Severe hpn. Causes of chronic renal failure: symptoms, methods of therapy and consequences. Blood clotting disorder

Modern medicine manages to cope with most acute kidney diseases and restrain the progression of most chronic ones. Unfortunately, about 40% of renal pathologies are still complicated by the development of chronic renal failure (CRF).

This term refers to the death or replacement of part of the structural units of the kidneys (nephrons) by the connective tissue and the irreversible impairment of the kidneys' functions in cleansing the blood of nitrogenous toxins, the production of erythropoietin, which is responsible for the formation of red blood elements, the removal of excess water and salts, as well as the reverse absorption of electrolytes.

The consequence of chronic renal failure is a disorder of water, electrolyte, nitrogen, acid-base balance, which leads to irreversible changes in the state of health and often causes death in the terminal variant of CRF. The diagnosis is made with violations that are recorded for three months or longer.

Today, CKD is also called chronic kidney disease (CKD). This term emphasizes the potential for the development of severe forms of renal failure, even in the initial stages of the process, when the glomerular filtration rate (GFR) has not yet been reduced. This allows you to more closely deal with patients with asymptomatic forms of renal failure and improve their prognosis.

Criteria for CRF

The diagnosis of CRF is made if the patient has had one of two types of renal disorders for 3 months or more:

• Damage to the kidneys with a violation of their structure and function, which are determined by laboratory or instrumental diagnostic methods. At the same time, GFR may decrease or remain normal.
• There is a decrease in GFR less than 60 ml per minute with or without kidney damage. This indicator of the filtration rate corresponds to the death of about half of the kidney nephrons.

What leads to CKD

Almost any chronic kidney disease without treatment, sooner or later, can lead to nephrosclerosis with kidney failure to function normally. That is, without timely therapy, such an outcome of any kidney disease as CRF is just a matter of time. However, cardiovascular pathologies, endocrine diseases, and systemic diseases can lead to renal failure.

• kidney disease: chronic glomerulonephritis, chronic tubulointerstitial nephritis, kidney tuberculosis, hydronephrosis, polycystic kidney disease, nephrolithiasis.
• Pathologies of the urinary tract: urolithiasis, urethral strictures.
• Cardiovascular diseases: arterial hypertension, atherosclerosis, incl. angiosclerosis of the renal vessels.
• Endocrine pathologies: diabetes.
• Systemic diseases: renal amyloidosis, .

How CKD develops

The process of replacing the affected glomeruli of the kidney with scar tissue is simultaneously accompanied by functional compensatory changes in the remaining ones. Therefore, chronic renal failure develops gradually with the passage of several stages in its course. The main cause of pathological changes in the body is a decrease in the rate of blood filtration in the glomerulus. The glomerular filtration rate is normally 100-120 ml per minute. An indirect indicator by which one can judge GFR is blood creatinine.

• The first stage of CKD is the initial

At the same time, the glomerular filtration rate remains at the level of 90 ml per minute (normal variant). There are confirmed kidney damage.

• Second stage

It suggests kidney damage with a slight decrease in GFR in the range of 89-60. For the elderly, in the absence of structural damage to the kidneys, such indicators are considered the norm.

• Third stage

In the third moderate stage, GFR drops to 60-30 ml per minute. At the same time, the process taking place in the kidneys is often hidden from view. There is no bright clinic. Perhaps an increase in the volume of urine excreted, a moderate decrease in the number of red blood cells and hemoglobin (anemia) and associated weakness, lethargy, decreased performance, pale skin and mucous membranes, brittle nails, hair loss, dry skin, decreased appetite. Approximately half of the patients have an increase in blood pressure (mainly diastolic, i.e. lower).

• Fourth stage

It is called conservative, as it can be restrained by drugs and, like the first one, does not require blood purification by hardware methods (hemodialysis). At the same time, glomerular filtration is kept at the level of 15-29 ml per minute. There are clinical signs of renal failure: severe weakness, decreased ability to work against the background of anemia. Increased urine output, significant urination at night with frequent nocturnal urges (nocturia). Approximately half of patients suffer from high blood pressure.

• Fifth stage

The fifth stage of renal failure got the name terminal, i.e. final. With a decrease in glomerular filtration below 15 ml per minute, the amount of urine excreted (oliguria) drops until it is completely absent in the outcome of the condition (anuria). All signs of poisoning the body with nitrogenous slags (uremia) appear against the background of disturbances in water and electrolyte balance, lesions of all organs and systems (primarily the nervous system, heart muscle). With such a development of events, the life of the patient directly depends on dialysis of the blood (cleansing it bypassing non-working kidneys). Without hemodialysis or kidney transplantation, patients die.

Symptoms of chronic renal failure

Appearance of patients

Appearance does not suffer until the stage when glomerular filtration is significantly reduced.

• Due to anemia, pallor appears, due to water and electrolyte disorders, dry skin.
• As the process progresses, yellowness of the skin and mucous membranes appears, a decrease in their elasticity.
• Spontaneous hemorrhages and bruising may occur.
• Because of the scratches.
• Characterized by the so-called renal edema with puffiness of the face up to the common type of anasarca.
• Muscles also lose their tone, become flabby, due to which fatigue increases and the patient's ability to work decreases.

Nervous System Damage

This is manifested by apathy, night sleep disorders and drowsiness during the day. Decreased memory, ability to learn. As chronic renal failure increases, pronounced lethargy and disorders of the ability to remember and think appear.

Violations in the peripheral part of the nervous system affect the chilliness of the limbs, tingling sensations, crawling. In the future, movement disorders in the arms and legs join.

urinary function

She initially suffers from a type of polyuria (an increase in the volume of urine) with a predominance of nocturnal urination. Further, CRF develops along the path of reducing the volume of urine and the development of edematous syndrome up to the complete absence of excretion.

Water-salt balance

• salt imbalance is manifested by increased thirst, dry mouth
• weakness, darkening of the eyes when standing up abruptly (due to sodium loss)
• excess potassium explains muscle paralysis
• respiratory disorders
• slowing of heartbeats, arrhythmias, intracardiac blockade up to cardiac arrest.

Against the background of an increase in the production of parathyroid hormones by the parathyroid glands, a high level of phosphorus and a low level of calcium in the blood appear. This leads to softening of the bones, spontaneous fractures, itchy skin.

Nitrogen imbalances

They cause an increase in blood creatinine, uric acid and urea, as a result of:

• with GFR less than 40 ml per minute, enterocolitis develops (damage to the small and large intestine with pain, bloating, frequent loose stools)
• ammonia smell from the mouth
• secondary articular lesions of the type of gout.

The cardiovascular system

• first, it reacts with an increase in blood pressure
• secondly, heart lesions (muscles -, pericardial sac - pericarditis)
• there are dull pains in the heart, cardiac arrhythmias, shortness of breath, swelling in the legs, liver enlargement.
• with an unfavorable course of myocarditis, the patient may die on the background of acute heart failure.
• pericarditis can occur with the accumulation of fluid in the pericardial sac or the precipitation of uric acid crystals in it, which, in addition to pain and expansion of the boundaries of the heart, gives a characteristic ("funeral") pericardial rub when listening to the chest.

hematopoiesis

Against the background of a deficiency in the production of erythropoietin by the kidneys, hematopoiesis slows down. The result is anemia, which manifests itself very early in weakness, lethargy, and decreased performance.

Pulmonary complications

characteristic of the late stages of CKD. This is a uremic lung - interstitial edema and bacterial inflammation of the lung against the background of a fall in immune defenses.

Digestive system

It reacts with decreased appetite, nausea, vomiting, inflammation of the oral mucosa and salivary glands. With uremia, erosive and ulcerative defects of the stomach and intestines appear, fraught with bleeding. Acute hepatitis also becomes a frequent companion of uremia.

Kidney failure during pregnancy

Even a physiological pregnancy significantly increases the load on the kidneys. In chronic kidney disease, pregnancy exacerbates the course of the pathology and can contribute to its rapid progression. This is due to the fact that:

• during pregnancy, increased renal blood flow stimulates the overstrain of the renal glomeruli and the death of some of them,
• deterioration of conditions for reabsorption of salts in the tubules of the kidney leads to the loss of high volumes of protein, which is toxic to the kidney tissue,
• increased work of the blood coagulation system contributes to the formation of small blood clots in the capillaries of the kidneys,
• deterioration in the course of arterial hypertension during pregnancy contributes to glomerular necrosis.

