Acute renal failure in children

Acute renal failure in children is a non-specific syndrome of various etiologies, developing due to a sudden shutdown of homeostatic functions of the kidneys, which is based on renal tissue hypoxia with subsequent predominant damage to the tubules and the development of interstitial edema. The syndrome is manifested by increasing azotemia, electrolyte imbalance, decompensated acidosis and impaired ability to excrete water.

The term “acute renal failure” was first proposed by J. Merill (1951) to replace the previous designations “anuria” and “acute uremia”.

Acute renal failure in children is a non-specific syndrome that develops as a result of acute transient or irreversible loss of homeostatic renal function caused by hypoxia of the renal tissue with subsequent predominant damage to the tubules and edema of the interstitial tissue (Naumova V.I., Papayan A.V., 1991).

Acute renal failure can develop in children of any age with many diseases: nephritis (infectious-allergic glomerulonephritis, toxic or drug-induced tubulointerstitial nephritis), infectious diseases (HFRS, leptospirosis, yersiniosis, etc.), shock (hypovolemic, infectious-toxic, traumatic), myoglobin and hemoglobinuria (traumatic rhabdomyolysis, acute hemolysis), intrauterine fetal hypoxia and many other pathological conditions.

In the recent past, organic kidney damage accompanied by anuria resulted in the death of patients in 80% of cases. Currently, thanks to the widespread introduction of efferent therapy methods (dialysis, hemofiltration, etc.) into clinical practice, it has been possible to significantly reduce mortality. According to A. S. Doletsky et al. (2000), today, with ARF in children, it is about 20%, and in newborns - from 14 to 73%.

ICD-10 codes

• N17. Acute renal failure.
• N17.0. Acute renal failure with tubular necrosis.
• N17.1. Acute renal failure with acute cortical necrosis.
• N17.2. Acute renal failure with medullary necrosis.
• N17.8. Other acute renal failure.
• N17.9. Acute renal failure, unspecified.

Epidemiology of acute renal failure

On average, acute renal failure occurs in 3 children per 1,000,000 population, of which 1/3 are infants.

In the neonatal period, the incidence of acute renal failure requiring dialysis is 1 in 5,000 newborns. According to official data, acute renal failure is the cause of 8-24% of all admissions to the neonatal intensive care unit. In the age group from 6 months to 5 years, the incidence of acute renal failure is 4-5 per 100,000 children. In this age group, the main cause of acute renal failure is hemolytic uremic syndrome. In school age, the incidence of acute renal failure depends primarily on the prevalence of diseases of the glomerular apparatus of the kidneys and is 1 per 100,000 children.

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Causes of Acute Renal Failure in Children

As early as 1947, I. Truit and co-authors put forward the theory of renal ischemia as the main cause of ARF. They believed that anuria and uremia are caused by prolonged reflex spasm of the vessels of the renal cortex, which contributes to the cessation of glomerular filtration, some increase in reabsorption and degenerative-necrotic changes in the distal convoluted tubules and the ascending part of the loop of Henle. Truett's vascular shunt as a pathogenetic basis for shock damage to the kidneys subsequently received general recognition. Oligoanuria at the shock stage of toxic nephropathy is explained by blood flow bypassing the Malpighian glomeruli, and ongoing hypoxia of the renal tissue, especially its cortex, contributes to the development of autolytic necrosis of the proximal tubules, as well as organic ARF.

Clinically, there are 2 forms of acute renal failure in children: functional (FR) and organic (ORF). The first occurs as a result of a violation of the VEO, often against the background of dehydration, as well as due to hemodynamic and respiratory disorders. It is believed that the changes in the kidneys observed in FR are reversible and cannot always be detected by conventional clinical and laboratory methods. The other form of renal failure (RF) is accompanied by distinct clinical manifestations: azotemia, electrolyte imbalance, decompensated metabolic acidosis and impaired ability of the kidneys to excrete water.

The most obvious clinical symptom of renal failure is oliguria. In adults and adolescents, oliguria is considered to be a decrease in diuresis > 0.3 ml / kg-h) or 500 ml / day, in infants - respectively > 0.7 ml / (kg-h) and 150 ml / day. With anuria in adults, the upper limit of the daily urine volume is considered to be diuresis > 300 ml / day, in infants > 50 ml / day.

