Acute renal failure in children

Acute renal failure in children is a nonspecific syndrome of various etiologies that develops in connection with a sudden shutdown of the homeostatic functions of the kidneys, which is based on hypoxia of the renal tissue followed by the primary damage to the tubules and the development of interstitial edema. The syndrome manifests itself as increasing azotemia, electrolyte imbalance, decompensated acidosis and impaired ability to release water.

The term "acute renal failure" was first proposed by J. Merill (1951) instead of the former designations "anuria" and "acute uremia".

Acute renal failure in children is a nonspecific syndrome that develops as a result of acute transient or irreversible loss of homeostatic renal function due to hypoxia of the renal tissue followed by primary damage to the tubules and edema of the interstitial tissue (Naumova VI, Papayan AV, 1991).

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

Organic kidney damage, accompanied by anuria, in the recent past in 80% of cases ended in the death of patients. Currently, due to the wide introduction of efferent therapy methods (dialysis, hemofiltration, etc.) into clinical practice, it was possible to significantly reduce the lethality. According to AS Doletsky and co-authors. (2000), today, with ARF in children, it is about 20%, in newborns - from 14 to 73%.

ICD-10 codes

• N17. Acute kidney 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 people, of whom 1/3 are infants.

In the newborn period, the incidence of acute renal failure requiring dialysis is 1 per 5000 newborns. According to official data, acute renal failure is responsible for 8-24% of all admission to the intensive care unit and resuscitation of newborns. At the age of 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. At school age, the incidence of acute renal failure depends, first of all, on the prevalence of diseases of the glomerular apparatus of the kidneys and is 1 per 100 000 children.

[1], [2], [3], [4], [5], [6], [7], [8], [9]

Causes of acute renal failure in children

As far back as 1947 I. Tgiyya et al. They advanced the theory of renal ischemia as the main cause of acute renal failure. They believed that anuria and uremia are caused by a prolonged reflex spasm of the vessels of the cortical substance of the kidneys, which help stop glomerular filtration, some increase in reabsorption and degenerative necrotic changes in the distal convoluted tubules and the ascending part of the loop of Henle. Vascular shunt Truet as a pathogenetic basis of shock damage to the kidneys subsequently received universal recognition. A bleeding bypassing the Malpighian glomeruli explains the oligoanuria in the shock stage of toxic nephropathy, and the continuing hypoxia of the renal tissue, especially of its cortex, promotes the development of autolytic necrosis of the proximal tubules, as well as organic arresters.

Clinically, there are 2 forms of acute renal failure in children: functional (FPN) and organic (actually OPN). The first occurs as a result of disturbance of VEO, more often against the background of dehydration, as well as due to disorders of hemodynamics and respiration. It is believed that changes in the kidneys observed in FPN are reversible and can not always be detected by conventional clinical and laboratory methods. Another form of renal failure (ARF) is accompanied by distinct clinical manifestations: azotemia, electrolyte imbalance, decompensated metabolic acidosis and impaired kidneys ability to release water.

The most symptomatic clinical symptom of kidney failure is oliguria. In adults and adolescents, diuresis> 0.3 ml / kg-h) or 500 ml / day is considered an oliguria, in infants -> 0.7 ml / (kg-h) and 150 ml / day, respectively. When anuria in adults, the upper limit of the daily volume of urine is considered diuresis> 300 ml / day, in infants> 50 ml / day.

Oliguria and acute renal failure are not synonymous. In patients with acute diuresis, there is not necessarily organic damage to the renal parenchyma. At the same time, oliguria is the main, most prominent clinical symptom of acute kidney failure in children.

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

• a stable spasm of afferent (bringing) arterioles, which reduces the flow of blood to the glomeruli;
• violation of intrarenal hemodynamics, primarily due to arteriovenous shunting of the blood flow (shunts of Troyet), sharply impoverishing the blood supply of the renal cortex;
• intravascular thrombogenic blockade, especially in bringing glomerular arterioles;
• decrease in the permeability of glomerular capillaries due to the fall of podocytes;
• blockade of tubules by cellular detritus, 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 basal membrane of the tubules), which is accompanied by free back absorption of the filtrate (primary urine) through the damaged basal membrane of the tubules into the interstitium of the kidneys;
• edema interstitium due to free penetration of primary urine through damaged tubular walls;
• alignment of the cortico-medullary osmotic gradient and blockade of the countercurrent multiplying apparatus of the kidneys by concentrating the urine;
• the growth of renal hypoxia due to compression of the intrarenal vessels with edema and shunting of blood in the kidneys;
• necrotic changes in the cortical substance of the kidneys (cortical necrosis), in which there is a high probability of death of patients at the height of arterial hypertension or the development of subsequent nephrosclerosis and CRF.

