Hemoglobinopathies

bone marrow pathology

Renal bone disease (mineral-bone disorders in CKD)

Renal bone disease is a severe complication of CKD, so early correction of serum calcium, phosphorus, and PTH levels is essential.

Target levels of parathyroid hormone depending on the stages of CKD

In order to correct hyperphosphatemia, it is necessary to use phosphate binders, depending on the phosphorus consumed with food: calcium-containing (cholecalciferol up to 3 g / day), as well as calcium-free (Sevelamer carbonate 3-6 tablets / day). Phosphate binders should be taken with meals.

For the treatment of secondary hyperparathyroidism, only after correction of hyperphosphatemia, it is necessary to use active forms of vitamin D (Alfacalcidol, Cinacalcet, Paricalcitol). The dose is selected depending on the initial level of PTH and the stage of CKD and under strict control of the level of phosphorus and PTH. If medical correction of secondary hyperparathyroidism is ineffective, indications are given for parathyroidectomy and sclerosis of the parathyroid glands.

Correction of hyperkalemia

Possible causes and principles of treatment of hyperkalemia:

The presence of hyperkalemia in combination with a relatively high level of creatinine in patients with CKD, obstructive uropathy, reflux nephropathy, or interstitial nephritis. A common cause is insufficient fluid intake. Treatment: fluid and sodium replacement

Taking potassium-sparing diuretics, ACE inhibitors, ARBs. Treatment: reduce doses or eliminate the drug.

With persistent hyperkalemia, exclude foods rich in potassium from the diet (eg, chocolate, potatoes, greens, fruits, dried fruits, juices, compotes), educate the patient and his family on this diet

All patients of 4-5 stages of CKD in a hospital should assess the state of acid-base balance according to the indications, in order to exclude hyperkalemia associated with severe acidosis.

In severe hyperkalemia, medical treatment is necessary. Correction of hyperkalemia begins at a plasma potassium level >5.5 mmol/l:

1) Intravenous administration of 4% solution of sodium bicarbonate 1-2 ml / kg for 20 minutes under the control of the acid-base state of the blood - the onset of action after 5-10 minutes, the duration of action is 1-2 hours.

2) Intravenous administration of 20% glucose at 1-2 g/kg with insulin - onset of action after 30-60 minutes, duration of action 2-4 hours.

3) Intravenous slow administration of 10% solution of calcium gluconate 0.5-1.0 ml/kg with monitoring of the number of heartbeats. Repeated administration until the ECG changes disappear - the onset of action is immediate, the duration of action is 30-60 minutes.

4) Inhalation of salbutamol.

5) Hemodialysis, peritoneal dialysis.

For treatment of other complications and conditions associated with comorbidities that exacerbate the severity and prognosis of patients with CKD, see the relevant protocols.

Other treatments

Dialysis therapy - see protocol Hemodialysis

Surgical intervention in a hospital setting

To ensure adequate vascular access for the purpose of high-quality blood purification from uremic toxins:

Implantation of a temporary dialysis catheter (for emergency indications)

Formation/removal of AVF (for program hemodialysis)

Suturing/excision of AVF aneurysm

Implantation/explantation of a synthetic vascular prosthesis

Implantation / explantation of a permanent catheter

For peritoneal dialysis -

Implantation/explantation of a peritoneal catheter (for peritoneal dialysis)

For morphological verification -

Kidney biopsy

With massive hematuria and proteinuria:

Nephrectomy unilateral

Nephrectomy bilateral

For the surgical treatment of hyperparathyroidism that is not corrected by medication

Parathyroidectomy

Sclerosis of the parathyroid glands.

Preventive actions:

Prevention of the above complications

Patient education on diet, prevention of infectious complications on peritoneal dialysis.

BP control at home with diary entries

Before starting renal replacement therapy, patients should be screened for viral infections, in particular viral hepatitis (B and C).

Patients who test positive for viral hepatitis B and C should receive dialysis therapy in a separate room, on a separate dedicated artificial kidney machine to prevent the spread of infection.

Patients not previously vaccinated and not infected with viral hepatitis should be vaccinated against viral hepatitis B before starting program dialysis.

Further management

Observation and rehabilitation of patients with CKD stages 1-3 is carried out by district therapists, GPs at the place of residence with the involvement of specialized specialists.

Patients suffering from stage 4-5 CKD require lifelong renal replacement therapy (peritoneal dialysis, hemodialysis, kidney transplantation). All patients on dialysis are prepared for a donor kidney transplant as soon as possible. Those

Patients who started treatment with peritoneal dialysis, if the treatment is not adequate due to the loss of function of the peritoneal peritoneum, are transferred to hemodialysis. Patients receiving hemodialysis therapy, if it is impossible to continue hemodialysis due to the problem of maintaining and creating vascular access, it is possible to transfer to peritoneal dialysis (in the absence of any contraindications).