Oliguria and acute renal failure are not synonyms. Patients with acute diuresis do not necessarily have organic damage to the renal parenchyma. At the same time, oliguria is the main, most noticeable clinical symptom of acute renal failure in children.

The main factors damaging the kidneys are circulatory hypoxia, DIC syndrome and nephrotoxins, which contribute to:

• persistent spasm of the afferent (afferent) arterioles, reducing blood flow to the glomeruli;
• disruption of intrarenal hemodynamics, primarily due to arteriovenous shunting of blood flow (Truett shunt), which sharply depletes the blood supply to the renal cortex;
• intravascular thrombogenic blockade, especially in the afferent glomerular arterioles;
• decreased permeability of glomerular capillaries due to the collapse of podocytes;
• blockage of tubules by cellular debris and protein masses;
• tubulointerstitial changes in the form of dystrophy or necrosis of the epithelium of the renal tubules (membranolysis and cytolysis), tubulorhexis (damage to the basement membrane of the tubules), which is accompanied by free reabsorption of the filtrate (primary urine) through the damaged basement membrane of the tubules into the interstitium of the kidneys;
• interstitial edema due to free penetration of primary urine through the damaged walls of the tubules;
• equalization of the cortico-medullary osmotic gradient and blockade of the countercurrent multiplier apparatus of the kidneys to concentrate urine;
• increasing renal hypoxia due to compression of intrarenal vessels by edema and shunting of blood in the kidneys;
• necrotic changes in the renal cortex (cortical necrosis), in which there is a high probability of death of patients at the height of acute renal failure or the development of subsequent nephrosclerosis and chronic renal failure.

All this is accompanied by a decrease in the rate of glomerular filtration, a sharp suppression of the concentration function of the renal tubules, oliguria and hyposthenuria.

In acute renal failure in children of different ages, various etiologic factors act as the leading ones. Thus, in the neonatal period, the main ones are hypoxia or asphyxia of the fetus, pneumopathy, intrauterine infections, sepsis, thrombosis of the renal vessels; at the age of 1 month to 3 years - HUS, primary infectious toxicosis, anhydremic shock; at the age of 3 to 7 years - viral or bacterial kidney damage, poisoning, traumatic and septic shock; at the age of 7-17 years - systemic vasculitis, glomerulonephritis, traumatic shock.

Causes of Acute Renal Failure

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Pathogenesis of acute renal failure

The pathogenesis of true ARF occurs in 4 successive phases (stages): pre-anuric, anuric, polyuric and restorative. The pre-anuric phase of ARF can be considered as the stage of the primary impact of etiologic factors on the kidney. In the anuric stage, the kidneys essentially lose their homeostatic functions: water, potassium, metabolites (in particular, ammonia, urea, creatinine - the so-called "middle" molecules) are retained in the blood and tissues, metabolic acidosis progresses. Excessive accumulation of toxic substances in the body leads to the phenomenon of uremia - ammonia poisoning. Restoration of diuresis in patients with ARF is almost always followed by the stage of excessive urine excretion - polyuria. During this period, renal vasoconstriction disappears, the permeability of glomerular capillaries is normalized.

When assessing renal function, it should be taken into account that diuresis in a child is the sum of mandatory and additional fluid loss by the kidneys. Mandatory diuresis is the amount of fluid required to fulfill the entire osmotic load, i.e. to excrete the volume of urine excreted by the kidneys working in the maximum concentration mode. In this case, the maximum osmolarity of urine in an adult is on average 1400 mosm/l, in a newborn - 600 mosm/l, in a child under 1 year - 700 mosm/l. Therefore, the younger the child, the greater the volume of mandatory diuresis. Thus, to excrete 1 mosm/l, an infant needs a diuresis of 1.4 ml, an adult - 0.7 ml. This means that in the absence of organic damage to the nephron, the decrease in diuresis cannot be unlimited and is limited to mandatory, and vice versa, the higher the osmotic load, the higher the diuresis.

To determine the osmoregulatory, concentration functions of the kidneys, it is necessary to determine the osmolarity of urine or the index of its relative density that correlates with it. To compare these indicators, E. K. Tsybulkin and N. M. Sokolov proposed the formula: OK = 26 x (OPM + 6), where OK is the osmotic concentration of urine, OPM is the relative density of urine.