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

In acute renal failure in children of different ages, various etiologic factors serve as the lead. Thus, during the newborn period, hypoxia or fetal asphyxia, pneumopathy, intrauterine infections, sepsis, renal blood vessels, at the age of 1 month to 3 years - HUS, primary infectious toxicosis, anhydrhythmic shock, at the age from 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

[10], [11], [12], [13], [14], [15], [16], [17], [18]

Pathogenesis of acute renal failure

The pathogenesis of the development of the true OPN occurs in the form of 4 consecutive phases (stages): predanuricheskoy, anuricheskoy, polyuric and reductive. The preanuric phase of OPN can be considered as a stage of the primary effect of etiological factors on the kidney. In the anuric stage, the kidneys lose their homeostatic functions: water, potassium, metabolites (in particular, ammonia, urea, creatinine - the so-called "medium" molecules) are delayed 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 replaced by the stage of excessive discharge of urine - polyuria. In this period, renal vasoconstriction disappears, the permeability of glomerular capillaries normalizes.

When evaluating renal functions, it should be borne in mind that diuresis in a child is the sum of mandatory and additional loss of fluid by the kidneys. By mandatory diuresis is meant the amount of fluid required to perform the entire osmotic load, i.e. For excretion of the volume of urine excreted by the kidneys operating in the maximum concentration regime. In this case, the maximum osmolarity of urine in an adult is on average 1400 mosm / l, for a newborn - 600 mosm / l, for a child under 1 year - 700 mosm / l. Therefore, the younger the child, the more he has the amount of mandatory diuresis. Thus, to isolate 1 mosm / l infant, a diuresis equal to 1.4 ml is necessary, to an adult - 0.7 ml. Hence, in the absence of organic damage to the nephron, the decrease in diuresis can not be unlimited and limited to mandatory, and vice versa, the higher the osmotic load, the higher the diuresis.

To determine the osmoregulatory, concentrating functions of the kidneys, it is necessary to determine the osmolality of the urine or the index of its relative density correlating with it. To compare these parameters, EK Tsybulkin and NM 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 any disease, so 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, the absolute oliguria is distinguished, which does not depend on the patient's water regime, and the relative oliguria observed when water is deficient in the body. The first of them relates to OPN, the second - to FPN. In some cases, anuria may be absent in patients with acute renal failure, while retaining the water-releasing function of the kidneys, however, the volume of injected fluid will always significantly exceed the volume of diuresis.

The combination of oliguria with hypersthenuria (PKM> 1.025) is an indication of FPN or the prednaric stage of OPN. The combination of oliguria with hyposthenuria testifies to a decrease in the filtration and concentration capacity of the kidneys, i.e., about the true arteries.

Examination of the urine sediment suggests a nosological form that led to impaired renal function. Thus, hematuria and proteinuria are observed in DIC syndrome or intracapillary glomerular damage. The presence in the sediment of granular and hyaline cylinders indicates hypoxia of the kidneys. Leukocyturia (neutrophilic) often occurs with acute inflammation of the kidneys (pyelonephritis, apostematous nephritis). Moderate lymphocyturia, eosinophiluria, proteinuria, cylindruria and micro-erythrocyturia, 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 creatinine in the blood (normal not more than 0.1 mmol / L) reflects a violation of kidney function. For creatinine of blood and urine, taking into account the minute diuresis, the glomerular filtration rate (clearance of endogenous creatinine) is determined, which is below the normal value (75-110 ml / min-1.73 m ² ). The concentration of urea (in norm 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 during sepsis, burns, severe injuries, etc.

Water-electrolyte imbalance in patients with arterial hypertension is manifested by an increase in the level of potassium in the blood up to 7 mmol / l and hyperhydration (up to anasarca, development of cerebral edema and lungs). The concentration of calcium in the blood is determined to be below 2.5 mmol / l. The sodium content is usually within the normal range (135-145 mmol / l) or there is a tendency to reduce it, since some of this electrolyte passes inside 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. For the oligoanuric stage of acute renal failure, hypo-isostenuria is typical - a decrease in OPM (<1,005) and urine osmolality (<400 mOsm / L) in all portions.