3. Progressive hyperazotemia (symptoms of uremia);

4. Uncontrolled arterial hypertension;

5. Severe progressive anemia (renal and / or post-hemorrhagic);

6. In case of complications of vascular access or peritoneal access;

7. Other complications requiring emergency treatment.

Information

Sources and literature

1. Minutes of the meetings of the Expert Commission on Health Development of the Ministry of Health of the Republic of Kazakhstan, 2013
   1. 1. Levey AS, Eckardt KU, Tsukamoto Y, et al. Definition and classification of chronic kidney disease: a position statement from Kidney Disease: Improving Global Outcomes (KDIGO). Kidney Int 2005; 67:2089. 2. KDOQI Clinical Practice Guidelines for Chronic Kidney Disease: Evaluation, Classification, and Stratification. Am J Kidney Dis, 2002, T.2 Suppl.1. P.1 - 246 3. Jander A, Nowicki M, Tkaczyk M et al. Does a late referral to a nephrologist constitute a problem in children starting renal replacement therapy in Poland? – A nationwide study. Nephrol Dial Transplant. 2006 Apr;21(4): 957-961. 4. Wuhl E, Schaefer F. Therapeutic strategies to slow chronic kidney disease progression. Pediatr Nephrol 2008; 23: 705-716 5. Mattoo TK. Epidemiology, risk factors, and etiology of hypertension in children and adolescents. In UpToDate Online 16.1. UpToDate1, Inc. Niaudet P (eds.). 2008 6. Association IPH: Blood Pressure Limits Chart. In, 2008 http://www.pediatrichypertension.org/BPLimitsChart.pdf 7. Strict blood-pressure control and progression of renal failure in children. ESCAPE Trial Group, Wuhl E, Trivelli A, Picca S et al. N Engl J Med. 2009 Oct22; 361(17): 1639-50 8. Rene G. VanDeVoorde, Bradley A. Warady. Management of Chronic Kidney Disease, from Pediatric Nephrology; 1676-1677; Springer 2009 9. Clinical practice recommendations for anemia in chronic kidney disease in children. Am J Kidney Dis 2006;47:86–108. 10. Rene G. VanDeVoorde, Bradley A. Warady. Management of Chronic Kidney Disease, from Pediatric Nephrology; 1666-1670; Springer 2009 11. Boehm M, Riesenhuber A, Winkelmayer WC, Arbeiter K, Mueller T, Aufricht C. Early erythropoietin therapy is associated with improved growth in children with chronic kidney disease. Pediatric Nephrol. 2007 Aug;22(8):1189-93 12. Jabs K. the effect of recombinant human erythropoietin on growth and nutritional status. Pediatr Nephrol 1996; 10: 324-327 13. Gerson A, Hwang W, Fiorenza J et al. Anemia and health-related quality of life in adolescents with chronic kidney disease. Am J Kidney Dis. 2004; 44: 1017-1023 14. On approval of the nomenclature, rules for the procurement, processing, storage, sale of blood and its components, as well as the rules for storage, transfusion of blood, its components and preparations. Acting order Minister of Health of the Republic of Kazakhstan dated November 6, 2009 No. 666. 15 Strivaths PR, Wong C, Goldstein SL. Nutrition aspects in children receiving maintenance hemodialysis: impact on outcome. Pediatr Nephrol 2008 Feb 22 16. Foster BJ, McCauley L, Mak RH. Nutrition in infants and very young children with chronic kidney disease. Pediatric Nephrol. 2011 Aug 28. 17. Wingen AM, Fabian-Bach C, Schaefer F et al. Randomized multi-center study of a low-protein diet on the progression of chronic renal failure in children. European Study Group of Nutritional Treatment of Chronic Renal Failure in Childhood. Lancet 1997; 349: 1117-1123 18. Pereira AM, Hamani N, Nogueira PC, Carvalhaes JT. Oral vitamin intake in children receiving long-term dialysis. J Ren Nutr. 2000 Jan;10(1): 24-9 19. Kucher A.G., Kayukov I.G., Esayan E.M., Ermakov Yu.A. Handbook of nutrition for patients with chronic renal failure. St. Petersburg, 2004. 20. Lesley Ress, Vanessa Shaw. Nutrition in children with CRF and on dialysis. Pediatric Nephrol. 2007; 22:1689 - 1702 21. Mehls O, Wuhl E, Tonshoff B et al. Growth hormone treatment in short children with chronic kidney disease. Acta Paediatr. 2008 Sep; 97(9): 1159-64 22. Katherine Wesseling-Perry, Isidro B. Salusky. chronic Kidney Disease Mineral ans Bone Disorder, from Pediatric Nephrology; 1755 - 1783; Springer 2009 23. National Kidney Foundation. K/DOQI clinical practice guidelines for bone metabolism and disease in chronic kidney disease. Am J Kidney Dis. 2003 Oct; 42(4 Suppl 3):S1-201 24. Shah SN, Abramowitz M, Hostetter TH et al. Serum bicarbonate level and the ptogression of Kidney Disease: A Cohort Study. Am J Kidney Disease, Vol 54 No 2, 2009:270-277 25. Clinical practice guidelines for nutrition in chronic renal failure. K/DOQI, National Kidney Foundation. Am J Kidney Dis 2000;35:S1–140. 26. Seikaly MG, Salhab N, Browne R. Patterns and time of initiation of dialysis in US children. Pediatr Nephrol 2005; 20:982-988 27. National Kidney Foundation. K/DOQI. 2006 updates clinical practice guidelines and recommendations. http://www.kidney.org/professionals/kdoqi/pdf/12-50-0210_JAG_DCP_Guidelines-HD_Oct06_SectionA_ofC.pdf 28. KDIGO for Anemia in Cronic Kidney Disease. 2012

Information

III. ORGANIZATIONAL ASPECTS OF PROTOCOL IMPLEMENTATION

List of developers
Tuganbekova S.K. - Deputy Director for Science of JSC "NSMC" Doctor of Medical Sciences, Professor, Chief Freelance Nephrologist of the Ministry of Health of the Republic of Kazakhstan
Narmanova O.Zh. - Professor of the Department of GP No. 2 of JSC "MUA", MD, independent accredited expert, nephrologist of the highest category
Gaipov A.E. - Head of OEKGK JSC "NSMC", nephrologist, Ph.D.
Smailov Zh.T. - chief freelance specialist in hemodialysis of the UZ of Astana, doctor of the highest category
Kokoshko A.I. - JSC "MUA" Associate Professor of the Department of Anesthesiology and Resuscitation, Ph.D.

Reviewers:

Karabaeva Aigul Zhumartovna - Doctor of Medical Sciences, Director of the Center for Postgraduate and Additional Professional Education of the Research Institute of K and WB, Almaty

Conflict of interest no.

Indication of the conditions for the revision of the protocol: Next review: no later than 3 years from the date of this approval or when new evidence becomes available.

Attached files

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What it is - Kidney failure is a serious functional disorder of the kidneys that results in fluid, electrolyte, and acid-base imbalances in the body.

Renal failure is characterized by a sharp decrease in the amount of urine excreted by the kidneys, up to its complete absence for a long time.

As a result, the work of all internal organs of a person is disrupted. The lack of adequate and timely treatment can lead to irreversible kidney damage, which will become a real threat to human life.

Causes of kidney failure

There are two forms of renal failure: acute and chronic. They differ in their manifestations and methods of treatment. Acute renal failure (ARF) sometimes becomes chronic.

AKI can occur as a result of shock of various origins, the harmful effects of poisons and toxic substances, infections, kidney diseases, and taking medications. OPN has a classification that is differentiated depending on the manifestations of the syndrome.

So, acute renal failure is divided into:

Chronic renal failure (CRF) most often develops as a result of diseases of the kidneys and urinary tract, as well as endocrine and cardiovascular diseases. This condition is characterized by a slow death of kidney tissues up to their complete destruction.

Moreover, CRF has four stages of its development:

Both acute and chronic renal failure have their own symptoms and manifestations.

Acute renal failure develops gradually, passing through several stages in its development, which are characterized by a certain set of symptoms.

There are four stages of ARF:

1) For the first, initial, stage of acute renal failure symptoms are mild. Clinical manifestations refer to the cause of the development of acute renal failure, for example, symptoms of poisoning due to exposure to poison or symptoms of the underlying disease. Thus, the primary specific symptom of acute renal failure is only a decrease in the amount of urine excreted. This condition can last for several days, during which signs of intoxication may appear with abdominal pain, slight swelling and pallor of the skin.

2) Second stage marked by the further development of oliguria up to anuria - the complete inability of the kidneys to produce urine. Symptoms become more severe due to the accumulation of urea in the blood. So, there are arrhythmias. hypertension. tachycardia. sometimes there are convulsions. Human reactions are inhibited, drowsiness occurs. In addition, extensive edema appears up to edema of the optic nerve head. On the part of the gastrointestinal tract (GIT), the patient may be tormented by nausea, vomiting and diarrhea.