The worse the filtration in the kidneys and the higher the creatinine numbers, the more unfavorable the conditions for the onset of pregnancy and its bearing. A pregnant woman with chronic renal failure and her fetus are faced with a number of pregnancy complications:

• Arterial hypertension
• nephrotic syndrome with edema
• Preeclampsia and eclampsia
• severe anemia
• and fetal hypoxia
• Delays and malformations of the fetus
• and premature birth
• Infectious diseases of the urinary system of a pregnant woman

Nephrologists and obstetricians-gynecologists are involved to decide on the appropriateness of pregnancy in each individual patient with CRF. At the same time, it is necessary to assess the risks for the patient and the fetus and correlate them with the risks that the progression of chronic renal failure every year reduces the likelihood of a new pregnancy and its successful resolution.

Treatment Methods

The beginning of the fight against CRF is always the regulation of diet and water-salt balance.

• Patients are advised to eat with a restriction of protein intake within 60 grams per day, with the predominant use of vegetable proteins. With the progression of chronic renal failure to stage 3-5, the protein is limited to 40-30 g per day. At the same time, they slightly increase the proportion of animal proteins, giving preference to beef, eggs and lean fish. The egg and potato diet is popular.
• At the same time, the consumption of foods containing phosphorus (legumes, mushrooms, milk, white bread, nuts, cocoa, rice) is limited.
• Excess potassium requires reducing the consumption of black bread, potatoes, bananas, dates, raisins, parsley, figs).
• Patients have to manage with a drinking regimen at the level of 2-2.5 liters per day (including soup and drinking pills) in the presence of severe edema or intractable arterial hypertension.
• It is useful to keep a food diary, which makes it easier to record protein and trace elements in food.
• Sometimes specialized mixtures are introduced into the diet, enriched with fats and containing a fixed amount of soy proteins and balanced in trace elements.
• Patients, along with the diet, may be shown an amino acid substitute - Ketosteril, which is usually added at GFR less than 25 ml per minute.
• A low-protein diet is not indicated for malnutrition, infectious complications of CRF, uncontrolled arterial hypertension, with GFR less than 5 ml per minute, increased protein breakdown, after surgery, severe nephrotic syndrome, terminal uremia with damage to the heart and nervous system, poor diet tolerance.
• Salt is not limited to patients without severe arterial hypertension and edema. In the presence of these syndromes, salt is limited to 3-5 grams per day.

Enterosorbents

They allow you to somewhat reduce the severity of uremia due to the binding in the intestine and the removal of nitrogenous toxins. This works in the early stages of chronic renal failure with the relative safety of glomerular filtration. Polyphepan, Enterodez, Enterosgel, Activated carbon, are used.

Anemia treatment

To stop anemia, Erythropoietin is administered, which stimulates the production of red blood cells. Uncontrolled arterial hypertension becomes a limitation to its use. Since iron deficiency may occur during treatment with erythropoietin (especially in menstruating women), therapy is supplemented with oral iron preparations (Sorbifer durules, Maltofer, etc., see).

Blood clotting disorder

Correction of blood clotting disorders is carried out with Clopidogrel. Ticlopedin, Aspirin.

Treatment of arterial hypertension

Drugs for the treatment of arterial hypertension: ACE inhibitors (Ramipril, Enalapril, Lisinopril) and sartans (Valsartan, Candesartan, Losartan, Eprosartan, Telmizartan), as well as Moxonidine, Felodipine, Diltiazem. in combinations with saluretics (Indapamide, Arifon, Furosemide, Bumetanide).

Phosphorus and calcium metabolism disorders

It is stopped by calcium carbonate, which prevents the absorption of phosphorus. Calcium deficiency - synthetic preparations of vitamin D.

Correction of water and electrolyte disorders

carried out in the same way as the treatment of acute renal failure. The main thing is to rid the patient of dehydration against the background of a restriction in the diet of water and sodium, as well as the elimination of acidification of the blood, which is fraught with severe shortness of breath and weakness. Solutions with bicarbonates and citrates, sodium bicarbonate are introduced. A 5% glucose solution and Trisamine are also used.

Secondary infections in chronic renal failure

This requires the appointment of antibiotics, antiviral or antifungal drugs.

Hemodialysis

With a critical decrease in glomerular filtration, the purification of blood from substances of nitrogen metabolism is carried out by hemodialysis, when slags pass into the dialysis solution through the membrane. The most commonly used apparatus is an "artificial kidney", less often peritoneal dialysis is performed, when the solution is poured into the abdominal cavity, and the peritoneum plays the role of a membrane. Hemodialysis for CRF is carried out in chronic mode. For this, patients travel for several hours a day to a specialized Center or hospital. At the same time, it is important to timely prepare an arterio-venous shunt, which is prepared at a GFR of 30-15 ml per minute. From the moment the GFR falls below 15 ml, dialysis is started in children and patients with diabetes mellitus, with GFR less than 10 ml per minute, dialysis is performed in other patients. In addition, indications for hemodialysis will be:

• Severe intoxication with nitrogenous products: nausea, vomiting, enterocolitis, unstable blood pressure.
• Treatment-resistant edema and electrolyte disturbances. Cerebral edema or pulmonary edema.
• Severe acidification of the blood.

Contraindications for hemodialysis:

• clotting disorders
• persistent severe hypotension
• tumors with metastases
• decompensation of cardiovascular diseases
• active infectious inflammation
• mental illness.

kidney transplant

This is a cardinal solution to the problem of chronic kidney disease. After that, the patient has to use cytostatics and hormones for life. There are cases of repeated transplants, if for some reason the transplant is rejected. Renal failure during pregnancy against the background of a transplanted kidney is not an indication for interruption of gestation. pregnancy can be carried to the required term and is usually resolved by caesarean section at 35-37 weeks.

Thus, Chronic Kidney Disease, which today replaced the concept of “chronic renal failure”, allows doctors to see the problem more timely (often when there are no external symptoms yet) and respond with the start of therapy. Adequate treatment can prolong or even save the patient's life, improve his prognosis and quality of life.

Chronic renal failure (CRF) is a violation of homeostasis caused by an irreversible decrease in the mass of active nephrons (MDN) of the kidneys. It occurs in all progressive kidney diseases and is manifested by a multi-symptomatic complex, reflecting the participation in this process of almost all organs and systems of the patient.

The activity of the kidneys ensures: 1) maintaining the volume of body fluids and maintaining an adequate amount of ions and osmotically active substances in them; 2) maintaining acid-base balance; 3) excretion of endogenous metabolites and exogenously administered substances; 4) synthesis of a number of biologically active substances (renin, prostaglandins, active metabolites of vitamin D3, natriuretic peptide urodilatin, etc.); 5) metabolism of proteins, lipids, carbohydrates. Violations of these functions entail a variety of clinical symptoms, increasing as the function of the kidneys decreases. The kidneys have great compensatory capabilities, only the loss of a significant MDN, approaching 60-70%, begins to be accompanied by clinical symptoms of CRF. The advanced symptomatology of CRF, called uremia or end-stage renal disease (ESRD), occurs when the size of the preserved nephron population approaches 10%.

The most common causes of CRF are glomerulonephritis, pyelonephritis and other interstitial nephritis, diabetic nephropathy (the latter in some countries, in particular in the USA, is one of the first causes of ESRD requiring hemodialysis treatment). At the same time, more and more often now we have to deal with chronic renal failure, which occurs in patients with gout, rheumatoid arthritis, nephropathies in SLE and systemic vasculitis, iatrogenic nephropathies, etc. In connection with the aging of the population of developed countries, angiogenic nephrosclerosis (hypertonic, atherosclerotic) and urological diseases accompanied by urinary tract obstruction (prostate hypertrophy, tumors, stones) are becoming increasingly important among the causes of CRF.

Data on the incidence of chronic renal failure are very contradictory, which is explained by the various possibilities of population analysis of this problem. According to our data, in a well-examined population of Moscow, it is 0.35%, while almost 90% of cases of CRF were in the elderly and senile. More definite data on the frequency of ESRD. On average, it can probably be estimated at 100-250 cases per million population. According to the European Renal Association (ERA-EDTA) Registry (1998), the incidence of ESRD requiring hemodialysis replacement therapy in Western European countries in 1995 ranged from 82 cases per million population in the Netherlands to 163 cases in Germany (mean 91 cases per million population). In the United States, this figure was 211 people per million - 1992 data. At the same time, there is an obvious increase in the frequency of chronic renal failure and ESRD in recent years, especially in highly developed countries. This fact is associated with a noticeable aging of the population of these countries - it is the elderly and old people, both due to involutive changes in the kidneys that significantly reduce their functional reserve, and due to the multimorbidity of senile pathology, among which kidney damage is quite frequent, and constitute the main array among patients with both CKD and ESRD. According to the same register, people aged 60 and over accounted for 58% in France, for example, and 61% in Italy.