In patients with arterial hypertension, metabolic acidosis is usually found in the blood.

The pre-tracheal (initial) stage of acute renal failure in children does not have a particular characteristic, but depends on the clinical manifestations of the disease that led to the OPN. The starting point of the diagnosis of the initial period of acute renal failure is a progressive oliguria, the rate of development of which may be different:

• acute (characteristic of shock) lasts 12-24 hours;
• average - 2-4 days (typical for HUS);
• gradual - 5-10 days, is observed at a number of bacterial infections (iersiniosis, 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, the level of azotemia and other manifestations of intoxication. All children have signs of impaired consciousness and nervous activity associated with brain edema. The motor activity of patients is lowered. Skin covers are pale, sometimes with a yellowish tinge, hemorrhagic eruptions 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 swelling spreads to the lower extremities. Perhaps the accumulation of free fluid in the abdominal cavity, in the inter pleural space. Sometimes the smell of ammonia from the mouth is determined. As a rule, there are shortness of breath, tachycardia. AD even in children of the first months of life can be higher than normal, but more often deviations are less pronounced. Cramps, uremic colitis are possible.

In the pre-dialysis period of the oligoanuric stage, anemia, sometimes thrombocytopenia, hyponatremia, progressive growth of azotemia are recorded in children: the urea level reaches 20-50 mmol / l, creatinineemia 0.3-0.6 mmol / l. There is a possibility of hyperkalemia (> 7.0 mmol / l), which is dangerous due to cardiodepressive action of this electrolyte. Significantly (4-6 times more than normal), the blood concentration of "medium" molecules, which are a universal marker of endogenous intoxication and renal insufficiency, increases.

The clinical symptoms of acute renal failure in children on dialysis are leveled after 2-3 days. The edematous syndrome decreases, the function of the heart, lungs stabilizes. Gradually the consciousness clears up, anemia, acidosis are eliminated. There is sluggishness, a decreased appetite, pallor. In the presence of stress ulcers, gastric or intestinal bleeding may occur with a complication in the form of collapse.

The polyuric stage of OPN is manifested by a gradual increase in diuresis. The amount of urine exceeds the normal diuresis several times. In this period, the development of dehydration, hypokalemic syndrome in the form of lethargy, flatulence, transient paresis of limbs, tachycardia, typical changes in the ECG is possible. In children, the MT significantly decreases, the elasticity and turgor of tissues decrease. The motor activity is low, appetite is lowered in the first days.

ARF in this period, as in the phase of oligoanuria, remains low (1,001-1,005). Excretion of urine sodium, creatinine and urea also sharply decreases, so often at the beginning of the polyuric stage, dialysis is necessary to correct azotemia and reduce intoxication. At the same time, the excretion of potassium with urine increases substantially, which naturally leads to hypokalemia. In the urine sediment, the high content of leukocytes, erythrocytes, and cylinders remains for a long time, which is associated with the release of dead tubular epithelial cells and the resolution of interstitial infiltrates.

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

The recovery phase can last 6-12 months or more. Gradually normalized MT patients, the state of the cardiovascular system and the gastrointestinal tract, indicators of blood and urine tests. However, for a long time sluggishness and fast fatigue of children, low PKO, propensity to nocturia remain. 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 main points for diagnosis of acute renal failure in children is the detection of a decrease in diuresis in combination with disorders of VEO and azotemia. An essential condition for an accurate diagnosis of oligoanuria is the bladder catheterization.

In the urine of patients with a true, organic OPN, the following changes are detected: OPM <1.005, urine osmolarity <400 mosm / L, creatinine, urea concentration and concentration ratio (creatinine concentration ratio in urine to that in blood - UCr / PCr), and also increased concentration of sodium ions in urine (UNa> 20mM / l). In these patients, the reabsorption of sodium in the renal tubules is suppressed.

FPN (or prerenal stage of OPN) is accompanied by an increase in OPM (> 1,025), urea content and concentration factor, as well as a decrease in UNa (20 mmol / l). The latter is due to the maximum reabsorption of sodium in the kidneys with FPN.

In the differential diagnosis of FPN and OPN, loading tests can be used.