3) The third stage is recovery. A person begins to feel better due to the fact that kidney function gradually returns to normal. The symptoms of intoxication disappear, the normal functioning of all internal organs is restored. The recovery period depends on the degree of kidney damage, the causes of acute renal failure and the adequacy of treatment.

4) Sometimes experts highlight fourth stage. which means the whole range of processes aimed at restoring the functionality and condition of the kidneys to the original parameters. In general, the recovery period can last several months.

Symptoms of chronic renal failure

Symptoms also develop in stages. Chronic renal failure is characterized by gradual kidney damage with slowly progressive symptoms. So, a person can suffer from CRF for several months and even years.

1) For the latent stage of chronic renal failure characterized by mild symptoms. Clinical manifestations are more related to the underlying disease, which caused the development of CRF. As chronic renal failure progresses, a person may begin to suffer from increased fatigue, which will be especially noticeable during high physical exertion, from weakness, drowsiness and dry mouth, which will increase the person's need for drinking water. Perhaps the development of polyuria - an increase in the volume of urine excreted by the kidneys.

2) Next stage- the stage of clinical manifestations, the name of which speaks for itself. There are functional failures in the work of the kidneys, which is expressed in a sharp decrease in the amount of urine excreted. This entails a change in the composition of the blood, which will be seen in the tests. Weakness and general fatigue of the patient progress. There is constant dryness in the mouth and thirst. From the gastrointestinal tract, symptoms such as nausea, stomach pain, and bad breath appear. possible diarrhea and vomiting. Due to a strong decrease in appetite, a person can significantly lose weight. Neurological disorders also appear, which are expressed in insomnia, headaches and apathy. There may be problems with the cardiovascular system, which will be expressed in arrhythmia and tachycardia. In addition, there may be pain in the bones and joints.

3) next stage is the stage of decomensation, which is characterized by the addition of additional secondary symptoms. Since a person with CRF in most cases has a hard time with tonsillitis, pharyngitis and acute respiratory infections, complications may develop up to pneumonia and pulmonary edema. In addition, a number of other complications may appear, the occurrence of which depends on the condition of the person.

4) Last stage of chronic renal failure marked by many symptoms that greatly impair a person's quality of life. The final stage is characterized by a general decrease in mood in conjunction with neurological symptoms. Severe swelling appears, the skin acquires a yellowish tint. Urine that is not excreted by the kidneys is passed out with sweat, which explains the persistent bad breath from a person with CKD.

On the part of the gastrointestinal tract, vomiting, heartburn and diarrhea can be observed. There is a strong intoxication of the body, which leads to functional disorders in the work of other organs. Thus, the production of necessary hormones decreases in a person, general immunity decreases, which leads to the development of various diseases that a person is not able to cope with on his own. Without treatment, changes in internal organs eventually become irreversible, leading to death.

Renal failure treatment

Acute renal failure is a reversible process. Treatment consists primarily in eliminating the cause of acute renal failure, which will avoid further negative effects on the kidneys. This is achieved through intensive therapy. Normal kidney function is restored by hemodialysis or peritoneal dialysis, which allows the kidneys to fully recover. The prognosis of acute renal failure in most cases is favorable.

Treatment chronic renal failure depends on the general condition of the person, on the causes of chronic renal failure and on the neglect of the disease. Therapy is carried out aimed at treating the root cause of chronic renal failure, as well as at equalizing all metabolic processes in the human body.

Therapy should also be aimed at slowing the progression of kidney damage. The success of treatment largely depends on the person, that is, on how responsibly he approaches the execution of all the doctor's prescriptions. In the last stage of CKD, regular dialysis or a healthy kidney transplant is necessary.

The prognosis of chronic renal failure is quite favorable if treatment is started at the initial stage or the stage of clinical manifestations. The prognosis of CRF in the final stage depends on the possibility of kidney transplantation. If there is such an opportunity, then this gives a person a chance for a significant extension of life, which will practically not differ in any way from the life of healthy people.

Which doctor should I contact for treatment?

If, after reading the article, you assume that you have symptoms characteristic of this disease, then you should seek the advice of a urologist.

Prognosis for life in end-stage renal disease

The end stage of chronic renal failure has ceased to be a verdict since the appearance and improvement of blood purification devices that replace renal functions. But even with effective and complete treatment, the life expectancy of a person in the terminal stage of CRF is limited to the next 10-15 years. No doctor can say exactly how long a person with broken kidneys will live.

Periods of the terminal stage of chronic renal failure

The reasons for a significant deterioration in the functional state of the kidneys with the formation of CRF are a sharp decrease in the number of nephrons in the parenchyma. Most often, their death occurs against the background of a complicated course of chronic renal diseases, in which proper treatment was not carried out or there were deep anatomical and functional lesions of the kidneys.

Regardless of the causative factors, the terminal stage of chronic renal failure is divided into several periods:

Determination of the exact condition of the patient is required for the choice of treatment tactics: at 1 and 2 periods, there are still opportunities for the application of effective therapies. In the 3rd and 4th periods, when irreversible changes occur in vital organs, it is extremely difficult to hope for a positive trend in treatment.

Basic Treatments

All therapeutic measures in the terminal stage of chronic renal failure are carried out in a hospital and are divided into conservative and surgical methods. The vast majority of patients will require all possible treatment options for renal failure, which will be used in stages.

Conservative treatment

The main methods used in all patients in the last stage of chronic renal failure include diet therapy and antitoxic effects on the blood.

1. Detoxification. Terminal CRF is characterized by a sharp deterioration in the work of the kidneys to cleanse the body of toxins and harmful substances formed in the process of life. Basic treatment implies mandatory blood detoxification. The doctor will prescribe various options for droppers, with the help of which it will be possible to partially remove toxic substances, replacing the work of diseased kidneys.

Dialysis

Any conservative methods of treatment for chronic renal failure, especially in the terminal stage, are not effective enough. It is optimal to use modern treatment methods that almost completely replace the lost kidney function. With chronic renal failure, the main type of therapy is dialysis, the essence of which is to pass the liquid through a special filter with the separation and removal of harmful substances. Dialysis can be used in any period of the terminal stage.

2. peritoneal dialysis. The inner surface of the abdomen consists of the peritoneum, which is a natural filter. It is this property that is used for continuous and effective dialysis. With the help of the operation, a special catheter tube is placed inside the abdomen, in which there is a dissolving liquid (dialysate). The blood flowing through the vessels of the peritoneum gives off harmful substances and toxins that are deposited in this dialysate. The solvent liquid must be changed every 6 hours. Replacing the dialysate is technically simple, so the patient can do it on their own.
3. Hemodialysis. For direct blood purification in the treatment of chronic renal failure, an artificial kidney device is needed. The technique involves taking blood from a sick person, cleaning it through the filter of the apparatus and returning it back to the vascular system of the body. The efficiency is much higher, so it is usually necessary to carry out the procedure lasting 5-6 hours 2-3 times a month.

kidney transplant

An operative method of treatment for kidney transplantation is carried out only in the 1st and 2nd periods of the clinical course of the terminal stage of chronic renal failure. If the doctor at the stage of examination discovered severe and irreversible changes in vital organs (heart, liver, lungs), then it is pointless to do a kidney transplant. In addition, surgery is contraindicated for severe pathologies of the endocrine system, mental illness, stomach ulcers and the presence of an acute infection anywhere in the body.