Despite the differences in the etiological factors leading to the development of CRF, the morphological changes in the kidneys in advanced CRF are quite similar and are characterized by glomerulosclerosis, tubulo-interstitial fibrosis, sclerosis of the intrarenal arteries and arterioles, and hypertrophy of the remaining nephrons. The morphological specificity of the initial kidney damage is lost in this case. Changes in intraglomerular hemodynamics characteristic of chronic renal failure are characterized by hypertension due to a decrease in the tone of the afferent arteriole of the glomerulus and / or efferent arteriole, and hyperfiltration with loss of functional renal reserve. Functional changes are accompanied by glomerular hypertrophy, the severity of which, apparently, affects the rate of further progression of CRF.

Pathogenesis of chronic renal failure

A progressive decrease in MDN and/or a decrease in glomerular filtration (CF) in each separately functioning nephron is accompanied by the accumulation of some (more than 200 are already known) and the deficiency of other biologically active substances. The resulting disproportions of inhibitors and stimulators of metabolic processes lead to a regulatory imbalance at the level of the whole organism, which is very complex and little studied.

Adaptation to these conditions, both at the level of the kidney and at the level of the body, closes many "vicious circles", ultimately leading to the defeat of all human organs and systems. It is in the cumulative action of the diverse biochemical, metabolic and pathophysiological anomalies inherent in this condition that the essence of CRF should be seen.

Nevertheless, with some products of the metabolism of proteins and amino acids, in particular with guanidine compounds (methyl- and dimethylguanidine, creatine, creatinine, guanidinosuccinic acid), symptoms of CRF such as malaise, anorexia, nausea, vomiting, headache can be associated with a certain degree of tolerance. pain; with the accumulation of methylguanidine - hypertriglyceridemia and impaired absorption of calcium in the intestine; with the accumulation of guanidinosuccinic acid - functional disorders of the platelet link of hemostasis.

With nitrogen-containing substances with a higher molecular weight, with the so-called medium molecules (with a molecular weight of 300 to 3500), including a number of polypeptide hormones, in particular insulin, glucagon, parathyroid hormone (PTH), growth hormone, luteinizing hormone, prolactin, link the effect on the number of erythroid cells in the bone marrow of patients and on the incorporation of iron into hemoglobin, the development of polyneuropathy, the effect on lipid and carbohydrate metabolism, and on immunity. However, various biologically active substances have different toxic effects. The latter is more clearly seen in PTH, which, along with the mobilization of calcium from the bones and the development of osteodystrophy, is believed to be responsible for triglyceridemia and atherosclerosis acceleration, polyneuropathy, impotence, and some other manifestations of uremia, which brings it closer to the concept of "universal uremic toxin". However, medium molecules accumulate in the blood of patients not only with uremia, but also with a number of other serious diseases (shock, coma, myocardial infarction, meningitis, pancreatitis, etc.), which rather reflects the severity of the condition of patients and organ (multiple organ) failure, their true importance in the pathogenesis of CKD continues to be controversial.

As a result of the progressive deterioration of the functional state of the kidneys, the state of both the extracellular environment and cells with their interactions changes more and more significantly (for example, the formation of peptide-insulin complexes blocks specific cellular insulin receptors and thereby disrupts glucose utilization), and the body as a whole.

Violation of the transmembrane flow of fluid and ions in chronic renal failure is accompanied by an increase in the intracellular sodium content, a decrease in the intracellular potassium content, osmotically induced cell overhydration, and a drop in the transcellular electrical potential. There is a decrease in ATPase activity, in particular in erythrocytes and brain cells. The functional ability of erythrocytes, leukocytes, platelets, skeletal muscle cells changes significantly, which can be easily correlated with anemia, a tendency to infections, hemorrhages, myopathies, etc., so characteristic of uremia.

The inability of the kidneys to provide water and electrolyte balance leads to the accumulation of excess water and sodium in the body, to total overhydration and arterial hypertension. There is evidence that already with the onset of a decrease in glomerular filtration, there is a clear tendency to increase blood pressure, the formation of hypertrophy and diastolic dysfunction of the left ventricle.

Early emerging hyperinsulinism, secondary hyperparathyroidism, and changes in the blood lipid profile predispose to the formation of metabolic polysyndromes with a high atherogenic index in such patients.

Clinical manifestations of CKD and ESRD

1. Violations of the water-electrolyte balance and acid-base balance. The most fundamental function of the kidneys, the ability to adequately excrete water, begins to suffer most early. This is due to a violation of their ability to concentrate urine, with the approach of the osmolarity of urine to the osmolarity of blood plasma. When the state of isostenuria is reached, in order to excrete an adequate amount of osmotic metabolites (about 600 mosm / kg of water are formed per day), the kidneys must secrete at least 2 liters of obligate water, which leads to forced polyuria, one of the earliest symptoms of CRF. At the same time, the range of fluctuations in excreted urine narrows to the limit, and a sharp change in the patient's drinking regimen can lead to both rapid dehydration of the body and equally rapid overhydration of it. Both can cause a variety of cardiovascular disorders and electrolyte imbalances, especially dangerous for the elderly and senile.

The balance of sodium, potassium and magnesium is relatively adequately maintained until the end stage of chronic renal failure (until the CF drops below 15 ml / min), after which the kidneys become unable to respond to sharp fluctuations in their intake from food. Lack of dietary sodium, as well as excessive use of diuretics, easily lead to its negative balance, an increase in the amount of extracellular fluid, a decrease in the rate of CF, and a rapid increase in azotemia. Failure to follow a potassium-restricted diet leads to hyperkalemia, which acidosis may also contribute to. At the same time, persistent hyperkalemia with normal potassium intake, absence of oliguria and acute acidosis may be due to hyporeninemic hypoaldosteronism. The latter is often combined with diabetes. An increase in magnesium concentration may be accompanied by respiratory failure and muscle paralysis. ASC is maintained by the kidney by reabsorption of bicarbonates by the proximal tubules and secretion of hydrogen ions by the distal tubules in the form of ammonia and titratable acids. Large functional reserves allow the kidney to maintain a normal AFR up to a decrease in MDN by 80% of the norm. The increase in acidosis is accompanied by respiratory disorders such as Ambyurget's respiratory rhythms or Kussmaul-Meier breathing.

2. Violation of phosphorus-kalyschevo exchange. Secondary hyperparathyroidism. The first signs of a violation of phosphorus-calcium metabolism are ascertained quite early. Already with a decrease in CF to 80-60 ml / min, with normal or slightly reduced concentrations of calcium and phosphorus, a decrease in the level of calcitriol, which blocks the absorption of calcium in the intestine, and an increase in the level of PTH are found. It is possible that it is the decrease in the synthesis of calcitriol, followed by hypocalcemia as a result of a decrease in the absorption of the latter in the intestine, that is the starting point for excessive synthesis of PTH. With a drop in CF to 25 ml / min, hyperphosphatemia and hypocalcemia occur (especially due to ionized calcium). Acidosis contributes to an increase in ionized calcium fraction, and rapid correction of acidosis can dramatically reduce the level of ionized calcium and cause acute hypocalcemia with tetany and seizures. Hypocalcemia is promoted by a high level of calcitonin, which blocks the transmembrane transport of calcium ions, and a lack of kidney production of 1,25 (OH) 2D3 (an active derivative of vitamin D), which disrupts calcium absorption in the intestine. Hypocalcemia stimulates further synthesis of PTH, the excretion of which by the kidneys is also impaired. A distinct picture of secondary hyperparathyroidism develops with fibrous osteitis - osteoporosis, osteofibrosis, often with osteomalacia, the pathogenesis of which is not completely clear. Along with bone changes, which are combined by the term "renal osteodystrophy", patients with uremia may develop extraosseous or metastatic calcification, especially when the calcium-phosphorus product exceeds 60. Common sites of metastatic calcification are medium-sized blood vessels, subcutaneous tissue, articular and periarticular tissues, eyes, myocardium and lungs. Manifestations of this process can be a symptom of "red eyes", debilitating pruritus, arthropathies, "pseudohypertension" syndrome with calcification of the brachial artery, calcification of the arteries of the heart and brain (heart attack, stroke), pulmonary hypertension syndrome, a total violation of microcirculation. The symptom complex of secondary hyperparathyroidism as a result of the multifaceted action of parathyroid hormone can be supplemented by peripheral neuropathy, encephalopathy, cardiomyopathy, erosive and ulcerative lesions of the stomach and intestines, and impotence.

3. Metabolism of proteins, carbohydrates, fats. Damage to the proximal tubules of the kidneys, which metabolizes peptides with a molecular weight of less than 60,000, leads to a deficiency of amino acids, especially essential ones, and histidine is transferred to the same category. With inadequate intake of amino acids from food (low-protein diets), protein deficiency progresses, muscle loss, cachexia, and tissue repair processes are disrupted.