Pathogenesis of acute renal failure

Symptoms of Acute Renal Failure in Children

Acute renal failure in children is not an independent syndrome, but develops as a complication of some disease, therefore its clinical signs are closely intertwined with the symptoms of the underlying disease.

The most noticeable and early symptom of acute renal failure in children is a decrease in diuresis. In this case, a distinction is made between absolute oliguria, which does not depend on the patient's water regime, and relative oliguria, observed with a water deficit in the body. The first of them is related to ARF, the second - to FPN. In some cases, a patient with ARF may not have anuria while maintaining the water-excreting function of the kidneys, but the volume of fluid administered will always significantly exceed the volume of diuresis.

The combination of oliguria with hypersthenuria (OPM> 1.025) is an indicator of FPN or pre-uric stage of ARF. The combination of oliguria with hyposthenuria indicates a decrease in the filtration and concentration capacity of the kidneys, i.e. true ARF.

The study of urine sediment allows us to assume the nosological form that led to the impairment of renal function. Thus, hematuria and proteinuria are observed in DIC syndrome or intracapillary damage to the glomeruli. The presence of granular and hyaline cylinders in the sediment indicates renal hypoxia. Leukocyturia (neutrophilic) often occurs in acute inflammation of the kidneys (pyelonephritis, apostematous nephritis). Moderate lymphocyturia, eosinophiluria, proteinuria, cylindruria and microerythrocyturia, as a rule, reflect the development of allergic, metabolic or toxic tubulointerstitial nephritis. Azotemia indicates a violation of the excretory function of the kidneys and the state of homeostasis in sick children. The main marker of azotemia is the concentration of creatinine and urea. An increase in the creatinine content in the blood (normally no more than 0.1 mmol/l) reflects a violation of the renal function. The glomerular filtration rate (endogenous creatinine clearance) is determined by the creatinine in the blood and urine, taking into account the minute diuresis, which in acute renal failure is below the normal value (75-110 ml/min-1.73 m2 ⁾. The concentration of urea (normally 3.3-8.8 mmol/l) reflects not only the state of the excretory function of the kidneys, but also the catabolic processes occurring in the child's body, which are activated by sepsis, burns, severe injuries, etc.

Water and electrolyte imbalance in patients with ARF is manifested by an increase in the potassium level in the blood to 7 mmol/l and hyperhydration (up to anasarca, development of cerebral and pulmonary edema). The concentration of calcium in the blood is determined at a level below 2.5 mmol/l. The sodium content is often within the normal range (135-145 mmol/l) or there is a tendency for it to decrease, since part of this electrolyte passes into the cells, replacing potassium, and the other is freely removed with urine. The latter is due to a sharp decrease in sodium reabsorption in the renal tubules due to their damage. The oligoanuric stage of ARF is characterized by hypoisosthenuria - a decrease in the OPM (< 1.005) and urine osmolarity (< 400 mosm/l) in all portions.

In patients with ARF, metabolic acidosis is usually detected in the blood.

The preanuric (initial) stage of acute renal failure in children does not have any special characteristics, but depends on the clinical manifestations of the disease that led to ARF. The reference point for diagnosing the initial period of ARF is progressive oliguria, the rate of development of which can be different:

• acute (characteristic of shock) lasts 12-24 hours;
• average - 2-4 days (typical for HUS);
• gradual - 5-10 days, observed in a number of bacterial infections (yersiniosis, leptospirosis, etc.).

The oligoanuric stage lasts 2-14 days or more (according to research, 22 days with a positive outcome of the disease). The clinical picture is determined by the symptoms of the underlying disease, as well as the degree of hyperhydration, hyperkalemia, azotemia level and other manifestations of intoxication. All children have signs of impaired consciousness and nervous activity associated with cerebral edema. The motor activity of patients is reduced. The skin is pale, sometimes with a yellowish tint, hemorrhagic rashes are possible, less often - scratching due to itching. The outer covers are pasty to the touch. First of all, the face, eyelids swell, then the edema spreads to the lower limbs. Accumulation of free fluid in the abdominal cavity, in the interpleural spaces is possible. Sometimes the smell of ammonia is determined from the mouth. As a rule, there is shortness of breath, tachycardia. Blood pressure even in children of the first months of life can become higher than normal, but more often the deviations are expressed to a lesser extent. Convulsions and uremic colitis are possible.