The selection of a donor kidney is of great importance. The best option is a close relative (mother, father, brother or sister). In the absence of relatives, you can try to get a donor organ from a suddenly deceased person.

Medical technologies make it possible to perform a kidney transplant without much difficulty, but the main thing is not the operation at all, but further treatment to prevent rejection of the transplanted organ. If everything went well and without complications, then the prognosis for life is favorable.

Any treatment of end-stage renal failure pursues the main goal - the restoration of basic renal functions. In the initial period of the terminal stage of the disease, it is best to perform a kidney transplant, especially if all vital organs are fully functional. For cardiopulmonary and liver failure, the doctor will prescribe various options for dialysis. A prerequisite for therapy is diet and regular detoxification courses. The result of a complex therapeutic effect will be the longest possible preservation of human life.

Kidney failure: how to treat, what diet and nutrition

Kidney failure is a pathological condition of the kidneys, in which they do not fully perform their work in the required volume as a result of any disease. This process leads to a change in the constancy of the body's self-regulation, and as a result, the work of its tissues and organs is disrupted.

Renal failure can occur in acute (ARF) and chronic (CRF) forms.

The causes of kidney failure vary depending on the form of the disease. There are several reasons that cause ROP:

4. Prerenal, that is, the disease is caused by heart failure, collapse, shock, severe arrhythmias, a significant reduction in circulating blood volume (possibly in case of blood loss).
5. Renal, in which the death of the renal tubules is caused by the action of heavy metals, poisons, alcohol, drugs, or due to insufficient blood supply to the kidney; sometimes the cause is acute glomerulonephritis or tubulointerstitial nephritis.
6. Postrenal, that is, as a result of acute bilateral blockage of the ureters in urolithiasis.

Chronic glomerulonephritis and pyelonephritis, systemic diseases, urolithiasis, neoplasms in the urinary system, diseases with impaired metabolism, vascular changes (high blood pressure, atherosclerosis) and genetic diseases are considered to be the causes of CRF.

Symptoms of the disease

Signs of renal failure depend on the severity of changes in renal function, on the duration of the disease and on the general condition of the body.

There are four degrees of acute renal failure:

7. Signs of renal failure of the initial phase: a decrease in the amount of urine, a decrease in blood pressure, an increase in heart rate.
8. The second phase (oliguric) is to reduce the amount of urine or to stop its production. The patient's condition becomes severe, as almost all body systems are affected and there is a complete metabolic disorder that threatens life.
9. The third phase (recovery or polyuric) is characterized by an increase in the amount of urine to a normal level, but it almost does not remove any substances from the body, except for salts and water, therefore, in this phase, the danger to the patient's life remains.
10. Renal failure of the 4th degree consists in the normalization of urine output, kidney function returns to normal after 1.5-3.5 months.

Signs of kidney failure in people who have a chronic form are a significant decrease in the amount of working tissues of the kidneys, which leads to azotemia (an increase in the level of nitrogenous substances in the blood). Since the kidneys cease to cope with their work, these substances are excreted in other ways, mainly through the mucous membranes of the gastrointestinal tract and lungs, which are not designed to perform such functions.

The syndrome of renal insufficiency quickly leads to the development of uremia, when self-poisoning of the body occurs. There is a rejection of meat food, bouts of nausea and vomiting, a regular feeling of thirst, a feeling of cramps in the muscles and pain in the bones. An icteric shade appears on the face, and when breathing, the smell of ammonia is felt. The amount of urine excreted and its density are greatly reduced. Kidney failure in children proceeds according to the same principles as in adults.

Complications of the disease

The end stage of renal failure is due to the complete loss of kidney function, due to which toxic products accumulate in the patient's body. Terminal renal failure provokes complications such as gastroenterocolitis, myocardial dystrophy, hepatic-renal syndrome, pericarditis.

Hepato-renal insufficiency means progressive oliguric renal failure in the presence of liver disease. With hepatic-renal syndrome, vasoconstriction occurs in the cortical region of the kidneys. This syndrome in cirrhosis is considered as the last stage of the development of the disease, which leads to the retention of water and sodium ions.

Diagnostic methods

Diagnosis of kidney failure includes determining the amount of creatinine, potassium and urea in the blood, as well as constant monitoring of the amount of urine excreted. They can use ultrasound, radiography and radionuclide methods.

To diagnose chronic renal failure, a set of advanced biochemical blood and urine tests, filtration rate analysis, and urography are used.

Medical treatment

Treatment of renal failure is carried out in the intensive care unit or intensive care units of the hospital. At the slightest complications, you should immediately seek medical help. Today it is possible to treat patients with acute renal failure using an artificial kidney machine while the kidney functions are being restored.

If treatment is started in a timely manner and carried out in full, then the prognosis is usually favorable.

During therapy, disturbed metabolic processes are treated, diseases that aggravate chronic renal failure are identified and treated. At a later stage, permanent hemodialysis and kidney transplantation are required.

Medicines for renal failure are used to reduce metabolic processes: anabolic hormones - testosterone propionate solution, methylandrostenediol. To improve renal microcirculation, you need to use trental, chimes, troxevasin and complamin for a long time. To stimulate urine output, a glucose solution is prescribed with the introduction of insulin or diuretics from the furosemide group. If there is a high concentration of nitrogen in the blood, then the gastrointestinal tract is washed with a solution of sodium bicarbonate, due to which nitrogenous slags are removed. This procedure is carried out on an empty stomach, before meals, once a day.

Antibiotics for renal failure are used in reduced doses, since the rate of their excretion is significantly reduced. The degree of chronic renal failure is taken into account and the dose of antibiotics is reduced to 2 or 4 times.

Treatment of the disease with folk methods

How to treat kidney failure without the use of antibiotics and other medicines is described in the recipes listed below.

11. Take lingonberry leaves, chamomile, motherwort grass, string flowers, dandelion and violets in half a teaspoon. This collection is poured with a glass of boiled water, insisted for about 1 hour and taken in a third of a glass 5 times a day.
12. The second recipe: mix mint, St. John's wort, lemon balm, calendula 1 tbsp. l. In a saucepan, pour the herbal mixture with 2 cups of boiled water and bring to a boil. Pour the prepared infusion into a thermos and leave overnight. Take 100 ml per day.
13. Folk remedies for kidney failure include the use of watermelon peels, which have a diuretic effect. Take 5 tbsp. l. chopped watermelon rinds per liter of water. It is necessary to fill the crusts with water, leave for an hour and take several times throughout the day.
14. Pomegranate peel and rose hips also have a slight diuretic effect. Take them in equal parts and fill with two glasses of boiled water. Insist for half an hour in warmth and take up to 2 glasses a day.

