Kidney failure in children: what it is and how to cope with the disease. Renal failure in a child Acute renal failure in children treatment principles

Acute renal failure in children is a nonspecific syndrome of various etiologies that develops due to a sudden shutdown of the homeostatic functions of the kidneys, which is based on hypoxia of the renal tissue, followed by 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) instead of the previous designations "anuria" and "acute uremia".

Acute renal failure in children is a nonspecific syndrome that develops as a result of an acute transient or irreversible loss of homeostatic kidney function due to hypoxia of the renal tissue, followed by predominant damage to the tubules and swelling of the interstitial tissue (Naumova V.I., Papayan A.V., 1991).

Acute renal failure can develop in children of any age with many diseases: with 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.

Organic kidney damage, accompanied by anuria, in the recent past in 80% of cases ended in the death of patients. At present, due to the widespread introduction of efferent methods of therapy (dialysis, hemofiltration, etc.) into clinical practice, it has been possible to significantly reduce mortality. According to A. S. Doletsky et al. (2000), today, with acute renal failure in children, it is about 20%, 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 of the 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 accounts for 8-24% of all admissions 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 frequency 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.

Causes of acute renal failure in children

Back in 1947, I. Tgiya et al. put forward 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 renal cortex, which contributes to the termination 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. Truet's vascular shunt as a pathogenetic basis for shock kidney damage later received universal recognition. The blood flow bypassing the Malpighian glomeruli explains oligoanuria at the shock stage of toxic nephropathy, and the ongoing hypoxia of the renal tissue, especially its cortical substance, contributes to the development of autolytic necrosis of the proximal tubules, as well as organic acute renal failure.

Clinically, there are 2 forms of acute renal failure in children: functional (FPN) and organic (actually AKI). The first occurs as a result of a violation of the VEO, more often against the background of dehydration, as well as due to hemodynamic and respiratory disorders. It is believed that changes in the kidneys observed in FPI are reversible and cannot 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 a violation of the ability of the kidneys to excrete water.

Oliguria is the most manifest clinical symptom of renal insufficiency. 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 volume of urine is considered to be diuresis\u003e 300 ml / day, in infants\u003e 50 ml / day.

Oliguria and acute renal failure are not synonyms. Patients with an acute decrease in 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 and nephrotoxins, contributing to:

sustained spasm of afferent (bringing) arterioles, which reduces blood flow to the glomeruli;
violation of intrarenal hemodynamics, primarily due to arteriovenous shunting of blood flow (Truet's shunt), which sharply impoverishes the blood supply to the renal cortex;
intravascular thrombogenic blockade, especially in the afferent glomerular arterioles;
decrease in the permeability of glomerular capillaries due to the collapse of podocytes;
blockade of tubules by cellular detritus, proteinaceous 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;
edema of the interstitium due to the free penetration of primary urine through the damaged walls of the tubules;
alignment of the cortico-medullary osmotic gradient and blockade of the work of the countercurrent-multiplier apparatus of the kidneys for concentrating urine;
an increase in renal hypoxia due to compression of intrarenal vessels by 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 acute renal failure or the development of subsequent nephrosclerosis and chronic renal failure.

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

In acute renal failure in children of different ages, various etiological factors act as the leading ones. So, in the neonatal period, 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, anhydrous 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.

The pathogenesis of acute renal failure

The pathogenesis of the development of true acute renal failure proceeds in the form of 4 successive phases (stages): pre-uric, anuric, polyuric and recovery. The preanuric phase of acute renal failure can be considered as the stage of the primary impact of etiological 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 "medium" 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. Recovery of diuresis in patients with acute renal failure is almost always replaced by the stage of excessive urine output - polyuria. During this period, renal vasoconstriction disappears, the permeability of glomerular capillaries normalizes.

When evaluating 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. Obligatory diuresis is understood as the amount of fluid necessary to fulfill the entire osmotic load, i.e., to excrete the volume of urine excreted by the kidneys operating in the maximum concentration mode. At the same time, 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 old - 700 mosm / l. Therefore, the younger the child, the greater the volume of obligatory diuresis. So, to release 1 mosm / l, an infant needs diuresis equal to 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 obligatory, 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 an indicator 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.

Symptoms of acute renal failure in children

Acute renal failure in children is not an independent syndrome, but develops as a complication of a 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. At the same time, absolute oliguria is distinguished, which does not depend on the patient's water regime, and relative, observed with a lack of water in the body. The first of them is related to OPN, the second - to FPN. In some cases, a patient with acute renal failure may not have anuria while maintaining the water-excretory function of the kidneys, however, the volume of fluid injected will always significantly exceed the volume of diuresis.

The combination of oliguria with hyperstenuria (OPM> 1.025) is an indicator of FPI or the pre-uric stage of AKI. The combination of oliguria with hypostenuria indicates a decrease in the filtration and concentration ability of the kidneys, i.e., true acute renal failure.

The study of urine sediment suggests a nosological form that led to impaired renal function. So, hematuria and proteinuria are observed with DIC or intracapillary damage to the glomeruli. The presence of granular and hyaline cylinders in the sediment indicates hypoxia of the kidneys. Leukocyturia (neutrophilic) often occurs with acute inflammation of the kidneys (pyelonephritis, apostematous nephritis). Moderate lymphocyturia, eosinophiluria, proteinuria, cylindruria, and microerythrocyturia usually 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 content of creatinine in the blood (normally not more than 0.1 mmol / l) reflects a violation of the renal function. According to blood and urine creatinine, taking into account minute diuresis, the glomerular filtration rate (endogenous creatinine clearance) is determined, which is lower than the normal rate in acute renal failure (75-110 ml / min-1.73 m 2). 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 during sepsis, burns, severe injuries, etc.