Hyperinsulinism, insulin resistance of tissues and impaired glucose tolerance are detected early in patients with chronic renal failure (already with a decrease in CF to 80 ml / min), i.e. the so-called uremic pseudodiabetes with an extremely rare development of ketoacidosis. Catabolism intensifies in response to energy insufficiency, while tissues, the energy metabolism of which is provided by glucose (the brain), are the first to suffer. The accumulation of inhibitors of gluconeogenesis leads to the activation of an alternative pathway with the formation of lactic acid, as a result of which these patients are prone to the development of lactic acidosis.

In chronic renal failure, already with an increase in blood creatinine to 3 mg%, the clearance of mevalonate, the main precursor of cholesterol synthesis, decreases, the rate of removal of triglycerides from plasma decreases, while at the same time, due to inhibition of the activity of lipoprotein lipase, their cleavage decreases, and the synthesis of VLDL is stimulated. There is also a change in lipid subfractions - a decrease in HDL levels and an increase in the ratio between apo E and apo A lipoproteins. All this contributes to the acceleration of atherogenesis and leads to high mortality of these patients from cardiovascular diseases (in 50-60% of cases).

4. Changes in the blood system. The most striking manifestations of changes in the blood system in patients with CRF are anemia and hemorrhagic diathesis. Anemia, which is observed in 80% of patients with compensated CRF and in 100% with ESRD, is caused both by a progressive decrease in the synthesis of erythropoietins by the kidneys and by changes in the erythrocytes themselves, which become more rigid and prone to agglutination and hemolysis. The synthesis of hemoglobin also suffers due to the accumulation of its inhibitors.

Under conditions of uremia, platelet function is impaired. This is associated, in particular, with the accumulation of guanidinosuccinic acid and other inhibitors of platelet aggregation. The result is an increase in bleeding time, although clotting time, prothrombin and partial thromboplastin time remain within the normal range. The consequences of this are easily occurring ecchymosis, bruising, internal bleeding.

5. Damage to the nervous system. On the part of the peripheral nervous system, progressive peripheral polyneuropathy is noted. At first, the damage to the sensory nerves is more pronounced than the motor ones; the lower extremities are affected to a greater extent, as well as the distal extremities. Its initial manifestations can be characterized by a violation of vibration sensitivity, paresthesia, a burning sensation of the skin of the extremities, and restless legs syndrome. In the future, muscle weakness, muscle twitches, hand tremors, cramps in the calf muscles join. In severe cases, paresis of the limbs may develop.

Symptoms from the central nervous system undergo dynamics from rapid fatigue, memory loss, sleep disturbances to severe lethargy and arousal, acute psychoses, epileptiform seizures, cerebrovascular accidents, coma. This is due to a violation of the hydration of brain cells and a violation of intracellular energy.

6. Damage to the cardiovascular system and lungs. The functioning of the cardiovascular system is influenced by many factors - disorders of the renin-angiotensive system, prostaglandin deficiency, an increase in the volume of extracellular fluid, fluctuations in sodium excretion, hyperkalemia, etc. The most common complication of CRF is arterial hypertension, observed in 50-80% of patients. A small proportion of them develop a syndrome of malignant arterial hypertension with severe hyperreninemia, encephalopathy, seizures, plasmorrhagia in the retina and edema of the optic nerve papilla.

In the majority of patients in the late stages of chronic renal failure, cardiomyopathy is stated, which, in addition to overloading the heart with hypertension and hypervolemia, is based on anemia, acidosis, electrolyte imbalance, coronary artery lesions, etc. Its manifestations are a variety of cardiac arrhythmias and congestive heart failure.

One of the most formidable complications of uremia is pericarditis. Its genesis remains insufficiently clear; unlike pericarditis of another etiology, it is accompanied by the formation of hemorrhagic fluid in the pericardial cavity. Pericarditis can cause cardiac tamponade, severe heart failure, "shell heart"; it occupies one of the leading places among the "uremic" causes of death, the idea of ​​\u200b\u200bit as a "death knell of the uremic" can only be changed with the help of timely intensive dialysis. Fluid retention in the body may be accompanied by the development of pulmonary edema. However, even in the absence of hyperhydration, against the background of normal or slightly elevated intracardiac and pulmonary pressure, a special, characteristic only of uremia, picture of the "water lung" can be observed. Radiologically, it is characterized by the shape of a "butterfly wing", which reflects the stagnation of blood in the vessels of the roots of the lungs and the increased permeability of the membranes of the alveolar capillaries. This pulmonary edema is easily corrected with vigorous dialysis.

With uremia, the development of pneumonitis is also possible, manifested morphologically by a decrease in the elasticity of the lung tissue, primarily due to hyalinosis of the alveolar membranes and interstitial-alveolar edema. However, this pathology does not have typical clinical manifestations.

7. Damage to the digestive organs. The so-called dyspeptic syndrome is observed in almost all patients with CRF, although its severity does not always correlate with the degree of azotemia. It is believed that in its genesis, the progressively increasing vicarious function of the gastrointestinal tract (intestinal ureolysis can increase the formation of ammonia by 5-6 times), the increase in the content of gastrin due to a decrease in its metabolism in the kidneys, and secondary hyperparathyroidism are of particular importance. The consequence of this is the development of erosive and ulcerative gastroenterocolitis, often complicated by bleeding from various parts of the gastrointestinal tract. The occurrence of the latter is also facilitated by a violation of the platelet link of hemostasis.

All patients with severe CRF are characterized by complaints of decreased appetite or anorexia, nausea, and vomiting. Uremic breath is characteristic, due to the conversion of saliva urea to ammonia, the appearance of the latter is often combined with unpleasant taste sensations.

Perhaps the development of reactive pancreatitis, manifested by girdle pain, gas and stool retention, hyperamylasemia. Rarely, uremic pseudoperitonitis occurs with a characteristic absence of hyperthermia and a shift in the leukocyte count.

With ESRD, liver damage is possible with progressive hypoproteinemia and hypobilirubinemia, an increase in the synthesis of melanin and urochromes and a decrease in their excretion. In this case, skin pigmentation becomes characteristic - yellow-brown with an ashy tint.

8. Violation of immunity. Impaired immunity in patients with CRF may be due to the underlying disease that led to CRF, such as glomerulonephritis, SLE, systemic vasculitis, etc., treatment of the underlying disease with steroids or cytostatics, the effect of uremia on immunocompetent cells. Leukocytes of patients with uremia are characterized by a decrease in chemotaxis and phagocytic activity. Delayed hypersensitivity reactions suffer. Antibody reactions to some antigens (eg, tetanus, diphtheria) remain normal, to others (eg, typhoid O and H, influenza) are reduced.

Infections are one of the most common causes of death in ESRD patients. The most frequent types of infectious complications in the pre-dialysis era were pneumonia and colibacillary sepsis; in patients receiving hemodialysis treatment, angiogenic sepsis came out on top, the source of which is vascular access. The causative agent of angiogenic sepsis is almost always gram-positive flora, while septicopyemia often develops, including with the development of septic endocarditis.

Thus, CKD and, especially, ESRD are clinical syndromes so extensive, covering so many areas of internal medicine, that there is “enough room for everyone” in their study.

CRF can be reversible only in extremely rare cases. As a rule, it progresses (even when the original kidney disease loses its severity and passes into a latent phase) and ends with the terminal stage, requiring the inclusion of methods that replace kidney function. The process in the kidneys can acquire the features of non-inflammatory nephrosclerosis, and the CF rate curve continues to decrease almost linearly over time. However, this process can be accelerated under the influence of acute dehydration and hypovolemia (sharp restriction of dietary sodium, excessive diuretic therapy), obstruction and urinary tract infection, hypercalcemia and hyperuricemia. Risk factors for the progression of kidney disease, regardless of the underlying disease, are: arterial hypertension, severe proteinuria, smoking, hyperlipidemia and hyperhomocysteinemia. At the same time, the first three of these factors are, according to multivariate analyses, highly significant and independent.

Of particular importance for determining the severity of renal failure is the determination of the level of serum creatinine or creatinine clearance (CC). Dynamic monitoring of the blood creatinine level or the reciprocal of the creatinine level (1 / creatinine level), as well as the rate of CF, allows you to get a fairly clear picture of both the stage of CRF and its progression.

Treatment of CKD and ESRD

Treatment of CRF is carried out mainly by conservative methods, treatment of ESRD by methods that replace kidney function (programmed hemodialysis, chronic peritoneal dialysis, kidney transplantation).

For the purpose of secondary prevention of chronic renal failure, careful monitoring of the activity of the initial renal process, its systematic and adequate treatment, and active clinical examination of patients should be carried out.

Treatment of chronic renal failure is both pathogenetic and symptomatic and is aimed at correcting water and electrolyte disorders, normalizing blood pressure, correcting anemia, hyperphosphatemia and hyperparathyroidism, and preventing the accumulation of toxic metabolic products in the body.