In the pre-dialysis period of the oligoanuric stage, children experience anemia, sometimes thrombocytopenia, hyponatremia, and progressive increase in azotemia: the urea level reaches 20-50 mmol/l, creatininemia - 0.3-0.6 mmol/l. Hyperkalemia (> 7.0 mmol/l) is possible, which is dangerous due to the cardiodepressant effect of this electrolyte. The concentration of "medium" molecules in the blood, which are a universal marker of endogenous intoxication and renal failure, increases significantly (4-6 times higher than normal).

Clinical symptoms of acute renal failure in children undergoing programmed dialysis are eliminated in 2-3 days. Edema syndrome is reduced, cardiac and pulmonary function is stabilized. Consciousness gradually clears up, anemia and acidosis are eliminated. Lethargy, decreased appetite, and pallor persist. In the presence of stress ulcers of the gastrointestinal tract, gastric or intestinal bleeding with complications in the form of collapse may occur.

The polyuric stage of acute renal failure is manifested by a gradual increase in diuresis. The amount of urine exceeds normal diuresis several times. During this period, dehydration, hypokalemic syndrome in the form of lethargy, flatulence, transient paresis of the limbs, tachycardia, and typical changes in the ECG may develop. In children, MT is significantly reduced, elasticity and turgor of tissues are reduced. Motor activity is low, appetite is reduced in the first days.

During this period, as in the oliguria phase, the acute renal failure remains low (1.001-1.005). The excretion of sodium, creatinine and urea in the urine also decreases sharply, so it is often necessary to perform dialysis at the beginning of the polyuric stage to correct azotemia and reduce intoxication. At the same time, the excretion of potassium in the urine increases significantly, which naturally leads to hypokalemia. The urine sediment retains an increased content of leukocytes, erythrocytes, and cylinders for a long time, which is associated with the release of dead cells of the tubular epithelium and the resorption of interstitial infiltrates.

The duration of the polyuric stage is from 2 to 14 days. During this period, the probability of death of patients remains high due to decreased immunity and possible complications in the form of pneumonia, urinary tract infection, sepsis. With the overcoming of this critical stage of ARF, the prognosis improves significantly.

The recovery stage can last 6-12 months or more. Gradually, the patients' MT, the state of the cardiovascular system and gastrointestinal tract, blood and urine test results are normalized. However, lethargy and rapid fatigue of children, low OPM, and a tendency to nocturia persist for a long time. This is due to the slow regeneration of the epithelium of the renal tubules.

Symptoms of Acute Renal Failure

Types of acute renal failure

Diagnosis of acute renal failure in children

The reference points for diagnosing acute renal failure in children are the detection of decreased diuresis in combination with VEO disorders and azotemia. A mandatory condition for accurate diagnosis of oliguria is catheterization of the urinary bladder.

The following changes are detected in the urine of patients with true, organic ARF: OPM < 1.005, urine osmolarity < 400 mosm/l, decreased concentration of creatinine, urea and concentration coefficient (ratio of creatinine concentration in urine to that in blood - UСr/РСr), and increased concentration of sodium ions in urine (UNa > 20 mmol/l). These patients have inhibition of sodium reabsorption in the renal tubules.

FPN (or prerenal stage of ARF) is accompanied by an increase in the RMP (> 1.025), urea content and concentration coefficient, as well as a decrease in UNa (20 mmol/l). The latter is due to the maximum reabsorption of sodium in the kidneys during FPN.

In the differential diagnosis of FPN and ARF, stress tests can be used.

1. A test with the introduction of vasodilators (pentamine, euphyllin, etc.) helps to increase diuresis in oliguria caused by the centralization of blood flow.
2. Water loading and urine alkalization test. The patient is given intravenous fluid in a volume of approximately 2% of BW, or 20 ml/kg, over 1-2 hours. Hemodesis and 10% glucose solution are usually used in equal proportions. If the patient has FPN, diuresis increases and RMP decreases over 2 hours. In the presence of metabolic acidosis, 2-3 ml/kg of 4.2% sodium bicarbonate solution is additionally administered. If the urine remains acidic, there is a high probability of ARF.
3. A test with the introduction of saluretics is carried out in the absence of dehydration against the background of persistent oliguria. The absence of diuresis indicates ARF. It should be remembered that the introduction of a large dose of Lasix (> 10 mg / kg) against the background of ARF is dangerous, so it is advisable to divide it into parts and introduce it fractionally over 1-2 hours. Usually they start with a dose of 2 mg / kg, after 1 hour, if there is no effect, another 3-5 mg / kg. Lasix acts more effectively against the background of continuous dopamine infusion at a dose of 1-3 mcg / (kg min), preliminary administration of rheoprotectors and sodium bicarbonate in age-appropriate doses.