Water and electrolyte imbalance in patients with acute renal failure is manifested by an increase in the level of potassium in the blood up to 7 mmol / l and hyperhydration (up to anasarca, the 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 more often within the normal range (135-145 mmol / l) or there is a tendency to decrease it, 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 acute renal failure is characterized by hypoisosthenuria - a decrease in OPM (

In patients with acute renal failure in the blood, metabolic acidosis is usually detected.

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

the most acute (characteristic of shock) lasts 12-24 hours;
medium - 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 studies, 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 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 extremities. Accumulation of free fluid in the abdominal cavity, in the interpleural spaces is possible. Sometimes the smell of ammonia from the mouth is determined. As a rule, there are shortness of breath, tachycardia. Even in children of the first months of life, blood pressure may become higher than normal, but more often the deviations are less pronounced. Convulsions, uremic colitis are possible.

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

Clinical symptoms of acute renal failure in children on program dialysis are leveled after 2-3 days. The edematous syndrome decreases, the function of the heart and lungs stabilizes. Consciousness gradually clears up, anemia and acidosis are eliminated. Lethargy, decreased appetite, pallor persist. In the presence of stress ulcers of the gastrointestinal tract, gastric or intestinal bleeding may occur with a complication in the form of collapse.

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

OPN during this period, as well as in the phase of oligoanuria, remains low (1.001-1.005). Urinary excretion of sodium, creatinine and urea also sharply decreases, so dialysis is often necessary at the beginning of the polyuric stage to correct azotemia and reduce intoxication. At the same time, urinary excretion of potassium increases significantly, which naturally leads to hypokalemia. In the urine sediment, an increased content of leukocytes, erythrocytes, and cylinders persists 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 a decrease in immunity and the possible addition of complications in the form of pneumonia, urinary tract infections, and sepsis. With overcoming this critical stage of acute renal failure, the prognosis improves significantly.

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

Diagnosis of acute renal failure in children

The main points of diagnosis of acute renal failure in children is the detection of a decrease in diuresis in combination with disorders of the VEO and azotemia. A prerequisite for accurate diagnosis of oligoanuria is bladder catheterization.

In the urine of patients with true, organic acute renal failure, the following changes are detected: OPM 20 mmol / l). In these patients, inhibition of sodium reabsorption in the renal tubules is observed.

FPI (or prerenal stage of ARF) is accompanied by an increase in OPM (> 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 with FPI.

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

A test with the introduction of vasodilators (pentamine, eufillin, etc.) contributes to an increase in diuresis with oliguria due to the centralization of blood flow.
Test with water load and alkalization of urine. For 1-2 hours, the patient is injected intravenously with liquid in a volume equal to approximately 2% of the MT, or 20 ml / kg. Usually gemodez and 10% glucose solution are used in equal proportions. If a patient has FPI for 2 hours, diuresis increases and OPM decreases. Against the background of metabolic acidosis, an additional 2-3 ml / kg of 4.2% sodium bicarbonate solution is administered. If the acid reaction of urine persists, the probability of acute renal failure is high.
A test with the introduction of saluretics is carried out in the absence of dehydration against the background of persistent oligoanuria. The absence of diuresis indicates acute renal failure. It should be remembered that the introduction of a large dose of lasix (> 10 mg / kg) against the background of acute renal failure is dangerous, therefore it is advisable to divide it into parts and introduce fractionally within 1-2 hours. They usually start with a dose of 2 mg / kg, after 1 hour, if there is no effect, another 3-5 mg / kg is administered. Lasix works more effectively against the background of continuous infusion of dopamine at a dose of 1-3 mcg / (kgmin), preliminary administration of rheoprotectors and sodium bicarbonate at age-related doses.

Treatment of acute renal failure in children

The treatment of FPI or the pre-uric stage of acute renal failure is almost directly related to the treatment of the underlying disease and the correction of its manifestations that contribute to the development of renal failure, the “shock” kidney, and consists in protecting the kidneys from toxic and hypoxic damage. To do this, you need as quickly as possible:

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

Timely and vigorous anti-shock therapy (colloidal preparations in the amount of 10-20 ml/kg for 1-2 hours), the appointment of drugs of vasodilating and deaggregating action (rheopolyglucin, heparin; eufillin, trental, complamin, 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 at a rate of 2–4 μg/kg per minute (immediately after stabilization of hemodynamics for 1–3 days) is more often used. Mannitol (1 g of dry matter per 1 kg of BW of a child) in the form of a 10% solution (intravenously drip quickly - in 40-60 minutes) reduces spasm of the adductor and efferent arterioles of the renal glomeruli, stimulates the glomerular filtration rate and, due to the high osmolarity of the solution, provides a significant increase in diuresis . Lasix during this period is prescribed fractionally at a dose of up to 5-10 mg / kg. Enhances the diuretic effect of lasix by preliminary alkalization of urine by introducing a 4.2% solution of sodium bicarbonate intravenously (at a dose of 2-3 ml / kg).