The most important component of the complex treatment of chronic renal failure is diet. With the help of a diet, it is possible to achieve a decrease in the severity of intoxication, a decrease in the manifestations of secondary hyperparathyroidism, a decrease in the rate of progression of chronic renal failure and, therefore, a delay in the transition to renal replacement therapy.

The goals of diet therapy are achieved under the condition of optimal restriction of dietary nitrogen and phosphorus, sufficient energy value of food, satisfaction of the body's needs for essential amino acids and polyunsaturated fatty acids, optimal fluid and salt administration.

Diet therapy should begin at an early stage of chronic renal failure, when blood creatinine begins to exceed the normal limit. It is based on the restriction of protein and phosphorus with the simultaneous addition of essential amino acids, including histidine. When prescribing a diet, the food stereotype and habits of the patient should be taken into account.

In the stage of complete compensation of chronic renal failure, a normal diet for the patient with a protein content of about 1 g/kg of body weight is maintained, amino acid supplements are not required. At the stage of azotemia, restriction of dietary protein (0.8-0.5-0.4 g / kg of weight, depending on the level of azotemia) and phosphorus is required (egg yolk and poultry meat are excluded, and beef, fish, rice, potatoes are re-boiled in large amounts of water, which allows to reduce the amount of phosphates to 6-7 mg/kg/day, i.e. almost twice). It is recommended to supplement essential acids in the form of taking ketosteril 4-6-8 tablets 3 times a day with meals. The presence of calcium salts in the composition of ketosteril promotes the binding of phosphates in the intestine.

When a patient is transferred to hemodialysis treatment, protein intake expands to 1.0-1.3 g/kg of weight, the introduction of essential amino acids is preserved. The energy value of food should correspond to 30-35 kcal / kg / day, which is achieved by consuming a sufficient amount of carbohydrates (about 450 g) and fats (about 90 g). Energy requirements after age 50 decrease by 5%, and after age 60 by 10% over each subsequent decade. The amount of fluid consumed is compared with diuresis and should not exceed the amount of urine excreted per 500 ml. Sodium intake is limited on average to 5-7 g/day, although it is better to calculate it individually, taking into account the peculiarities of its excretion, the presence or absence of arterial hypertension and edema. It is necessary to exclude salted meat and fish, hard cheeses, ordinary bread baking.

In the treatment of hypervolemia, the first-line drug is furosemide in large doses; if it is ineffective, it can be combined with thiazides.

For the correction of arterial hypertension, first-line drugs are ACE inhibitors and angiotheisin receptor blockers, as they prevent the progression of chronic renal failure, left ventricular hypertrophy and coronary heart disease. However, with an increase in creatinine levels of more than 300 μmol / l, their appointment should be accompanied by strict control of both blood pressure and the state of kidney function, due to the possibility of a sharp and sometimes irreversible drop in it due to a decrease in the tone of the efferent arteriole of the glomerulus, a decrease in hydrostatic and filtration pressure in it. It should be borne in mind the possibility of developing hyperkalemia and worsening anemia during treatment with these drugs. Second-line drugs are calcium channel blockers. The drug and its dose are selected individually. Considering that arterial hypertension is a highly significant and independent risk factor for the progression of chronic renal failure, it is necessary to achieve not a decrease, but normalization of blood pressure in these patients. Serious attention should be paid to secondary hyperparathyroidism. In its genesis, phosphate retention is important, leading to inhibition of 1-alpha-hydroxylase of the kidneys and a decrease in the synthesis of 1,25 (OH) 2 vitamin D, inadequate low secretion of calcitriol, hypersecretion of PTH.

To prevent its development and progression, calcium salts are used, preferably calcium carbonate up to 3-4 g / day (the possibility of hypercalcemia should be borne in mind), with an increase in the level of parathyroid hormone by more than 2-3 times, it is possible to prescribe small doses of 1.25 (OH) 2 vitamin D. A placebo-controlled study showed that it was low doses of this vitamin that prevented an increase in PTH without increasing calcium levels in the blood and urine. It is possible to use rocaltrol (calcitriol), also starting with small doses (0.25 mcg per day).

In the treatment of anemia, recombinant erythropoietins are currently widely used - recormon (eprex) up to 2000 IU 3 times a week. The best results are obtained with the simultaneous intravenous administration of iron preparations (ferrum-lek).

To weaken the manifestations of dyspeptic syndrome, it is possible to use hofitol (purified juice extract of fresh leaves of the field artichoke), preferably intramuscularly or intravenously slowly 1-2 times a day, 5-10 ml each.

In order to increase sexual function in men, it is possible to use testosterone preparations (andriol for oral administration at 80-120 mg / day or silfadenil), in women - conjugated estrogens and progestogens (especially with anovulation and high levels of luteinizing hormone). Dyslipidemia and hyperhomocysteinemia as factors of atherogenesis and progression of chronic renal failure also require close attention. For the correction of dyslipidemia, apparently, atorvastatin, which affects both cholesterol and triglyceride levels, can become a first-line drug. Correction of homocysteinemia requires replenishment of folate deficiency, i.e. administration of folic acid.

Oral sorbents (SNK charcoal, oxidized starch, coconut charcoal), which previously had certain hopes, did not justify these hopes due to insufficient extraction from the body, primarily of creatinine and water. Preparation of the patient for dialysis treatment, along with psychological preparation, requires timely imposition of vascular access (it is believed that this should be done already when the CF drops to 25–20 ml/min) and vaccination against hepatitis B.

Currently in foreign literature instead of the term HPN, which is considered obsolete and characterizes only the fact of an irreversible impairment of kidney function, the term is used "chronic kidney disease" with a mandatory indication of the stage. At the same time, it should be emphasized that the establishment of the presence and stage of CKD in no way replaces the main diagnosis.

Clinical picture

The course of chronic renal failure varies, but more often it grows slowly and gradually with periods of exacerbations and remissions. CKD increases rapidly with exacerbation of the underlying pathological process in the kidneys(for example, glomerulonephritis or pyelonephritis), as well as upon infection(ARI, influenza, tonsillitis, pneumonia, furunculosis, etc.). This is important, as timely treatment can improve kidney function. A sign of exacerbation of chronic renal failure is a decrease in diuresis, a significant increase in urea and creatinine, a violation of the acid-base balance of the blood and an increase in anemia. In the most severe cases of malignant subacute glomerulonephritis, the end stage of chronic renal failure can develop as early as 6-8 weeks from the onset of the disease.

In the initial (latent) stage, there are few clinical manifestations, the body more or less copes with maintaining the constancy of the internal environment. But then deviations begin to grow. In this stage, the symptoms are determined by the underlying disease, often general weakness, fatigue, decreased ability to work.

SKIN

In the initial stage of chronic renal failure, the skin usually pale, which is associated with anemia, tk. produced in the kidneys erythropoietin- a hormone that stimulates the formation of red blood cells. Subsequently, the skin acquires yellowish bronze tint and the urine gradually becomes discolored, which looks like jaundice. However, this change in skin color is associated with urinary urochrome retention in the body. In the terminal stage of chronic renal failure, patients are tormented by itching, and the skin is covered with a kind of white " uremic frost» from white crystals of urea. Let me remind you that normally excreted in the urine 20-35 g of urea per day.

"Uremic frost" from urea crystals on the skin of a negro.

Due to severe itching and a decrease in immunity, there are often pustular infections.

Skin itching with chronic renal failure.

BONE SYSTEM

Due to the violation of phosphorus-calcium metabolism, a lot of parathyroid hormone, which "washes" calcium from the bones. arises osteomalacia- the bones become less strong, hurt, they often have pathological fractures(bones break from small efforts, which normally does not happen). In chronic renal failure, the content also increases uric acid in the blood (hyperuricemia), which leads to the deposition of urate in tissues and periodic bouts of inflammation in the joints - gout.

NERVOUS SYSTEM

Initially, patients realize that they have severe kidney disease; arises response to illness, which goes through a series of stages, starting with negation. Patients are depressed, mood changes often, thoughts of suicide are possible. This reaction to the disease is more common in cancer patients, but for additional information I will give these stages here:

1. Negation or shock ("it can't be").
2. Anger and aggression(“why me”, “why me”).
3. « Bargain» (search for methods of treatment, drugs).
4. Depression and alienation (“I don’t want anything”, “I don’t need anything”, “everything is indifferent”).
5. Acceptance of your illness and building a new life (rethinking your life).

In the future, as nitrogenous metabolic products accumulate in the blood, muscle twitching sometimes painful cramps in the calf muscles. In the terminal stage of chronic renal failure, severe nerve damage is characteristic ( polyneuropathy) with pain and atrophy (reduction in volume) of the muscles.

Polyneuropathy in chronic renal failure causes pain and muscle atrophy.

Since chronic renal failure usually causes malignant arterial hypertension(increased and very stable blood pressure), then often there are strokes.