Principles of diet therapy in renal failure

Diet in kidney failure plays an important role - it is necessary to adhere to a diet low in protein and salt, to exclude drugs that have a toxic and damaging effect on the kidneys. Nutrition in kidney failure depends on several general principles:

15. It is necessary to limit the intake of proteins to 65 g per day, depending on the phase of kidney disease.
16. The energy value of food increases due to the increased consumption of fats and carbohydrates.
17. Diet for kidney failure is reduced to the use of a variety of fruits and vegetables. In this case, it is necessary to take into account the content of proteins, vitamins and salts in them.
18. Appropriate culinary processing of products is carried out to improve appetite.
19. The intake of sodium chloride and water into the body is regulated, the amount of which affects the presence of puffiness and blood pressure indicators.

Sample diet menu for kidney failure:

First breakfast: boiled potatoes - 220g, one egg, sweet tea, honey (jam) - 45g.

Lunch: sweet tea, sour cream - 200g.

Dinner: rice soup - 300g (butter - 5-10g, sour cream - 10g, potatoes - 90g, carrots - 20g, rice - 20g, onions - 5g and tomato juice - 10g). The second is served with vegetable stew - 200 g (from carrots, beets and rutabaga) and a glass of apple jelly.

Dinner: rice milk porridge - 200g, sweet tea, jam (honey) - 40g.

Prognosis for the disease

With timely and adequate treatment, the prognosis for acute renal failure is quite favorable.

In the chronic variant of the disease, the prognosis depends on the stage of the process and the degree of impaired renal function. In the case of compensation for the work of the kidneys, the prognosis for the patient's life is favorable. But in the terminal stage, the only life-sustaining options are permanent hemodialysis or a donor kidney transplant.

Stage 4 Chronic Kidney Failure (CKD)

Stage 4 chronic renal failure is a serious stage of renal disease with a glomerular filtration rate of 15-30 ml/min. A severe decrease in kidney function will cause systemic symptoms. Patients in this stage, on the one hand, should pay special attention to diet, lifestyle changes in order to manage the disease situation and not burden the kidneys, and on the other hand, receive treatment to improve the kidney situation and avoid threatening complications.

As kidney function deteriorates, metabolites can accumulate in the bloodstream and cause a medical condition called Anemia. Because the kidneys cannot produce erythropoietin efficiently, and the hormone stimulates the production of blood cells, patients with stage 4 kidney failure will become anemic. The kidneys regulate electrolyte balance, and in stage 4 kidney failure, it was common for patients to suffer from high calorie, high phosphorus, low calcium, high sodium, and the like. High potassium will lead to arrhythmia, high sodium will threaten fluid retention and increase blood pressure, and high phosphorus will cause diseased bones.

The symptom of stage 4 chronic renal failure mainly includes:

* Weakness. Feeling tired is the result of a symptom of anemia in stage 4.

* Change in urination. Urine may be frothy and the foam persists for a long time. This is a sign of increased protein in the urine. Blood in the urine will cause the color of the urine to be dark orange, brown, tea-colored, or red. The person may pass more or less urine, or go to the bathroom frequently at night.

* Difficulty falling asleep. Itchy skin, restless legs, or muscle cramps may keep the sufferer awake and have difficulty falling asleep.

* Nausea. Chronic kidney failure can cause vomiting or nausea.

* Lack of appetite. The patient has no desire to eat and often complains of a metallic or ammonia taste in the mouth.

* Cardiovascular diseases. In stage 4 chronic renal failure, various factors, including high blood pressure, water and salt retention, anemia and toxic substances, will increase the risk for patients to develop heart failure, arrhythmias, myocardial damage, and the like.

* Symptoms in the nervous system. Early symptoms mainly include insomnia, poor concentration, memory loss. In some cases, patients suffer from tingling, numbness, coma, insanity and others.

Stage 4 patients usually require a blood test creatinine. hemoglobin, calcium, potassium and calcium in order to learn how the kidneys work and how to reduce the risk of complications. After determining the result of the analysis, the doctor will advise the patient on the best opinion of the treatment. Because diet is a necessary part of the treatment, so a dietitian will also be necessary for the treatment. And the dietitian will examine the result of the analysis and give the patient his own dietary plan. A proper eating plan helps preserve kidney function and overall health.

Some of the basic dietary advice in stage 4 kidney failure mainly includes the following:

Calculate protein intake. Proteins are sources of nutrition for the human body. However, too much protein is harmful because it will produce more nitrogenous waste. Protein intake of 0.6 g per kilogram per day is beneficial when your glomerular filtration rate falls below 25, or approximately 25% of kidney function remains. You should ask your doctor how much protein is available per day and remember that at least half of the protein comes from high quality sources like egg white, lean meats, fish, etc.

Sodium restriction. Too much sodium can cause large fluid retention. And this will lead to swelling and shortness of breath in a person. A person in stage 4 kidney failure should avoid processed foods and prepare meals with low sodium or sodium ingredients. Most diets start with a goal of 1500-2000 mg per day or as recommended by your doctor.

Maintain a healthy body weight. If you want to maintain a healthy weight by burning calories, and now you need to exercise regularly.

Taking cholesterol. Replace saturated fats with unsaturated fats and eat a low-fat diet overall. This may help reduce the risk of cardiovascular disease.

Other Tips. You should limit your potassium intake if the lab results are above the normal range. If the patient has too much fluid content, then he will limit fluid intake. Fluid retention symptoms mainly include swelling in the legs, arms, face, high blood pressure, and shortness of breath.

In order to prolong kidney health, patients in stage 4 kidney failure should take the medicine recommended by the doctor to control blood pressure, anemia and other situations. People in stage 4 will probably lose kidney function further, and end up with dialysis. In addition to a basic management plan to control the progress of the disease, proper treatment will help improve kidney function from a bad state to a better state, and therefore dialysis will not be necessary. And this will be done with the combination of Western medicine and traditional Chinese medicine.

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Renal failure and anuria

Acute renal failure- a condition in which there is a sudden cessation or a very sharp decrease in the function of both kidneys or a single kidney. As a result of the development of such a state, azotemia . which increases rapidly, and severe water and electrolyte disturbances are also noted.

In the same time anuria is a serious condition of the body, in which the flow of urine into the bladder completely stops, or no more than 50 ml of it enters during the day. A person suffering from anuria does not have both urination and the urge to urinate.

What's happening?

In the pathogenesis of the disease, the leading is a violation of blood circulation in the kidneys and a decrease in the level of oxygen delivered to them. As a result, there is a violation of all important functions of the kidneys - filtration . excretory . secretory . As a result, the content of nitrogenous metabolism products sharply increases in the body, and metabolism is seriously disturbed.

In about 60% of cases, signs of acute renal failure are observed after surgery or injury. About 40% of cases of the disease manifest themselves in the treatment of patients in a hospital. In rare cases (about 1-2%), this syndrome develops in women during pregnancy .