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

Hemodialysis is carried out using artificial kidney machines and dialyzers. The patient's blood and a special dialysis solution flow in the dialyzer at a high rate (100-300 ml/min) on opposite sides of a semi-permeable membrane with a very large area. Through the membrane, ions and metabolites are exchanged along a concentration gradient, as a result of which a large amount of toxic substances are removed from the child's body quite quickly, and the indicators of VEO and CBS are leveled. Removed from the body and excess water due to filtration.

Absolute indications for dialysis therapy are:

hyperkalemia (> 7 mmol / l);
severe hyperhydration with symptoms 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 / (l day), which is the main sign of hypermetabolism.

Dialysis is carried out daily during the entire period of anuria. The duration of program dialysis is 4-5 hours. On the 1st day, in order to avoid disequilibration (redistribution of water into cells due to slower leaching of urea from them and the creation of an osmotic pressure gradient), it is better to dialysis twice; the 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 transfusion of blood is currently practically not used in children with acute renal failure. In the first months of life, in the absence of the ability to provide venous access, as well as in the real danger of hypotensive reactions against the background of hemodialysis, preference is given to peritoneal dialysis. The dialysis membrane during its implementation is the child's own peritoneum, 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 avoids disequilibration and collapse. In older children, low-flow veno-venous hemofiltration or permanent hemodiafiltration is used (in adult patients, when used per day, it is removed with subsequent adequate replacement of up to 40-60 liters of fluid).

When establishing the diagnosis of acute renal failure, the first priority of the doctor in the predialysis period is to determine the volume of fluid needed by the child. Its daily volume is calculated taking into account the following indicators: perspiration + diuresis + pathological losses. Normally, per day, imperceptible losses in newborns are 30 ml / kg, in children under 5 years old - 25 ml / kg, in older children - 15 ml / kg (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 loss with vomiting and stool, are taken into account. The entire required volume of liquid is prescribed partly 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 restriction of sodium chloride 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%) glucose solution with insulin is administered intravenously. The latter is prescribed at the rate of 1 unit per 4-5 g of glucose. Potassium salt in the oligoanuric period of acute renal failure is not prescribed to patients. To carry out the pharmacological protection of the body from the action of high concentrations of potassium circulating in the blood, a 10% solution of calcium chloride is injected intravenously in an amount of 0.2-0.5 ml / kg, it is better to inject it drip. For the sorption of potassium ions, it is possible to use ion exchange resins inside.

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

During the period of dialysis therapy, it is necessary to choose drugs taking into account their dialyzing ability. In this regard, if antibiotic therapy is necessary, preference is given to penicillins or cephalosporins, which have a good dialyzing ability. On the contrary, it is necessary to refrain from prescribing cardiac glycosides, especially in saturation doses, since they accumulate in patients with acute renal failure.

When convulsions occur in children with acute renal failure, GHB is used at a dose of 50-100 mg / kg, it is possible in combination with benzodiazepines (seduxen, etc.). If convulsions occur against the background of hypertension (hypertensive crisis, eclampsia), emergency dialysis with ultrafiltration is necessary. Prior to the start of dialysis, children with a hypertensive crisis can be prescribed capoten (under the tongue) at a dose of 1-6 mg / (kg per day), apressin (0.1-0.5 mg / kg), a-blockers (prazosin, cardura), less commonly used clonidine (under the tongue or intravenously). It is possible to prescribe 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 Hg st.). If there is no effect, sodium nitroprussind (1-8 µg/kgmin) or perlinganite (0.1-1.0 µg/kgmin) is used intravenously.

At critical indicators (Hb

During the period of polyuria, compensation for fluid losses, correction of the electrolyte composition, and especially the introduction of potassium ions to children are very important. If it is not possible to monitor 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 addition of infectious, purulent complications in children, so aseptic conditions are of great importance when performing procedures.

It's important to know!

The causes of acute renal failure are not completely clear, but four main mechanisms of its development are noted: tubular obstruction; interstitial edema and passive reverse flow of glomerular filtrate at the level of tubules; disorder of hemodynamics of the kidney; disseminated intravascular coagulation.

Kidney failure in a child is a rare occurrence due to organ dysfunction and rapid progression. In the absence of timely medical care, the baby may die. Therefore, each parent needs to know her symptoms and the treatment that the baby will need.

There are many reasons why children begin to fail kidneys. This is the formation of an anomaly of organs during intrauterine development or the activity of the pathogen in the baby's body after his birth. Therefore, the disease can be acquired or congenital.

Causes of the development of the disease in a newborn

In newly born babies, renal failure is diagnosed when both kidneys are congenitally absent or when the heart muscle and the entire cardiovascular system are not properly formed. In newborns, pathology also develops due to the appearance of blood clots in the veins, vascular disease of the arteries of the urinary organ.

Acute renal failure in children or its chronic form appears when there is a violation of the outflow of urine or infection of the urinary tract. A pathological condition awaits a baby after a difficult birth or when his body is dehydrated due to intrauterine infection.

Babies up to 12 months

The causes of kidney failure in infants are metabolic problems, intestinal infections, congenital and acquired diseases that provoke the death of many blood elements.

older children

A chronic or acute type of pathological condition develops as a result of acute infectious diseases. Intoxication of the body with medications or nephrotoxic agents can provoke a disease at this age. Organ injuries, sepsis, hemorrhages and burns can also be causes. In adolescents, acute renal failure can be triggered by the formation of calculi in the kidneys, which causes a violation of the outflow of urine.