THE CARDIOVASCULAR SYSTEM

The kidneys regulate blood pressure levels. In chronic renal failure due to renal blood flow disorders and activation of the renin-angiotensinogen-aldosterone system the level of blood pressure steadily rises to high numbers and at the same time it is extremely difficult to go astray. This can be regarded as a kind of diagnostic sign: if the "non-renal" patient's blood pressure is much more difficult to lower than before, he needs to check the kidneys(at least - to pass a urine test according to Nechiporenko).

Headache, dizziness, discomfort and pain in the heart, arrhythmias, shortness of breath up to pulmonary edema due to overload of the left ventricle. In the future, adversely affect anemia and acidosis. May develop uremic myocarditis and pericarditis.

RESPIRATORY SYSTEM

As mentioned just above, it can develop " nephrogenic pulmonary edema due to the accumulation of fluid in the body and weak heart function. due to penetration of urea mucosal irritation, which leads to laryngitis, tracheitis, bronchitis and pneumonia due to reduced immunity.

DIGESTIVE SYSTEM

Mucous membranes of the stomach and small intestine highly permeable to urea, which can hydrolyze to ammonia, annoying and damaging them. There may be a perversion of taste, nausea, vomiting, ammonia smell in the mouth, increased salivation, ulceration of the oral mucosa, gastrointestinal bleeding. The most common infectious complications are stomatitis and parotitis.

Laboratory indicators

BLOOD with uremia (end-stage renal failure): increasing anemia(hemoglobin drops to 40-50 g / l and below), toxic leukocytosis up to 80-100? 10 9 /l with the formula shifted to the left. The number of platelets is reduced ( thrombocytopenia), which is one of the causes of bleeding in uremia and further reduces the level of hemoglobin.

URINE: in the initial period, changes are determined by the underlying disease. As chronic renal failure increases, these changes smooth out, and it becomes difficult to determine the primary disease by urinalysis. Found in urine protein, leukocytes, erythrocytes, cylinders.

In the early stages of chronic renal failure blood potassium levels are usually low due to polyuria ("forced diuresis"). Sodium levels are also reduced due to the restriction of its use with food, and especially with damage to the tubules (for example, with pyelonephritis). Definitely evolving acidosis(acidification of the internal environment) due to a violation of the excretion of acids by the kidneys, the formation of ammonia in the tubular cells and increased secretion of bicarbonates. Acidosis manifests itself drowsiness, skin itching and low body temperature.

Because the the active form of vitamin D is produced in the kidneys, chronic renal failure leads to a sharp calcium malabsorption in the intestines and to a decrease in the level of calcium in the blood (hypocalcemia). Hypocalcemia may present paresthesia(tingling sensation and "goosebumps" on the skin), muscle twitches and cramps. According to the feedback mechanism, more parathyroid hormone enters the bloodstream, which “washes out” calcium from the bones. In the terminal stage of CRF, the level of magnesium (drowsiness, weakness) and phosphorus (due to the “dissolution” of bones by parathyroid hormone) in the blood increases.

About treatment

First of all, it is necessary to treat the underlying disease that caused chronic renal failure. Without this, the rest of the treatment will be ineffective. Important avoid nephrotoxic drugs(e.g. aminoglycoside antibiotics).

On a diet limit the amount of protein up to 50-40 g (up to 25-18 g) of protein per day, which reduces the formation of nitrogenous metabolic products. High caloric content of food (1800-3000 kcal / day) is provided by carbohydrates and fats. The consumption of meat and fish is completely prohibited, eggs, butter and vegetable oil, honey, vegetables and fruits are allowed. Such a diet with a complete set of essential amino acids allows reuse urea nitrogen for protein synthesis. In a hospital setting, patients with chronic renal failure are prescribed a diet 7a(according to Pevzner), in the terminal stage on hemodialysis - a diet 7g.

In the early stages of chronic renal failure, anticoagulants(heparin) and antiplatelet agents(chimes, trental), which improve blood circulation in the kidneys. In the terminal stage, these drugs are contraindicated, because. increase bleeding.

Necessarily reduce high blood pressure, although this is difficult to do - you have to prescribe antihypertensive drugs from different groups. Furosemide (Lasix) is used in high doses, and thiazide diuretics (hydrochlorothiazide) are ineffective in CRF.

Potassium and sodium imbalance eliminated by diet, the appointment of panangin, glucose with insulin and potassium, as well as the intake of table salt. To combat anemia, the use of erythropoietin preparations is most effective.

Herbal preparations are used to reduce azotemia lespenephril and hofitol which increase renal blood flow. May be appointed anabolic steroid, which enhance protein synthesis and reduce the formation of urea. Exists method of excretion of nitrogen metabolism products through the intestines with controlled diarrhea. For these purposes, a choice of magnesium sulfate, sorbitol (xylitol) or a special solution (NaCl, KCl, CaCl 2 , Na 2 CO 3 , mannitol) is used. However, there is a danger here dehydration and electrolyte (ionic) imbalance therefore, it is safer to use hemodialysis. In the absence of arterial hypertension and heart failure, prescribe dry hot air sauna, after which the general condition of many patients improves significantly.

In the terminal stage of chronic renal failure, the so-called renal replacement therapy(RT), which includes program hemodialysis, permanent peritoneal dialysis and kidney transplantation. The methods are complex, they cannot be described here in a nutshell. Mortality among patients with end-stage chronic renal failure is 22% per year.

The conservative stage of chronic renal failure requires the transfer of patients to the II group of disability, the terminal - to the I group.

References:

1. « Practical Guide to Nephrology» ed. A. S. Chizha, 2001.
2. « Problems of diagnosis and conservative therapy of chronic renal failure”, Medical Council magazine, No. 11-12, 2010 http://medi.ru/doc/a240513.htm

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19 comments to the article "Chronic renal failure (CRF)"

Diabetes is not the main cause of CKD.

On the mentioned page medi.ru/doc/a240513.htm it is claimed that " diabetes mellitus is currently the leading cause of terminal CKD both in developed and developing countries - it is the main disease in 20-40% patients starting renal replacement therapy for the first time.

They also write on the fence.
The main cause is essential and symptomatic arterial hypertension. And then diabetes.

The main cause is essential and symptomatic arterial hypertension. And then diabetes.

And is it very important? Treatment-resistant hypertension, as a rule (except for tumors of the endocrine system, CNS lesions, vascular stenosis) is a consequence of kidney damage.

Important because both symptomatic and essential are treated effectively. And the presence of a large number of chronic renal failure in the country is a sign of its rapid marginalization and degradation.

this is no longer a question for medicine ... but for the "country"

Important because both symptomatic and essential are treated effectively

POORLY respond to therapy, especially in patients with ESRF. I speak responsibly, because I have to do with it.

My mother has a terminal stage of chronic renal failure, but she is not given group 1. What law or other document states that the first group is placed at the terminal stage? Something on the Internet I can not find a specific document where this would be clearly indicated.

The first group of disability is assigned to those patients who cannot serve themselves on their own. If a patient with end-stage renal failure regularly undergoes hemodialysis, then his condition is satisfactory, and he is able to take care of himself.

If a patient with terminal CRF for some reason lives without renal replacement therapy, then his condition worsens significantly, and here the 1st group of disability may well be put.

If you do not agree with the decision of the Bureau of Medical and Social Expertise, you can appeal it:
invalid.ru/expert.htm#appeal

Group 1 is given to people who have irreversible changes in the body - terminal CRF - is such! And dialysis patients - potential for group 1 disability - definitely! It’s just that in this state the “socially oriented policy” is aimed at eliminating the sick and old ...

The 1st group of disability is given if the patient cannot serve himself on his own and needs outside help. With regular dialysis should give the 2nd group.

It is precisely to such doctors that my last words of the commentary apply.

After all, it is those who sit on the commission who determine how you, the patient, live and how self-service is available to you! They don't see when a dialysis patient is dragged home and also on dialysis! And yet, dialysis is not available in all places - people go God knows where in such a state!

Interestingly, but they themselves did not try to be in this shoes and “enjoy” disability and still just live on that handout, which they called a pension, the state? Thank God, I got on the commission DOCTOR, MAN! Former military doctor! - He knew for sure that on dialysis - this is 1 group for life!

And you, dear Emergency Doctor, do not get sick! And remember that NO ONE is immune from such a disaster! Be merciful to the sick, and not to the state - it doesn't matter - they will plunder!

I am not a member of the commission and will not be able to get into it with all my desire, since narrow specialists of certain specialties are taken there. I'm just trying to convey to patients how they will be looked at and what they can expect.

Disability is benefits, pension supplements (yes, small, but there are many disabled people) and one of the indicators of health care, so the commission is forced to conduct a strict screening.

I just have no words for your comment, dear emergency doctor ...