Distinguish acute and chronic stages of renal failure. The clinic of acute renal failure can develop over several hours. If the diagnosis is carried out in a timely manner, and all measures have been taken to prevent such a condition, then the kidney functions are fully restored. Presentation of treatment methods is carried out only by a specialist.

Several types of acute renal failure are defined. prerenal renal failure develops as a result of an acute violation of blood flow in the kidneys. Renal renal failure is the result of damage to the renal parenchyma. Postrenal renal failure is a consequence of a sharp violation of the outflow of urine.

The reasons

The development of acute renal failure occurs during the receipt of traumatic shock, in which tissues are damaged. Also, this condition develops under the influence of reflex shock, a decrease in the amount of circulating blood due to burns, and a large loss of blood. In this case, the state is defined as shock kidney . This occurs in serious accidents, severe surgical interventions, injuries, myocardial infarction . transfusion of incompatible blood.

The state called toxic kidney . manifested as a result of poisoning with poisons, intoxication of the body with medications, alcohol abuse, substance abuse, radiation.

Acute infectious kidney - a consequence of serious infectious diseases - hemorrhagic fever . leptospirosis . It can also occur in the course of a severe course of infectious diseases, in which dehydration develops rapidly.

Acute renal failure also develops due to obstruction of the urinary tract. This happens if the patient has a growing tumor, there are stones, thrombosis, embolism of the renal arteries is observed, or an injury to the ureter occurs. In addition, anuria sometimes becomes a complication of acute pyelonephritis and acute glomerulonephritis .

During pregnancy, acute renal failure is most often observed in the first and third trimesters. In the first trimester, this condition may develop after abortion . especially carried out in non-sterile conditions.

Renal failure also develops due to postpartum hemorrhage, as well as preeclampsia in the last weeks of pregnancy.

There are also a number of cases when it is not possible to clearly determine the reasons why the patient develops acute renal failure. Sometimes this situation is observed when several different factors affect the development of the disease at once.

Symptoms

Initially, the patient does not directly show symptoms of renal failure, but signs of the disease that leads to the development of anuria. These can be signs of shock, poisoning, directly symptoms of the disease. Further, the symptoms in children and adults are manifested by a decrease in the amount of urine excreted. Initially, its amount decreases to 400 ml daily (this condition is called oliguria ), later the patient excretes no more than 50 ml of urine per day (determined anuria ). The patient complains of nausea, he also has vomiting, appetite disappears.

A person becomes lethargic, drowsy, he has a lethargy of consciousness, and sometimes convulsions and hallucinations appear.

The condition of the skin also changes. It becomes very dry, turns pale, swelling and hemorrhages may appear. A person breathes often and deeply, he has tachycardia . heart rhythm is disturbed and blood pressure rises. There may also be loose stools and bloating .

Anuria is cured if the treatment of anuria was started in a timely manner and carried out correctly. To do this, the doctor must clearly determine the causes of anuria. If therapy is carried out correctly, then the symptoms of anuria gradually disappear and a period begins when diuresis is restored. During the improvement of the patient's condition, anuria is characterized by a daily diuresis of 3-5 liters. However, in order for health to be fully restored, it takes from 6 to 18 months.

Thus, the course of the disease is divided into four stages. At the initial stage, a person's condition directly depends on the cause that provoked kidney failure. At the second, oligoanuric stage, the amount of urine decreases sharply, or it may be completely absent. This stage is the most dangerous, and if it continues for too long, coma and even death are possible. In the third, diuretic stage, the patient gradually increases the amount of urine that is excreted. Then comes the fourth stage - recovery.

Diagnostics

A patient with suspected renal failure or with signs of anuria is assigned a series of examinations. First of all, this is a consultation with a urologist, biochemical and clinical blood tests, ultrasound, intravenous urography. Anuria is easy to diagnose, since by questioning the patient it can be understood that he has not had urination and urge to urinate for a long time. To differentiate this condition from acute urinary retention, a bladder catheter is performed to confirm the absence of urine in the bladder.

Treatment

All patients who have symptoms of acute renal failure should be urgently taken to a hospital, where diagnosis and subsequent treatment is carried out in the intensive care unit or in the nephrology department. The leading role in this case is as early as possible the start of treatment of the underlying disease in order to eliminate all the causes that led to kidney damage. Given the fact that the pathogenesis of the disease is most often determined by the effect of shock on the body, it is necessary to promptly carry out anti-shock measures . The classification of the types of the disease is of decisive importance in the choice of treatment methods. So, in case of renal failure caused by blood loss, it is compensated by the introduction of blood substitutes. If poisoning occurs initially, gastric lavage is mandatory to remove toxic substances. In severe renal failure, hemodialysis or peritoneal dialysis is necessary.

A particularly serious condition is caused by the terminal stage of chronic renal failure. In this case, kidney function is completely lost, and toxins accumulate in the body. As a result, this condition leads to serious complications. Therefore, chronic renal failure in children and adults must be properly treated.

Treatment of renal failure is carried out gradually, taking into account certain stages. Initially, the doctor determines the reasons that led to the patient showing signs of kidney failure. Next, steps must be taken to achieve a relatively normal amount of urine that is excreted in a person.

Depending on the stage of renal failure, conservative treatment is carried out. Its goal is to reduce the amount of nitrogen, water and electrolytes that enter the body so that this amount matches that which is excreted from the body. In addition, an important point in the restoration of the body is diet with renal failure, constant monitoring of his condition, as well as monitoring of biochemical parameters. Especially careful attitude to treatment should be if there is renal failure in children.

The next important step in the treatment of anuria is dialysis therapy . In some cases, dialysis therapy is used to prevent complications already in the early stages of the disease.

An absolute indication for dialysis in a patient is symptomatic uremia, the accumulation of fluid in the patient's body, which cannot be removed using conservative methods.

Particular attention is paid to the nutrition of patients. The fact is that both hunger and thirst can dramatically worsen a person's condition. In this case, it is shown low protein diet . that is, the diet should be dominated by fats, carbohydrates. If a person cannot eat on his own, glucose and nutritional mixtures must be administered intravenously.

Complications

The course of acute renal failure is often complicated by infectious diseases. It is in this course that the disease can be fatal.

As a complication of the cardiovascular system is circulatory failure . arrhythmias . hypertension . pericarditis . Often in acute renal failure, there is a manifestation of neurological disorders. Patients who are not on dialysis may experience severe drowsiness . disturbances of consciousness, trembling and other disorders of the nervous system. More often, these disorders develop in older people.

From the side gastrointestinal tract complications also develop frequently. It can be nausea, anorexia, intestinal obstruction.

Prevention

In order to prevent the development of such a dangerous condition of the body, first of all, it is necessary to provide timely qualified assistance to those patients who have a high risk of developing acute renal failure. These are people with severe injuries, burns; those who have just undergone a major operation, patients with sepsis, eclampsia, etc. Very carefully, you should use those medications that are nephrotoxic .