Symptomatic manifestations of pathology

Signs of kidney failure in a child do not differ from the manifestations in an adult. There are the following common symptoms of kidney failure in children:

emptying frequent;
the amount of fluid released does not correspond to the norm;
bad feeling;
symptoms of body poisoning: nausea, vomiting, diarrhea;
increase in body temperature;
change in color of the epidermis to yellow;
formation of stones and sand in paired organs;
tremor;
decreased muscle tone;
swelling of the hands, feet.

The study of urine shows an increase in the level of protein in it. Nephrotic syndrome is a clear sign of the development of renal failure in children. It almost never occurs in adults.

Acute disease

Acute renal failure in children - intoxication of the body with toxins and other harmful substances that accumulate due to the cessation of organs.

In the first days of the development of the disease, general malaise, nausea and other signs of poisoning are observed. In the first two weeks of the disease, the clinical picture is supplemented by uremia, the blood is saturated with nitrogenous toxins. Further, the water-electrolyte balance is disturbed, diuresis, the child loses weight dramatically. At stage 4, there is a decrease in symptoms, the so-called clinical recovery.

If you do not start treating the pathology in a baby in a timely manner, it will develop into a chronic form.

Chronic kidney failure

Chronic renal failure in children can progress for a long time, leading to complete dysfunction of paired organs. Pathology is divided into congenital and acquired types. There are 4 stages of its development: latent, compensated, intermittent and terminal.

At the first sign of improper kidney function in children, parents need to urgently contact a pediatrician. He will prescribe the necessary tests and refer you to a nephrologist.

Diagnosis of a pathological condition

The acute form of insufficiency is detected on the basis of the symptoms described above and the results of laboratory tests. In urine, there is an increase in creatinine, urea, sodium. The density and osmolarity of urine decreases, the presence of casts and leukocytes is detected. A blood test reveals a decrease in the filtration function by 25%, creatinine in the fluid increases sharply, and the potassium content decreases.

Additionally, doctors prescribe a hardware examination using ultrasound, magnetic resonance imaging of the urinary organs, bladder and ureters. If necessary, x-rays and cystoscopy are done.

In children, it is diagnosed on the basis of a survey, in which the presence of diseases of the genitourinary system of a chronic type in the baby is revealed. A blood test shows a reduced level of glomerular filtration, leukocytosis, an increase in potassium and a decrease in hemoglobin. ECG reveals noise and expansion of the boundaries of the heart muscle, tachycardia. There is an increase in blood pressure.

Differential diagnosis is carried out with acute glomerulonephritis and encephalopathies.

Urgent measures

With an attack of acute renal failure in a baby, parents should call an ambulance. It is forbidden to take any action independently.

In a medical institution, the child will have a gastric lavage, and sorbents will be introduced into the digestive system. Hemodialysis or hemosorption is performed as a last resort when the infant is in danger of death. After the crumbs, you can not feed for some time, until all vital signs return to normal.

Treatment methods for the disease

In the acute form of kidney failure, therapy is aimed at detoxifying the body, restoring blood volume and its circulation in the kidney tissue. With the timely detection of pathology, the following medicines will give a good effect:

diuretics;
vasodilators;
anti-shock medications;
blood thinners.

In most cases, babies under one year of age are prescribed hemodialysis for acute renal failure. If the disease is complicated by hyperglycemia, pulmonary or cerebral edema, hypertension, an “artificial kidney” is also indispensable here.

Adolescents are additionally prescribed plasmapheresis, that is, they filter the blood. Antibacterial drugs are used to prevent infection. During the recovery period, it will be appropriate to take potassium, glucose and electrolyte mixtures.

In the chronic form of the pathology, complex treatment of the kidney and all affected organs is carried out. The treatment regimen includes such drugs (as prescribed by the doctor):

Antamicides. Reduce the amount of phosphorus in the blood.
D vitamins and calcium. Normalize calcium metabolism.
Means for lowering blood pressure in hypertension.
Diuretics (to increase diuresis).
Iron in the development of anemia.

If uremia progresses, hemodialysis is put on the baby. After the child's condition improves, they return to conservative treatment. To achieve stable remission for many years, the most effective method is organ transplantation.

Complications when ignoring the disease

Kidney failure greatly complicates the life of the child. He needs constant hemodialysis. Pathology provokes deviations in the development of the baby, disability. Due to the neglect of the disease, the child may develop defects of the central nervous system, anemia, ischemia, atherosclerosis. The outcome is deplorable - the death of the crumbs. In the case of an organ transplant, the baby needs to take expensive medications in order for the kidney to take root.

Preventive rules

In order for the child's kidneys to work properly, you need to monitor his nutrition and the amount of fluid he drinks per day. The baby should not overcool the back, injure the lower back. With a hereditary predisposition to the disease, you need to take the child to regular preventive examinations for timely diagnosis.

Do not forget about the importance of treating all diseases of the genitourinary system. Any infection can become a provoking factor for the development of renal failure.

Kidney failure is not a death sentence for children. But it is important to diagnose in a timely manner and follow all the instructions of the attending physician. With acute renal failure in newborns, a number of complications develop, the disease becomes chronic. Here, the outcome will depend on the cause of the disease and the success of therapy. For older children, the prognosis is better. In 75% of cases, it is possible to achieve a complete restoration of the functioning of the urinary organs.

Long-term kidney diseases of various etiologies are accompanied by a persistent violation of their work. Very often, impaired renal function turns into insufficiency, which is confirmed by specific clinical and laboratory syndromes, united under the name "chronic renal failure" (CRF). Ignorance of the risk factors for CRF, early symptoms of its development leads to difficulties in both timely diagnosis and selection of effective treatment, and this often leads to death.