You try to explain to patients who are in a difficult life situation about benefits, about a large number of disabled people, and so on ... yes, “care” for our budget is part of your competence ... Keep going, just leave this profession, please don’t treat patients with money in mind, and not about the end result of their profession ...

Dear my “fellow soldiers” – patients of the hemodialysis department and after transplantation! Living in our country and still finding yourself in a situation of illness, all of you are potentially heroes! Please do not give up, fight for yourself, achieve adequate dialysis and receive all the necessary drugs - the Constitution, Laws and the Convention on the Rights of Persons with Disabilities have not been canceled yet! Write to all authorities, to patient nephrological organizations - adequate therapy is the key to the safety of your body!

Those who got on dialysis - this is 1 gr. disability! Know it! Now, after transplantation, if you came to her with a non-life-long group, they give both groups 2 and 3, so your doctors should write as clearly as possible in the extracts for the commission all vital violations of your health - in detail and truthfully with a recommendation for a high degree of the group! severe diseases of the internal organs, with a progressive course, severe joint deformities, and so on. other

Know that in the country for a long time already there has been a surplus of budgetary funds, the tax authorities of the regions are collecting a lot of money - and only for the population they will never be! And if you don't make yourself known. apply to the prosecutor's office, the press, etc. - they will simply “forget” about you, and this only plays into the hands of our system - do not let yourself be destroyed!

Remember that you have loved ones who care about you!

I live in Belarus, money is tight here. We exist largely thanks to the help of Russia.

In the Russian Federation, the budget surplus is primarily due to high prices for exported oil. If it falls, as it has already happened, the budget will immediately crack at the seams. And what to do when you have to cut social spending drastically, as recently in Greece? Psychologically, it is much easier not to receive something at all than to receive it and then return it.

Whatever the reason for the surplus, sick people should not worry at all - they are citizens of the state! And if there are worthless managers in this state, they need to be changed, the sooner the better.

In Russia, there is an immensely huge bureaucracy, corruption and fabulous salaries and benefits for officials! And what about the medical market - it's generally Yaroslavna's cry! Even medicines under DLO are actually bought above the commercial retail price, and written off at a price even higher! And you think that patients should take into account something else… Hmm… yes, no, it’s easier to put everything in its place at the place of residence and defend yourself once, another time the officials will not want to contact you. But this is my opinion and my experience - for example, my conscience will not allow me to “rob” my family, forcing me to spend extra money on what can be shaken out of this empty state.

The fact that somewhere there is some money does not mean that they are in medicine. About 20 cents are allocated for food for one patient per day, the same amount for medicines and about 15 cents per day the doctor receives in his hands for one patient.

Chronic renal failure (CRF) refers to severe pathologies of the urinary system, in which there is a complete or partial decrease in kidney function. The disease develops rather slowly, goes through several stages of its development, each of which is accompanied by certain pathological changes in the functioning of the kidneys and the whole organism. Chronic renal failure can occur in different ways, but in the vast majority of cases, the disease has a progressive course, which is accompanied by periods of remission and exacerbation. With the timely diagnosis of the disease, the necessary medical therapy, its development can be slowed down, thereby stopping the manifestation of more severe stages.

It is possible to determine at what stage CRF is located with the help of laboratory and instrumental studies. A biochemical blood test has good information content, the results of which help determine the type of disease, concomitant diseases, stages of chronic renal failure, as well as the level of creatine in the blood.

Creatinine is an important component of blood plasma, which is involved in the energy metabolism of tissues. Excreted from the body with urine. When creatinine in the blood is elevated, this is a sure sign of impaired kidney function, as well as a signal of a possible development, the stages of which directly depend on its level.

In addition to the increased level of creatinine in the blood plasma, doctors also pay attention to other indicators: urea, ammonia, urates and other components. Creatinine is a waste product that must be removed from the body, so if its amount exceeds the allowable rate, it is important to take immediate action on it.

The norm of creatinine in the blood in men is 70-110 µmol / l, in women 35-90 µmol / l, and in children - 18-35 µmol / l. With age, its amount increases, which increases the risk of developing kidney disease.

In nephrology, the disease is divided into stages of chronic renal failure, each of which requires an individual approach to treatment. The chronic form most often develops against the background of long-term pathologies in the urinary system or after an acute form, in the absence of proper treatment. Very often, early degrees of renal failure do not cause any discomfort to a person, but when there are other chronic diseases in the anamnesis: then the clinic will be more pronounced, and the disease itself will progress rapidly.

CRF in medicine is considered as a symptom complex that manifests itself in the death of kidney nephrons caused by progressive pathologies. Given the complexity of the disease, it is divided into several stages, forms and classifications.

Determining the stage of CKD by blood creatinine

Ryabov classification

The classification of chronic renal failure according to Ryabov consists of indicators of the three main stages of the disease and the amount of creatinine in the blood plasma.

Latent (stage 1) - refers to the initial and reversible forms of the disease. They classify it:

1. Phase A - creatinine and GFR are normal.
2. Phase B - creatinine is increased to 0.13 mmol / l, and GFR is reduced, but not less than 50%.

Azotemic (stage 2) - a stable progressive form.

1. Phase A - creatinine 0.14-0.44, GFR 20-50%.
2. Phase B - creatinine 0.45-0.71, GFR 10-20%.

Uremic (stage 3) - progressive.

1. Phase A - creatinine level 0.72-1.24, GFR 5-10%.
2. Phase B - creatinine 1.25 and above, GFR< 5%.

GFR classification

In addition to the classification of CRF by creatinine, doctors pay attention to the glomerular filtration rate (GFR), which is calculated using a special formula. Kidney damage according to GFR is divided into 5 stages:

• 0 – GFR ˃ 90 ml/min;
• I – GFR 60–89 ml/min;
• II - GFR 30–59 ml/min;
• III – GFR 15–30 ml/min;
• IV - GFR ˂ 15 ml/min.

Regardless of the classification of CRF, the creatinine stage and the level of glomerular filtration rate are the most important indicators of a biochemical blood test. In the process of its development, the disease goes through 4 stages. Clinical signs can be recognized by stages, each of which has a characteristic clinic.

Latent stage of CKD

Latent - the initial stage of renal failure, in which the level of GFR, as well as creatinine, are within the normal range or slightly increased. The functionality of the kidneys is not impaired at the 1st degree, so the symptoms practically do not bother the person. At this stage of the disease, ammonia synthesis and urine osmolarity decrease, and there are no significant deviations in the test results. With the development of a latent form of CRF, symptoms are absent or may show up in the form of other abnormalities.

Patients during this period may complain of:

• jumps in blood pressure;
• increased fatigue;
• dry mouth;
• intense thirst.

If at this stage the disease is diagnosed, adequate treatment is carried out, the prognosis for recovery is quite favorable.

Compensated stage

Stage CKD 2, which is also called polyuric or compensated. At this stage, the level of all indicators is above acceptable standards. The work of the kidneys at this stage is compensated by other organs. The clinic is more pronounced, the patient has the following symptoms:

• chronic fatigue in the morning;
• strong and constant thirst;
• decrease in body temperature;
• anemia;
• pale, yellowish skin color;
• high blood pressure;
• decrease in the density of urine;
• frequent urination.

At this stage of the disease, glomerular filtration and urine osmolarity are markedly reduced. The patient develops acidosis, protein metabolism is disturbed, the urge to urinate becomes more frequent. Proper and timely treatment will keep the disease under control, reduce the risk of the disease progressing to more serious stages.

Intermittent stage

Stage 2-B - intermittent, in which the level of creatinine in the blood significantly exceeds the norm - 4.5 mg / dl. During this period, the amount of urine increases by 2 times, calcium and potassium decrease. The patient is concerned about the following symptoms:

• muscle twitching;
• constant fatigue;
• convulsions;
• signs of anemia;
• hypertension;
• nausea;
• urge to vomit;
• anorexia;
• bloating.

The third stage is accompanied by the appearance of polyuria and nocturia, there are also changes in the skin, which becomes flabby, loses its natural color, weakness and periodic pain in the joints may also be present.

At the intermittent stage, the work of the kidneys deteriorates significantly, the person becomes susceptible to various viral infections, and appetite disappears. Treatment is carried out in a complex, consists of symptomatic and systemic drugs.

terminal stage

The last and most severe form of chronic renal failure, in which the kidneys refuse to perform their functions. The terminal stage of chronic renal failure is accompanied by severe symptoms that disrupt the functioning of the whole organism. Accompanied by the following symptoms:

• mental disorder;
• itching, dryness and flabbiness of the skin;
• convulsions;
• memory loss;
• smell of ammonia from the mouth;
• swelling of the body and face;
• nausea, vomiting;
• bloating, stool problems;
• rapid weight loss.