1. A sample with the introduction of vasodilator drugs (pentamine, euphyllin, etc.) contributes to an increase in diuresis in oliguria due to centralization of the blood flow.
2. A sample with a water load and alkalinization of urine. The patient is intravenously injected with a liquid in a volume equal to about 2% of MT, or 20 ml / kg for 1-2 hours. Usually, haemodesis and 10% glucose solution are used in equal proportions. If the patient has FPN for 2 h, diuresis increases and the POM decreases. Against the background of metabolic acidosis, 2-3 ml / kg of 4.2% sodium bicarbonate solution is additionally administered. If the acid reaction of urine is maintained, the risk of acute arterial hypertension is high.
3. A sample with the introduction of saluretics is performed in the absence of dehydration against the backdrop of persisting oligoanuria. The absence of diuresis is indicative of acute renal failure. It should be remembered that the introduction of a large dose of lasix (> 10 mg / kg) against the background of arterial shock is dangerous, so it is advisable to divide it into parts and inject it within 1-2 hours fractional. Begin usually with a dose of 2 mg / kg, after 1 hour in the absence of the effect, another 3-5 mg / kg is administered. Lasix acts more effectively against the background of continuous infusion of dopamine at a dose of 1-3 μg / (kgmin), pre-administration of reoprotectors and sodium bicarbonate at age doses.

Diagnosis of acute renal failure

[19], [20], [21], [22],

Treatment of acute renal failure in children

Treatment FPN or prednuricheskoy stage of acute renal failure is almost directly related to the therapy of the underlying disease and the correction of its manifestations that promote the development of renal failure, the "shock" kidney and consists in protecting the kidney from toxic and hypoxic damage. For this you need as quickly as possible:

1. to restore BCC (blood pressure and CVP);
2. improve microcirculation at the periphery;
3. to eliminate hypoxemia and acidosis;
4. to carry out effective detoxification with the use (if necessary) of antibiotics, antiviral drugs, efferent methods (hemosorption, plasmapheresis).

Timely and vigorous anti-shock therapy (colloid preparations in the volume of 10-20 ml / kg for 1 -2 h), the appointment of vasodilating and disaggregating agents (rheopolyglucin, heparin, euphyllin, trental, komplin, etc.), IT and diuretics (lasix , mannitol) can prevent the development of organic renal failure.

In recent years, in order to improve renal blood flow, dopamine infusion is used at a rate of 2-4 μg / kg per minute (immediately after hemodynamic stabilization for 1-3 days). Mannitol (1 g of dry matter per 1 kg MT of the child) in the form of a 10% solution (intravenously drip quickly - for 40-60 minutes) reduces the spasm of the leading and retracting arterioles of the renal glomeruli, stimulates the glomerular filtration rate and, due to the high osmolarity of the solution, . Lasix during this period is prescribed fractional dose of 5-10 mg / kg. Strengthens the diuretic effect of Lasix pre-alkalinization of urine by administering a 4.2% solution of sodium bicarbonate drip intravenously (at a dose of 2-3 ml / kg).

The absence of the effect of the therapy, the preservation of anuria, the appearance and growth of edema are the basis for establishing the diagnosis of arthritis in the stage of anuria and the solution of the question of the use of dialysis (hemodialysis or peritoneal dialysis).

Hemodialysis is performed with the help of "artificial kidney" apparatus and dialyzers. The patient's blood and a special dialysis solution flow in the dialyzer at high speed (100-300 ml / min) on opposite sides of a semipermeable membrane with a very large area. Through the membrane there is an exchange of ions and metabolites along the concentration gradient, as a consequence of which a large number of toxic substances are removed from the child's body quite quickly, the WEO and CBS parameters are equalized. Removed from the body and excess water due to filtration.

Absolute indications for dialysis therapy are:

• hyperkalemia (> 7 mmol / l);
• marked hyperhydration with phenomena of eclampsia, pulmonary edema, brain;
• a 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 / (d day), which is the main sign of hypermetabolism.

Dialysis is performed daily throughout the anuria period. The duration of dialysis program is 4-5 hours. On the 1st day, dialysis is better to be performed twice to avoid dissequibilization (redistribution of water inside the cells due to slower washing out of urea and the graduation of osmotic pressure); duration of the session is about 2 hours with an interval of 6-8 hours. In older children, there is a need for dialysis in the first days of the polyuric stage.