Chronic renal failure (CRF) is a pathological condition of the body that gradually develops as a result of the progressive course of diseases of the urinary system. CRF is not even a disease, but a clinical and laboratory symptom complex, which is characterized by the accumulation of nitrogen metabolism products (protein) in the body, subsequently a violation of acid-base balance, metabolism, the development of anemia, increased blood pressure and changes in other internal organs. CRF, in fact, is a complication of various kidney diseases.

Causes of kidney failure

The causes of chronic renal failure include congenital, acquired or hereditary, often chronically occurring, diseases of the urinary system. The leading position is occupied by glomerulonephritis, followed by:

pyelonephritis, interstitial nephritis;
scleroderma, periarteritis nodosa, systemic lupus erythematosus;
amyloidosis of the kidneys;
renal artery stenosis, essential arterial hypertension;
tubulopathies, Fanconi syndrome, poisoning with heavy metals and drugs;
hereditary nephritis;
obstructive diseases of the upper (tumors, stones) and lower (anomalies in the development of the urethra and bladder neck) urinary tract.

An interesting fact is that in children under the age of 3 years, the development of chronic renal failure is due to severe anomalies in the structure of the urinary tract, hereditary tubulopathies and dysplasia of the renal tissue. In this case, the work of the kidneys can remain compensated for a long time.

In children over the age of 10, acquired kidney diseases (glomerulonephritis, kidney damage in diabetes mellitus, tuberculosis, systemic diseases) prevail over the others.

I would like to note the children who are at risk for the development of CRF:

with sclerosing glomerulonephritis;
children with impaired intrauterine development of the urinary system and, as a result, structural anomalies at birth;
boys with hereditary nephritis;
children with complex tubulopathies;
with obstructive kidney disease, accompanied by recurrent pyelonephritis;
lack of effect from properly selected therapy.

To suspect this ailment, what should I look for?

With CRF, the emotional sphere of the child suffers: he becomes irritable, often naughty and cries, for which he is unfairly punished.

Parents need to know the clinical signs of this disease in order to suspect in a timely manner and immediately, only with the help of a doctor, begin therapeutic measures. The main symptoms are determined by a violation of the water and electrolyte balance, peripheral circulation, the state of the cardiovascular system, the central and peripheral nervous system, and the nature of damage to internal organs.

So, in order.

1. With congenital and hereditary nephropathy, already at the age of 3 years, growth retardation is most often noted, which is combined with a decrease in muscle tone, thinning of the subcutaneous fat layer. The emotional sphere of the child also suffers: there is excessive aggressiveness, tearfulness, which is assessed by parents as pampering and only leads to aggravation of relations with the child and unfair punishments.

2. Kidney dysfunction inevitably leaves its mark on the skin. In the initial stages, the skin becomes dry, then itching and peeling appear, it acquires a yellowish tint. The pallor of the skin is due to the development of anemia and intoxication. In the terminal stage, the skin becomes yellow-earthy in color, on the trunk and extremities there are elements of a hemorrhagic rash (small or large bruises in the form of dots, spots, stripes from purple to scarlet, which do not disappear and do not change color when pressed). In the process of progression of CRF, nails can also suffer - they become brittle, leukonychia appears (white stripes or spots inside the nail).

3. A special role in metabolic processes is played by sweat glands, especially apocrine glands (located on the scalp: head, armpits, pubis, perineum). During the compensatory stage of development of chronic renal failure, they begin to work actively, which leads to increased sweating, and this, in turn, causes itching in the perineum and anus, sweat has a golden yellow color. But a decrease in sweating is characteristic of the decompensated stage of chronic renal failure; as it progresses, the hair color changes, increased fragility and loss are noted, uremic gray hair may appear due to the adsorption of urea on the hair.

4. Bone damage is manifested by stiffness in the knee, ankle, sacral region, pain in the bones and joints at night. There are no radiological changes in the bone tissue. For older children, characteristic manifestations are inflammation of the joints due to the deposition of uric acid and its salts in the synovial fluid.

5. Hypertension in this pathology is characterized as the main sign of damage to the cardiovascular system. At the initial stage of chronic renal failure, tachycardia (rapid heartbeat) and systolic murmur at the apex of the heart can be determined. Later, the boundaries of relative cardiac dullness expand to the left, electrolytic and dystrophic changes in the myocardium are visible on the ECG. When examining the fundus, narrowing of the arteries and dilation of the veins, hyperemia and edema, aneurysms of arterioles are visible. Almost half of the patients develop heart failure and uremic pericarditis. Therefore, very important research methods for the timely diagnosis of effusion in the pericardial cavity are chest x-ray and echocardiography (ultrasound of the heart).

6. At various stages of CRF, patients have a violation of external respiration, pulmonary circulation and respiratory failure. Clinically, this is manifested by hard breathing, shortness of breath, wet rales of various sizes, and percussion - a honeycomb lung. On the radiograph, there is an increase in the pulmonary pattern, darkening zones at the roots of the lungs, and sometimes a picture of hydrothorax. Chronic hypoxia in patients with chronic renal failure leads to a change in the nail phalanges by the type of drumsticks and watch glasses. These very bright signs are visible to the naked eye even to people who have absolutely nothing to do with medicine.