In connection with a pronounced violation of the kidneys, all organs and systems suffer. The patient's condition is severe, there is a high risk of death. The end stage of chronic renal failure is accompanied by a high level of creatinine in the blood, which causes a general intoxication of the body.

At this stage of the disease, the kidneys practically do not work, urine is not excreted, it enters the bloodstream. The only way to save a person's life is considered to be a kidney transplant or permanent hemodialysis, which helps cleanse the blood of toxins. Thanks to hemodialysis, a person can live for many years, but the procedure must be performed regularly in a hospital setting.

Conclusion

Life expectancy in CKD directly depends on the stage at which the disease is detected, methods of treatment and lifestyle of a person. If the disease is diagnosed in the early stages, while the patient follows all the doctor's recommendations, follows a diet and takes the necessary medications, the prognosis is very favorable. Late stages of the disease give less chance of life, especially when the disease has acquired the terminal stage. If at this stage a person does not undergo hemodialysis or there is no possibility of a kidney transplant, the consequences are quite severe, and the patient himself dies within a few days or weeks.

With the development of chronic renal failure, classification is of paramount importance, since at each stage of the disease a person requires a special and individual approach to treatment.

Chronic kidney disease is a serious condition that can manifest itself due to a long-term pathological process in the kidney tissues, which lasts about 3 months. In the initial stages of the disease, the symptoms may go unnoticed, but as the nephrons are damaged, the clinic will be more pronounced, and in the end it can completely lead to complete disability and death of a person.

What is chronic renal failure (CRF), and what are the stages of CKD according to creatinine? Chronic renal failure is an irreversible impairment of kidney function. The kidneys are responsible for the elimination of many harmful metabolic products, the regulation of blood pressure and the acid-base balance in the body.

The development of chronic renal failure occurs gradually. At the onset of the disease, there may be no clinical symptoms or they may be uncharacteristic of the disease (for example, arterial hypertension). The glomerular filtration rate (GFR) classification is used to determine the stage of the disease.

Factors provoking CKD

Kidney dysfunction can occur both as a result of a sudden triggering of a damaging factor, and as a result of a long-term pathological process. In the first case, acute renal failure is diagnosed, which can result in a complete deterioration of health within a few months, the complete destruction of the structures of this organ.

If the kidney is damaged gradually due to the impact of a long-term pathological process lasting at least 3 months, then chronic kidney disease develops with the most severe consequences: severe chronic renal failure and an advanced stage of renal failure requiring therapy with hemodialysis.

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Among the main factors affecting the functioning of the kidneys, first of all, one can single out: circulatory disorders, specific and non-specific inflammatory processes and immunological factors that are toxic to the kidneys, urinary tract diseases, as well as chronic diseases such as diabetes mellitus and arterial hypertension.

Diagnostic methods

The main criteria for laboratory assessment of kidney function are: the amount of filtered plasma per unit time, the level of creatinine and urea in the blood serum, diuresis, that is, the amount of urine produced.

In addition, in the course of chronic renal failure, the patient deals with anemia and thrombocytopenia, hyperphosphatemia, hypocalcemia and hypercalcemia, impaired regulation of blood volume, most often with the development of arterial hypertension and acidosis. The loss of protein leads to numerous disorders associated with its deficiency - endocrine disruptions or immunodeficiency.

Symptoms of the disease

The main symptoms of chronic renal failure include:

• weakness, fatigue, malnutrition;
• low body temperature;
• violations of hydration of the body;
• change in the amount of urine excreted;
• decrease in immunity.

Initially, the renal glomeruli undergo hypertrophy. This means that the kidney is increasing in size. However, end-stage renal disease (uremia) is characterized by small kidneys.

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As the disease progresses, toxins accumulate in the blood - products of protein metabolism, resulting in an increase in the concentration of creatinine, urea and uric acid in the blood serum, which poison the entire body.

Stages of the chronic form

CRF classification:

1. Kidney disease with normal GFR - latent stage (GFR 90 and > 90 ml/min).
2. Early stage (GFR 60-89 ml/min).
3. Middle stage (GFR 30-59 ml/min).
4. Severe stage (GFR 15-29 ml/min).
5. End-stage (uremia) – GFR below 15 ml/min.

The development of chronic renal failure occurs gradually, with a glomerular filtration rate below 15 ml / min, renal replacement therapy is required. As GFR decreases, symptoms and complications from various organs and systems appear.

Each classification has its own clinical picture.

Stage I - clinical manifestations depend on the underlying disease (eg, diabetes mellitus, arterial hypertension). Blood pressure often rises. At this stage, the cause should be determined and the risk factors for developing kidney disease should be eliminated.

Stage II increases susceptibility to dehydration and urinary tract infections. Often coexists with vitamin D deficiency, which stimulates the parathyroid glands to secrete parathyroid hormone and develop secondary parathyroid hyperfunction. Some patients develop anemia, mainly caused by reduced production of erythropoietin in the kidneys.

In stage III, polyuria, nocturia occur, that is, nocturnal urination and increased thirst. Half of the patients develop arterial hypertension. Many patients have anemia, which can cause weakness, reduced physical activity, and easy fatigue.

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Stage IV CRF is characterized by symptoms of severe severity. There is discomfort from the gastrointestinal tract: loss of appetite, nausea and vomiting. Arterial hypertension occurs in more than 80% of patients. Many have left ventricular hypertrophy and heart failure.

At stage V of terminal renal failure, the symptoms that arise affect almost all organs and systems. Patients require renal replacement therapy (dialysis or kidney transplant), which causes regression of most symptoms of uremia.

Therapeutic measures

In the event of a sudden impairment of kidney function, the main goal is to eliminate its cause, for example, replenishing the loss of fluid in a state of dehydration, treating heart failure, restoring the patency of the urinary tract and blood vessels. Strict control of the balance of minerals is required, especially the concentration of potassium in the blood serum. It is very important to take into account the degree of kidney failure when taking medications, especially those taken constantly. To avoid severe complications and ensure the regeneration of the damaged parenchyma of the organ, renal replacement therapy is used.

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Chronic renal failure is an irreversible process, depending to a large extent on the type of underlying disease, the coexistence of other diseases, and the age and sex of the patient. Unfavorable factors are: male gender, smoking, hyperlipidemia and the amount of proteinuria. Treatment is aimed primarily at the underlying disease, the main goals are:

• normalization of blood pressure;
• balancing the level of glycemia in diabetes mellitus;
• treatment of hyperlipidemia;
• alignment of violations of water and electrolyte balance;
• discontinuation of drugs and substances with a neurotoxic effect;
• treatment of concomitant diseases;
• prevention and treatment of complications, in particular anemia.

In addition, it is necessary to strive to reduce the loss of protein in the urine, to an optimal value below 0.3 g / day, for this, drugs from the group of inhibitors, receptor blockers, are used. To lower the level of cholesterol in the blood, the patient must take statins, fibrates and make lifestyle changes. Ultimately, if chronic renal failure has reached stage 5 of the disease, the patient is treated with a hemodialysis procedure.

Carrying out a hemodialysis procedure

When the level of GFR drops to a value of 15-20 ml/min/1.73 m 2 , the patient undergoes hemodialysis. Indications for dialysis are the following life-threatening conditions:

• uremic pericarditis;
• severe phase of arterial hypertension;
• chronic symptoms of nausea and vomiting;
• serum creatinine >12 mg/dl or urea >300 mg/dl.

Hemodialysis is carried out using a special device, popularly called an "artificial kidney", it provides a simultaneous flow of blood and fluid, dialysate, separated by a semi-permeable membrane, through which, according to the principle of diffusion (concentration difference) and ultrafiltration (pressure difference), metabolism is possible. Thus, the blood is purified from harmful metabolites and toxic compounds. The process lasts about 4-5 hours and is carried out mainly 3 times a week.

During a hemodialysis procedure, the patient receives heparin to prevent blood from clotting.

The opinions of doctors on the question of how long hemodialysis patients live are always different, however, the average life expectancy is 20 years. It is not uncommon in medical practice that patients live for more than 35 years.

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kidney transplant

Kidney transplantation is the only way to completely cure the disease of chronic renal failure. The operation entails a significant improvement in the quality of life in people previously treated with dialysis. Unfortunately, a kidney transplant requires tissue compatibility from a living or deceased donor. Therefore, a long waiting time is often required for the operation to take place. An organ transplant is needed for individuals whose serum creatinine concentration exceeds 6 mg/dL. After surgery, patients must take immunosuppressive drugs and steroids to prevent organ rejection. Contraindications for the operation are serious diseases of organs such as cancer, as well as age, atherosclerosis.

It is necessary to constantly monitor kidney function after surgery. According to the latest research data, after 5 years after the operation, about 80% of transplanted organs perform their functions. Unfortunately, the number of transactions performed is 3 times less than the number of people on the waiting list.