Diagnosis of acute renal failure

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Treatment of acute renal failure in children

Treatment of FPN or pre-uric stage of ARF is almost directly related to the therapy of the underlying disease and correction of its manifestations that contribute to the development of renal failure, "shock" kidney and consists of protecting the kidneys from toxic and hypoxic damage. To do this, it is necessary as quickly as possible:

1. restore the BCC (BP and CVP);
2. improve microcirculation in the periphery;
3. eliminate hypoxemia and acidosis;
4. carry out effective detoxification using (if necessary) antibiotics, antiviral drugs, efferent methods (hemosorption, plasmapheresis).

Timely and vigorous anti-shock therapy (colloidal preparations in a volume of 10-20 ml/kg for 1-2 hours), administration of vasodilator and anti-aggregating drugs (rheopolyglucin, heparin; euphyllin, trental, complamin, etc.), IT and diuretics (lasix, mannitol) can prevent the development of organic renal failure.

In recent years, dopamine infusion at a rate of 2-4 mcg/kg per minute (immediately after stabilization of hemodynamics for 1-3 days) has been used more often to improve renal blood flow. Mannitol (1 g of dry matter per 1 kg of the child's BW) in the form of a 10% solution (intravenously by drip quickly - 40-60 minutes) reduces spasm of the afferent and efferent arterioles of the renal glomeruli, stimulates the rate of glomerular filtration and, due to the high osmolarity of the solution, provides a significant increase in diuresis. Lasix is prescribed during this period in fractional doses of up to 5-10 mg/kg. The diuretic effect of Lasix is enhanced by preliminary alkalization of urine by administering a 4.2% sodium bicarbonate solution by drip intravenously (at a dose of 2-3 ml/kg).

The lack of effect from the therapy, the persistence of anuria, the appearance and increase of edema are the basis for establishing a diagnosis of acute renal failure in the anuria stage and deciding on the use of dialysis (hemodialysis or peritoneal dialysis).

Hemodialysis is performed using artificial kidney machines and dialyzers. The patient's blood and a special dialysate solution flow through the dialyzer at a high speed (100-300 ml/min) on different sides of a semipermeable membrane with a very large area. Ions and metabolites are exchanged through the membrane along the concentration gradient, as a result of which a large number of toxic substances are removed from the child's body rather quickly, and the VEO and KOS indicators are leveled. Excess water is also removed from the body due to filtration.

Absolute indications for dialysis therapy are:

• hyperkalemia (> 7 mmol/l);
• severe hyperhydration with symptoms of eclampsia, pulmonary and cerebral edema;
• rapid increase in uremic intoxication: an increase in the level of urea in the blood plasma by 20-30 mmol/(l day) and creatinine by 0.20-0.40 mmol/(l day), which serves as the main sign of hypermetabolism.

Dialysis is performed daily throughout the entire period of anuria. The duration of programmed dialysis is 4-5 hours. On the first day, in order to avoid disequilibration (redistribution of water inside the cells due to slower urea leaching from them and creation of an osmotic pressure gradient), dialysis is best performed twice; the session duration is about 2 hours with an interval of 6-8 hours. In older children, dialysis is also necessary in the first days of the polyuric stage.

Intestinal, gastric dialysis, and exchange transfusion are currently practically not used in children with ARF. In the first months of life, if venous access is not possible, as well as if there is a real risk of hypotensive reactions during hemodialysis, preference is given to peritoneal dialysis. The child's own peritoneum serves as a dialysis membrane during its implementation, which is washed with a dialysis solution introduced into the abdominal cavity through special catheters. With this method, blood purification is carried out almost continuously, which helps to avoid disequilibration and collapse. In older children, low-flow venovenous hemofiltration or continuous hemodiafiltration is used (in adult patients, when they are used, up to 40-60 liters of fluid are removed per day with subsequent adequate replacement).