7. Signs of damage to the gastrointestinal tract are the lining of the tongue, pain in the epigastric region (pit of the stomach), symptoms of gastritis, enterocolitis, intestinal bleeding. As CRF progresses, these symptoms worsen.

8. Normochromic is the leading and earliest sign of CRF. There is a decrease in the number of erythrocytes and the amount of hemoglobin, an increase in the number of old erythrocytes with a reduced ability to deform, the rate of hemoglobin synthesis also slows down due to pathological changes in the intracellular heme pool, in the bone marrow, young erythroid cells are prematurely destroyed. At the same time, the process of blood clotting is disturbed, the level of platelets and fibrinogen decreases, which, in turn, leads to an increase in bleeding time. Clinically, this is manifested by frequent nosebleeds, the formation of hematomas at the site of the slightest mechanical impact on the skin, gastric and intestinal bleeding in the terminal stage of CRF.

9. The most characteristic and dangerous are disturbances in water and electrolyte metabolism, which in turn cause a specific clinical picture. Increased formation and excretion of urine (polyuria) with insufficient fluid intake is accompanied by thirst, reduced skin turgor, and thickening of the blood due to an increase in hemoglobin. These signs for young children are very dangerous and can be fatal due to dehydration. Children complain of fatigue, drowsiness, thirst is accompanied by dryness of the tongue, reduced urine formation, muscle twitches appear, and body temperature rises. leads to disruption of all body systems. With accelerated excretion of sodium from the body, patients are characterized by an asthenic state, accompanied by muscle hypotension, low blood pressure, low body temperature, and a decrease in diuresis. In this case, there is no thirst, on the contrary, vomiting develops, the tongue is coated, but wet, migraine develops, joint pain, myalgia, sometimes there are convulsions. The above symptoms depend on the pathogenetically determined type of dehydration (intracellular or extracellular dehydration), but they rarely occur in isolation.

10. In the initial stages of the development of chronic renal failure, the amount of potassium in the blood serum is reduced. But the development of acidosis leads to hyperkalemia. Clinically, we see a decrease in reflexes, muscle weakness, lethargy. Changes on the ECG are also visible, indicating a decrease in the contractility of the ventricles of the heart, expanding the boundaries of the heart.

But hyperkalemia is manifested by muscle pain, nausea, ascending paralysis, tachycardia, arrhythmia, metallic taste in the mouth, apathy. These conditions are more typical for the terminal stage of chronic renal failure.

The level of magnesium in this pathology increases. The heart muscle also suffers from this - bradycardia (a different kind of blockade due to a violation of the conduction of electrical impulses through the conduction system of the heart).

There are no specific signs of a violation of the level of chlorine in the blood. Of course, a violation of the electrolyte state of the blood occurs due to changes in the level of micro- and macroelements in the complex, since everything in the body is interconnected.

Imbalance between phosphorus and calcium leads to osteodystrophy and soft tissue calcification. Elevated calcium levels can lead to neuromuscular disorders: tremor of the fingers, muscle twitches, vomiting occurs periodically.

At different stages of CRF, there is a decrease in the indicators of cellular and humoral immunity, which causes the addition of bacterial complications.

What is needed for diagnosis?

The main methods for diagnosing CRF are urine, blood tests and ultrasound of the retroperitoneal organs.

Diagnosis of CRF at different stages of development is based not only on clinical symptoms, but also on the basis of laboratory data: general urinalysis, complete blood count, coagulogram, biochemical blood test, Nechiporenko urinalysis, Zemnitsky urinalysis, ultrasound of the kidneys and abdominal organs , ECG, study of the level of hormones of endocrine glands.

If a child has a lag in physical development, dry scaly skin, pallor of the skin, bags under the eyes, especially in the morning, nausea, complaints of fatigue, subfebrile temperature, thirst (the child drinks 2-3 liters or more), nighttime urination requires a thorough nephrological examination.

The following definition of oliguric renal failure in newborns is generally accepted:

Urine output below 1 ml/kg/hour for more than 24 hours.
No increase in diuresis in response to fluid loading.
The combination of the two previous factors with a serum creatinine level above 130 mmol / l.

Although urine output is reduced in most young children with acute renal failure, solute retention is observed in some patients with normal urination, which is reflected in an increase in serum creatinine (neoliguric renal failure). The frequency of oliguric acute renal failure in newborns ranges from 1 to 6% among all patients in intensive care units. Causes of acute renal failure in newborns are traditionally divided into 3 groups: prerenal, renal and postrenal. This division, based on the location of the lesion, is important because assessment, treatment, and prognosis in these three groups can be quite different.

Prerenal acute renal failure. The most common cause of AKI in the neonatal period is impaired renal perfusion, occurring in up to 70% of oliguric children. Prerenal AKI can occur in any clinical situation where there is otherwise normal renal hypoperfusion. Although prompt correction of the low perfusion condition usually restores renal function, however, with untimely infusion therapy, parenchymal kidney damage may develop.

Etiology of acute renal failure in newborns

Prerenal causes

Reduced plasma volume; bleeding, dehydration, sepsis
Other causes of renal hypoperfusion: hypoxia, respiratory distress syndrome, congestive and heart failure, shock

Renal Causes

Congenital anomalies of the kidneys: bilateral agenesis, bilateral multicystic (dysplasia), polycystic
Vascular lesions: renal artery or vein thrombosis
Ischemic: shock, bleeding, dehydration, sepsis, hypoxia, respiratory distress syndrome
Nephrotoxic: aminoglycoside antibiotics
Uric acid: neonatal hyperuricemia

Post-renal causes

Bilateral obstruction: posterior urethral valve, urethral trauma, congenital phimosis, urethral diverticulum, neurogenic bladder, megacystis-megaureter syndrome
Obstructive lesion of the only functioning kidney: obstruction of the ureteropelvic segment

Renal acute renal failure.