In order to prevent the development of chronic renal failure, which develops as a consequence of a number of kidney diseases, it is necessary to prevent exacerbation of pyelonephritis, glomerulonephritis. It is important for chronic forms of these diseases to follow a strict diet prescribed by a doctor. Patients with chronic kidney disease should be regularly monitored by a doctor.

Stage 5 Chronic Renal Failure (CRF)

* Belching

* Shortness of breath caused by fluid accumulation

* Muscle cramp

* Tingling of hands and feet

* Difficulty concentrating

* Decreased urine output

* Feeling tired and getting weaker and weaker

* Change in urine color

* Increased skin pigmentation

The kidneys are very important for our health. In the stage of kidney failure, the kidneys are not able to efficiently excrete toxins and extra water from the body, and they are not yet able to do those that regulate blood pressure, maintain the balance of electrolytes like potassium, phosphorus, etc. and produce erythropoietin to stimulate the production of blood cells.

Patients with stage 5 renal failure require a nephrologist. Patients will suffer from urine test and blood test for creatinine and electrolyte, and the doctor will recommend treatment to reduce complications and make patients feel healthier. The doctor will probably recommend dialysis or some of their doctors will prepare a kidney transplant. There are two types of dialysis: peritoneal dialysis and hemodialysis. Before dialysis, there will be questions from patients. The essence of dialysis is only a method that helps patients live longer, but it cannot improve the kidneys and cause side effects. When dialysis is needed for patients, the doctor will simply advise taking this treatment and choosing which type to treat. As for kidney transplantation, patients will evaluate whether a transplant is possible, consider the risk of recurrence, and which kidney would be suitable.

If a person find natural treatments, then Chinese medicine treatment would be your choice. Treatment with Chinese medicines, despite its slow effects, compared with Western medicine, can nourish the kidneys, refrain from inflammation, speed up nutrient supplementation to repair damaged (not completely damaged) kidney cells, and accompanying with repairing the kidneys, the clinical symptoms/complications will be better under control and patients may feel much relieved.

Diet is so important in reducing the risk of complications and improving overall health that patients should see a dietitian. And the dietician will provide a dietary plan that is based on the personal laboratory result and the underlying disease situation. Dietary advice for stage 5 kidney disease includes:

More vegetables, grains and fruits can be included, but note to limit or avoid foods high in potassium and phosphorus. Limit total fat intake, and replace saturated fats with unsaturated ones. And it contributes to the prevention of cardiovascular diseases.

Limit your intake of high-sodium refined and processed foods, and have a low-sodium lunch.

Sufficient protein supplementation to supplement protein loss due to dialysis.

Goal for a healthy body weight by calorie intake based on body size and individual needs.

If the output of urine is less than 1 liter per day (nearly 32 ounces) and? serum potassium above 5.0, a low potassium diet is recommended.

Avoid foods high in potassium and keep track of your potassium levels by getting regular blood tests.

Limiting 2000 mg of calcium and phosphorus to 1000 mg is based on individual requirements.

Remember that there really is no diet that is right for every case of kidney disease. Patients need to make a diet plan based on the individual condition after talking with the doctor. Please note that this may be a kidney complication which can be dangerous. Check the condition of the disease as often as possible and communicate with your doctor regularly to know if there is a need for treatment or dietary changes.

If you have any questions, please contact us via phone +86-311-89261580 or email [email protected] or skype:hospital.kidney. We will answer your questions as soon as possible.

chronic renal failure b is the gradual decline in renal function due to the death of nephrons due to chronic kidney disease. At the initial stages, it is asymptomatic, later on, disorders of the general condition and urination, edema, and pruritus join. The gradual deterioration of kidney function leads to disruption of the body's vital functions, the occurrence of complications from various organs and systems. Diagnosis includes clinical and biochemical tests, Reberg and Zimnitsky tests, ultrasound of the kidneys, ultrasound of the renal vessels. Treatment of chronic renal failure is based on the treatment of the underlying disease, elimination of symptoms and repeated courses of extracorporeal hemocorrection.

General information

(CRF) is an irreversible violation of the filtration and excretory functions of the kidneys, up to their complete cessation, due to the death of renal tissue. CRF has a progressive course, in the early stages it manifests itself as a general malaise. With an increase in chronic renal failure - pronounced symptoms of intoxication of the body: weakness, loss of appetite, nausea, vomiting, swelling, skin - dry, pale yellow. Sharply, sometimes to zero, diuresis decreases. In the later stages, heart failure develops, pulmonary edema, bleeding tendency, encephalopathy, uremic coma. Shown hemodialysis and kidney transplant.

Causes of CRF

Chronic renal failure can be the outcome of chronic glomerulonephritis, nephritis in systemic diseases, chronic pyelonephritis, diabetic glomerulosclerosis, renal amyloidosis, polycystic kidney disease, nephroangiosclerosis and other diseases that affect both kidneys or a single kidney.

Pathogenesis

The pathogenesis is based on the progressive death of nephrons. Initially, renal processes become less efficient, then kidney function is impaired. The morphological picture is determined by the underlying disease. Histological examination indicates the death of the parenchyma, which is replaced by connective tissue. The development of CRF is preceded by a period of suffering from chronic kidney disease lasting from 2 to 10 years or more. The course of kidney disease before the onset of CRF can be divided into a number of stages. The definition of these stages is of practical interest, since it affects the choice of treatment tactics.

Classification

The following stages of chronic renal failure are distinguished:

1. Latent. Occurs without significant symptoms. Usually detected only by the results of in-depth clinical studies. Glomerular filtration is reduced to 50-60 ml/min, there is periodic proteinuria.
2. Compensated. The patient is worried about increased fatigue, a feeling of dry mouth. An increase in the volume of urine with a decrease in its relative density. Decreased glomerular filtration to 49-30 ml/min. Increased creatinine and urea levels.
3. Intermittent. The severity of clinical symptoms increases. There are complications due to the increasing CRF. The patient's condition changes in waves. Decreased glomerular filtration rate to 29-15 ml/min, acidosis, persistent increase in creatinine levels.
4. Terminal. It is characterized by a gradual decrease in diuresis, an increase in edema, gross violations of acid-base and water-salt metabolism. There are phenomena of heart failure, congestion in the liver and lungs, liver dystrophy, polyserositis.

CKD symptoms

In the period preceding the development of chronic renal failure, renal processes persist. The level of glomerular filtration and tubular reabsorption is not impaired. Subsequently, glomerular filtration gradually decreases, the kidneys lose their ability to concentrate urine, and renal processes begin to suffer. At this stage, homeostasis is not yet disturbed. In the future, the number of functioning nephrons continues to decrease, and with a decrease in glomerular filtration to 50-60 ml / min, the patient has the first signs of CRF.

Patients with a latent stage of CKD usually do not complain. In some cases, they note mild weakness and decreased performance. Patients with chronic renal failure in the compensated stage are concerned about a decrease in efficiency, increased fatigue, and a periodic feeling of dry mouth. With the intermittent stage of chronic renal failure, the symptoms become more pronounced. Weakness increases, patients complain of constant thirst and dry mouth. Appetite is reduced. The skin is pale, dry.