Intestinal, gastric dialysis, exchange blood transfusion is currently not used in children with ARF. In the first months of life, in the absence of the opportunity to provide venous access, as well as with a real risk of hypotensive reactions against hemodialysis, preference is given to peritoneal dialysis. Dialysis membrane during its operation is the child's own peritoneum, which is washed with a dialysis solution, introduced into the abdominal cavity by special catheters. With the help of this method, blood purification is carried out almost continuously, which avoids disacquisition and collapse. In older children, low-flux veno-venous hemofiltration or constant hemodiafiltration is used (in adults, when used daily, it is removed, followed by adequate substitution of up to 40-60 liters of fluid).

When establishing the diagnosis of acute renal failure, the primary task of a doctor in the pre-dialysis period is to determine the amount of fluid necessary for the child. The daily volume is calculated taking into account the following indices: perspirations + diuresis + pathological losses. Normally, per day, insignificant losses are 30 ml / kg in newborns, 25 ml / kg in children under 5 years, and 15 ml / kg in adults (300-350 ml / day in adults). These losses increase by 10 ml / kg with an increase in the body temperature of the child for each HS over 37.5 ° C and an increase in BH of 10 per minute compared with the norm. The amount of urine given by the child over the past 24 hours, as well as the pathological fluid loss with vomiting, stool, are taken into account. All the necessary volume of fluid is prescribed partially inside, the other part - intravenously.

For infants, breastmilk or adapted formula is given as a food, older children are assigned table number 7 according to Pevzner with restriction of table salt in the pre-dialysis period. Against the background of program dialysis, a strict salt-free diet is usually not used. The volume of food decreases in proportion to the calculated amount of liquid.

To correct energy deficiency in children with acute renal failure, a concentrated (20%) solution of glucose with insulin is injected intravenously. The latter is assigned at the rate of 1 unit per 4-5 g glucose. Potassium salt in the oligoanuric period is not prescribed for acute arterial hypertension. To carry out pharmacological protection of the body from the effects of high concentrations of potassium circulating in the blood, 10% calcium chloride solution is injected intravenously in the amount of 0.2-0.5 ml / kg, it is better to administer it drip. For the sorption of potassium ions, it is possible to use ion-exchange resins inside.

Taking into account the hypoalbuminaemia often detected in children with OPN, a solution of 5-10% albumin is injected intravenously at a rate of 5-8 ml / kg 2-3 times a week. Timely recovery of the oncotic plasma pressure also contributes to increased urination, improves response to lasix, and reduces encephalopathy.

In the period of dialysis therapy, it is necessary to choose medicines taking into account their dialyzing ability. In this regard, if you need to carry out antibacterial therapy, preference is given to penicillins or cephalosporins with good dialyzing ability. From the appointment of cardiac glycosides, especially in doses of saturation, it is necessary, on the contrary, to abstain, since in patients with ARF they are cumulated.

When seizures occur in children with OPN GHB is used in a dose of 50-100 mg / kg, can be combined with benzodiazepines (seduxen, etc.). If the seizures arose against the background of hypertension (eccentricity, eclampsia), emergency dialysis with ultrafiltration is necessary. Before the onset of dialysis, children with a hypertensive crisis can be prescribed a hood (under the tongue) at a dose of 1-6 mg / kg, apressin (0.1-0.5 mg / kg), a-blockers (prazosin, cardura), less commonly used Clonidine (under the tongue or intravenously). Possible appointment of calcium channel blockers (nifedipine) at a dose of 0.25-0.5 mg / kg or beta-blockers (anaprilin) at a dose of 0.1-0.3 mg / kg, especially in the presence of high diastolic blood pressure (> 100 mm ., st.). If there is no effect, nitroprussland sodium (1-8 μg / kgmin) or perlhenate (0.1-1.0 μg / kgmin) is dripped intravenously.

At critical indices (Hb <80 g / l, erythrocyte level <2.5-10 ¹² / l) correction of anemia is carried out by transfusion of fresh erythrocyte mass or washed erythrocytes. It is possible to use preparations of erythropoietin (eg, eprex).

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

How is acute renal failure treated?

How is acute renal failure prevented in children?

• Timely correction of BCC reduction, adequate measures aimed at combating shock, hypoxic-ischemic damage of organs and systems, exclusion of nephrotoxic drugs, monitoring of surgical patients in the post-operation period in terms of preventing the development of their DIC syndrome and infectious complications.
• Carrying out ultrasound of kidneys in children from the first months of life to exclude abnormalities of the development of the organs of the urinary system.