In renal acute renal failure, impaired renal function is associated with damage to the parenchyma at the cellular level. Usually this is one of the following 2 types of pathology: ischemia (acute tubular necrosis), nephrotoxic damage (aminoglycosides), congenital anomalies of the kidneys (polycystic), vascular disorders (thrombosis of the renal artery or vein, especially the only kidney).

Postrenal acute renal failure.

Postrenal acute renal failure develops when there is an obstruction to the flow of urine from both kidneys or from a single kidney. The most common causes of postrenal acute renal failure in newborns are the posterior urethral valve or bilateral obstruction of the vesicoureteral segment. Although these types of obstruction are usually correctable, however, with their long intrauterine existence, various degrees of irreversible changes in renal function may develop. AKI occurs as a result of an underlying anomaly, but on the other hand, already existing AKI can lead to secondary parenchymal damage.

Symptoms of acute renal failure in newborns

AKI in the newborn is manifested clinically by symptoms that are primarily characteristic of the underlying pathology, for example, sepsis, shock, dehydration, severe respiratory distress syndrome. Often there are nonspecific symptoms associated with uremia, namely, malnutrition, severe lethargy, vomiting, convulsions, hypertension,.

Diagnosis of acute renal failure in newborns

Evaluation of a newborn with acute renal failure should begin with a thorough history taking of both the patient and the family and examination. When prerenal causes of acute oliguria are suspected, increased fluid loading with or without furosemide is of both diagnostic and therapeutic value. If diuresis does not increase in response to these measures, further deeper determination of kidney function is necessary.

Laboratory research includes a complete blood count, determination of serum concentrations of urea, creatinine, electrolytes, uric acid, calcium and phosphorus. The level of creatinine in serum during the first few days of a child's life corresponds to that of the mother, and after the 1st week it is 35-44 mmol / l in a full-term newborn. The presence in the urine of erythrocytes, protein, cylinders is characteristic of parenchymal kidney damage.

In the differential diagnosis of renal renal failure and n rerenal azotemia in a patient with oliguria, the most valuable indicator is FEC a. The use of this test is based on the assumption that the renal tubules of a poorly perfused kidney voraciously reabsorb sodium, while a kidney with parenchymal or tubular damage is unable to reabsorb sodium. Accordingly, in most cases of oliguric renal failure in newborns, which developed against the background of renal causes, the FEC a indicator is more than 2.5%. FEC should be measured prior to furosemide administration. In addition, in very preterm infants, who normally have a high FEC a, the results of this test should be interpreted with caution.

It is an extremely valuable examination method that allows you to determine the size of the kidneys, their shape and localization, as well as the expansion of the excretory system and the condition of the bladder. If a posterior urethral valve or vesicoureteral reflux is suspected, voiding cystourethrography is indicated. An antegrade pyelography may also be needed to detect obstruction of the ureterovesical segment. However, a decrease in GFR and tubular function in newborns results in poor visualization of the kidneys and urinary tract on intravenous pyelography during the first few weeks of life. In addition, some radiopaque agents are nephrotoxic. Therefore, it is best to examine kidney function with a radioisotope scan using technetium-99.

Treatment of acute renal failure in newborns

Treatment should be carried out in parallel with diagnostic measures. In children with prerenal oliguria, fluid loading with or without furosemide usually increases urine output and improves renal function. With a posterior urethral valve, an urgent need to place a urinary catheter, while for other obstructive lesions in newborns, a “high” surgical (nephro- or ureterostomy) may be necessary. The fluid load is carried out at the rate of 20 ml/kg of an isotonic solution containing 25 mmol/l of sodium bicarbonate with an infusion of the specified volume for 1-2 hours. If during this time sufficient diuresis is not restored (2 ml of urine or more per kg in 1-2 hours), intravenous administration of furosemide at a dose of 2-3 mg / kg is indicated. The absence of an increase in diuresis after fluid loading in a newborn with normal cardiac output (hence normal renal perfusion) in the absence of urinary tract obstruction suggests the presence of parenchymal renal disease and requires appropriate treatment of oliguric or anuric renal failure.

Maintaining fluid balance is the basis of the treatment of a patient with acute renal failure. The daily fluid load should be equal to the sum of insensitive water loss, diuresis, and extrarenal fluid loss. In term infants, insensible water loss is 30-40 ml/kg/day, while preterm infants may require up to 70 ml/kg/day. When conducting fluid therapy, it is very important to measure the body weight of the newborn frequently. The electrolyte composition of the injected liquid is determined by the data of regular laboratory examinations. Insensitive water losses do not contain electrolytes and therefore must be replenished simply with an aqueous glucose solution.

Serious secondary disorders such as hyperkalemia, hyponatremia, hypertension, hypocalcemia, hyperphosphatemia, and metabolic acidosis can occur as a result of AKI. Therefore, in patients with acute renal failure, exogenous sources of potassium intake should be excluded first of all. However, many have an increase in serum potassium, which requires immediate active treatment to avoid cardiotoxicity. With a progressive increase in serum potassium concentration, therapy should begin with the use of sodium-potassium ion exchange resins (sodium polystyrene sulfonate in sorbitol, 1 g/kg rectally in an enema). In emergency situations, to prevent or treat already occurring cardiac, intravenous administration of sodium bicarbonate (1-2 mmol / kg), 10% calcium gluconate solution (0.5 ml / kg) and glucose (0.5-1.0 g / kg ) followed by the introduction of insulin (0.1-0.2 U/kg).