Patients with end-stage renal failure lose weight, their skin becomes gray-yellow, flabby. Characterized by itching, reduced muscle tone, tremor of the hands and fingers, small muscle twitches. Thirst and dry mouth intensify. Patients are lethargic, drowsy, unable to concentrate.

With an increase in intoxication, a characteristic smell of ammonia from the mouth, nausea and vomiting appear. Periods of apathy are replaced by excitement, the patient is inhibited, inadequate. Characterized by dystrophy, hypothermia, hoarseness, lack of appetite, aphthous stomatitis. The abdomen is swollen, frequent vomiting, diarrhea. Stool dark, offensive. Patients complain of excruciating skin itching and frequent muscle twitches. Anemia increases, hemorrhagic syndrome and renal osteodystrophy develop. Typical manifestations of chronic renal failure in the terminal stage are myocarditis, pericarditis, encephalopathy, pulmonary edema, ascites, gastrointestinal bleeding, uremic coma.

Complications

CRF is characterized by increasing disorders of all organs and systems. Blood changes include anemia due to both inhibition of hematopoiesis and a reduction in the life of red blood cells. Coagulation disorders are noted: prolongation of bleeding time, thrombocytopenia, a decrease in the amount of prothrombin. On the part of the heart and lungs, arterial hypertension is observed (in more than half of the patients), congestive heart failure, pericarditis, myocarditis. In the later stages, uremic pneumonitis develops.

Neurological changes in the early stages include distraction and sleep disturbance, in the later stages - lethargy, confusion, in some cases delirium and hallucinations. On the part of the peripheral nervous system, peripheral polyneuropathy is detected. On the part of the gastrointestinal tract in the early stages, a deterioration in appetite, dry mouth is detected. Later there is an eructation, nausea, vomiting, stomatitis. As a result of irritation of the mucosa during the release of metabolic products, enterocolitis and atrophic gastritis develop. Superficial ulcers of the stomach and intestines are formed, often becoming sources of bleeding.

On the part of the musculoskeletal system, CRF is characterized by various forms of osteodystrophy (osteoporosis, osteosclerosis, osteomalacia, fibrous osteitis). Clinical manifestations of renal osteodystrophy are spontaneous fractures, skeletal deformities, compression of the vertebrae, arthritis, pain in the bones and muscles. On the part of the immune system, lymphocytopenia develops in chronic renal failure. Reduced immunity causes a high incidence of purulent-septic complications.

Diagnostics

If the development of chronic renal failure is suspected, the patient needs to consult a nephrologist and conduct laboratory tests: a biochemical analysis of blood and urine, a Reberg test. The basis for the diagnosis is a decrease in the level of glomerular filtration, an increase in the level of creatinine and urea.

During the Zimnitsky test, isohyposthenuria is detected. Ultrasound of the kidneys indicates a decrease in the thickness of the parenchyma and a decrease in the size of the kidneys. A decrease in intraorganic and main renal blood flow is detected on ultrasound of the renal vessels. Radiocontrast urography should be used with caution due to the nephrotoxicity of many contrast agents. The list of other diagnostic procedures is determined by the nature of the pathology that caused the development of CRF.

Treatment of chronic renal failure

Specialists in the field of modern urology and nephrology have extensive capabilities in the treatment of CRF. Timely treatment aimed at achieving a stable remission can often significantly slow down the development of pathology and delay the appearance of severe clinical symptoms. When conducting therapy for a patient with an early stage of chronic renal failure, special attention is paid to measures to prevent the progression of the underlying disease.

Treatment of the underlying disease continues even in violation of renal processes, but during this period the importance of symptomatic therapy increases. If necessary, prescribe antibacterial and antihypertensive drugs. Shown sanatorium treatment. It is required to control the level of glomerular filtration, the concentration function of the kidneys, renal blood flow, the level of urea and creatinine. In case of violations of homeostasis, the acid-base composition, azotemia and water-salt balance of the blood are corrected. Symptomatic treatment consists in the treatment of anemic, hemorrhagic and hypertensive syndromes, maintaining normal cardiac activity.

Patients with chronic renal failure are prescribed a high-calorie (about 3,000 calories) low-protein diet that includes essential amino acids. It is necessary to reduce the amount of salt (up to 2-3 g / day), and with the development of severe hypertension, transfer the patient to a salt-free diet. The protein content in the diet depends on the degree of impaired renal function, with glomerular filtration below 50 ml / min, the amount of protein decreases to 30-40 g / day, with a decrease below 20 ml / min - up to 20-24 g / day.

With the development of renal osteodystrophy, vitamin D and calcium gluconate are prescribed. One should be aware of the danger of calcification of the internal organs caused by large doses of vitamin D in hyperphosphatemia. To eliminate hyperphosphatemia, sorbitol + aluminum hydroxide is prescribed. During therapy, the level of phosphorus and calcium in the blood is monitored. Correction of the acid-base composition is carried out with a 5% solution of sodium bicarbonate intravenously. In oliguria, to increase the volume of urine excreted, furosemide is prescribed at a dosage that provides polyuria. To normalize blood pressure, standard antihypertensive drugs are used in combination with furosemide.

With anemia, iron preparations, androgens and folic acid are prescribed, with a decrease in hematocrit to 25%, fractional transfusions of erythrocyte mass are performed. The dosage of chemotherapeutic drugs and antibiotics is determined depending on the method of excretion. Doses of sulfonamides, cephaloridine, methicillin, ampicillin and penicillin are reduced by 2-3 times. When taking polymyxin, neomycin, monomycin and streptomycin, even in small doses, complications may develop (neuritis of the auditory nerve, etc.). Patients with CRF are contraindicated in derivatives of nitrofurans.

The use of glycosides in the treatment of heart failure should be done with caution. The dosage is reduced, especially with the development of hypokalemia. Patients with an intermittent stage of chronic renal failure during an exacerbation are prescribed hemodialysis. After the patient's condition improves, they are again transferred to conservative treatment. Effective appointment of repeated courses.

With the onset of the terminal stage and the absence of the effect of symptomatic therapy, the patient is prescribed regular hemodialysis (2-3 times a week). Transfer to hemodialysis is recommended when creatinine clearance falls below 10 ml/min and its plasma level rises to 0.1 g/l. When choosing the tactics of therapy, it should be taken into account that the development of complications in chronic renal failure reduces the effect of hemodialysis and excludes the possibility of kidney transplantation.

Forecast and prevention

The prognosis for chronic renal failure is always serious. Sustainable rehabilitation and a significant prolongation of life is possible with timely hemodialysis or kidney transplantation. The decision on the possibility of carrying out these types of treatment is made by transplantologists and doctors of hemodialysis centers. Prevention involves the timely detection and treatment of diseases that can cause chronic renal failure.