When diagnosing ARF, the primary task of the doctor in the pre-dialysis period is to determine the volume of fluid required by the child. Its daily volume is calculated taking into account the following indicators: perspiration + diuresis + pathological losses. Normally, imperceptible losses per day are 30 ml / kg in newborns, 25 ml / kg in children under 5 years old, 15 ml / kg in older children (in adults - 300-350 ml / day). These losses increase by 10 ml / kg with an increase in the child's body temperature for each GS above 37.5 ° C and an increase in respiratory rate of 10 per minute compared to the norm. The amount of urine excreted by the child over the past day, as well as pathological fluid losses with vomiting and stool are taken into account. The entire required volume of fluid is partially prescribed orally, the other part - intravenously.

Infants are given breast milk or adapted milk formulas as food, older children are prescribed table No. 7 according to Pevzner with a limitation of table salt in the pre-dialysis period. A strict salt-free diet is usually not used against the background of program dialysis. The volume of food is reduced proportionally to the calculated amount of liquid.

To correct energy deficiency, children with acute renal failure are given a concentrated (20%) glucose solution with insulin intravenously. The latter is prescribed at a rate of 1 unit per 4-5 g of glucose. Potassium salt is not prescribed to patients in the oligoanuric period of ARF. To provide pharmacological protection of the body from the effects of high concentrations of potassium circulating in the blood, a 10% calcium chloride solution is administered intravenously in an amount of 0.2-0.5 ml/kg; it is best administered by drip. Ion exchange resins can be used internally to absorb potassium ions.

Considering the hypoalbuminemia often detected in children with ARF, a 5-10% albumin solution is administered intravenously at a rate of 5-8 ml/kg 2-3 times a week. Timely restoration of plasma oncotic pressure also promotes increased urination, improves the response to lasix, and reduces encephalopathy.

During dialysis therapy, it is necessary to select medications taking into account their dialyzing capacity. In this regard, if antibacterial therapy is necessary, preference is given to penicillins or cephalosporins, which have good dialyzing capacity. On the contrary, it is necessary to refrain from prescribing cardiac glycosides, especially in saturation doses, since they accumulate in patients with ARF.

In case of seizures in children with ARF, GHB is used in a dose of 50-100 mg/kg, possibly in combination with benzodiazepines (seduxen, etc.). If seizures occur against the background of hypertension (hypertensive crisis, eclampsia), emergency dialysis with ultrafiltration is necessary. Before dialysis, children with hypertensive crisis can be prescribed capoten (sublingually) in a dose of 1-6 mg/(kg/day), apressin (0.1-0.5 mg/kg), alpha-blockers (prazosin, cardura), less often clonidine is used (sublingually or intravenously). It is possible to prescribe calcium channel blockers (nifedipine) in a dose of 0.25-0.5 mg/kg or beta-blockers (anaprilin) in a dose of 0.1-0.3 mg/kg, especially in the presence of high diastolic blood pressure (> 100 mmHg). If there is no effect, sodium nitroprussin (1-8 mcg/kg/min) or perlinganit (0.1-1.0 mcg/kg/min) is used intravenously by drip.

In case of critical values (Hb < 80 g/l, erythrocyte level <2.5-10 ¹² /l), correction of anemia is performed by transfusion of fresh erythrocyte mass or washed erythrocytes. It is possible to use erythropoietin preparations (for example, eprex).

During the period of polyuria, it is very important to compensate for fluid loss, correct the electrolyte composition and especially to administer potassium ions to children. If there is no possibility of monitoring the potassium level in the blood, it is administered at a dose of 2-3 mmol/(kg-day). This period of the disease is fraught with the addition of infectious, purulent complications in children, therefore, aseptic conditions are of great importance when performing procedures.

How is acute renal failure treated?

How is acute kidney failure prevented in children?

• Timely correction of the decrease in circulating blood volume, adequate measures aimed at combating shock, hypoxic-ischemic damage to organs and systems, exclusion of nephrotoxic drugs, monitoring of surgical patients in the postoperative period in terms of preventing the development of DIC syndrome and infectious complications.
• Conducting ultrasound examination of the kidneys in children starting from the first months of life to exclude developmental abnormalities of the urinary system.