In children with oliguria, hyperhydration may develop hyponatremia and hypertension, which requires, first of all, restriction of the fluid load. High doses of intravenous furosemide (5 mg/kg) may be effective. With persistent asymptomatic hypertension, apressin is added parenterally (0.25-0.5 mg / kg every 4 hours). If persistent significant rises in LD are accompanied by clinical manifestations, diazoxide (5 mg/kg) is administered intravenously.

Hyperphosphatemia (serum phosphorus level greater than 2 mmol/l), which is often the cause of hypocalcemia associated with it, requires the use of milk formulas with a low content of phosphorus (Similak PM 60/40), as well as calcium carbonate that binds phosphate (50-100 mg /kg/day). The use of aluminum hydroxide for this purpose (phosphate binding) is contraindicated due to aluminum toxicity in children with renal insufficiency.

As a result of the retention of hydrogen ions, metabolic acidosis may develop, which requires the use of sodium bicarbonate.

The patient's nutrition (intravenous or enteral) should provide 100-120 calories and 1-2 g protein/kg/day. For enterally fed newborns, formulas low in phosphorus and aluminum are recommended, such as Similac PM 60/40. Active implementation of adequate nutrition greatly contributes to the restoration of kidney function, providing the necessary energy needs at the cellular level.

Although most neonates with acute renal failure are treated conservatively, peritoneal dialysis or long-term arteriovenous haemofiltration (DAHD) may be required in rare cases to treat the metabolic complications of fluid overload. Mortality in this group of patients usually exceeds 60%. In our hospital, over the past 6 years, we have performed peritoneal dialysis in 17 newborns with acute renal failure. Mostly these were patients undergoing open heart surgery. Although, according to the literature, the mortality rate in such patients is 90-100%, in our experience, the early initiation of peritoneal dialysis and the provision of adequate nutrition have reduced mortality in recent years to 38%.

The article was prepared and edited by: surgeon

(ARF) is a clinical syndrome of various etiologies, which is characterized by a pronounced and rapid decrease in glomerular filtration rate with the inability to maintain homeostasis.
Causes of acute renal failure:

Prerenal (functional acute renal failure);
Renal (organic acute renal failure);
Postrenal acute renal failure.

prerenal(functional surge arrester).
The main reason is hypovolemia (centralization of blood circulation and renal ischemia). Functional disorders of the kidneys develop (no organic changes). With timely elimination of renal ischemia, their function is fully restored. If the ischemia is prolonged (protracted), then a secondary organic lesion of the renal parenchyma may develop.

Functional acute renal failure develops when:

Hypovolemia (dehydration, intoxication,);
Violation of central hemodynamics (myocarditis, cardiac tamponade, myocardial infarction);
Violation of peripheral hemodynamics (, sepsis);
Occlusion of the renal vessels.

Renal(organic OPN).

There are three types of renal acute renal failure:

cortical necrosis.
Causes: hypovolemia, hypoxia, shock, hemolysis, endotoxins;
Necrotic papillitis - necrosis in the cerebral ball.
Causes: ethylene glycol poisoning, poisoning with alcohol substitutes, abuse of acetylsalicylic acid;
Interstitial nephritis.

Postrenal acute renal failure: develops when the outflow of urine below the renal pelvis is disturbed. Causes: urolithiasis, tumor, neurogenic bladder, traumatic injury to the ureters during gynecological operations.

OPN pathogenesis.

The development of acute renal failure is influenced by 2 factors: toxic and circulatory, for example, in case of chemical poisoning, a direct one is a toxic factor and an indirect one is a circulatory one.

The kidneys are characterized by a high intensity of blood circulation. 92.5% of the total amount of blood flows through the kidneys. There are 2 functional circles of blood circulation in the kidney. The large circle is cortical and the small circle is juxtamedullary. Blood circulation can switch from a large circle to a small one (shunting occurs).

Approximate schemes for the development of OPN:

Traumatic aggression - shock - renal ischemia - diffuse destruction of renal tubules - anuria - uremia - outcome;
Toxic aggression - severe poisoning - changes in the proximal tubules - anuria - uremia - outcome;
Enterocolitis - dehydration - collapse - renal ischemia - diffuse destruction of renal tubules - anuria - uremia - outcome.

OPN clinic

There are 4 periods of acute renal failure:

The period of action of the etiological factor. Duration from several minutes to hours;
Period of oligoanuria(can last up to 21-28 days). It is characterized by the development of oliguria or anuria. Uremic intoxication develops. Oliguria - decrease in diuresis less than 0.5 ml / kg per hour. Anuria - urine output less than 50 ml per day or urine output less than 0.3 ml / kg per hour.

During this period, complications in other systems may occur:

CNS - there may be encephalopathy (against the background of uremic intoxication, hyperhydration);
Circulatory system (may develop pericarditis, myocarditis);
Respiratory system (possible pneumonia, pleurisy);
Liver (kidneys and liver are interconnected, if kidney function is impaired, part of its functions is taken over by the liver);
The blood system (anemia may develop due to inhibition of blood formation, as well as a decrease in kidney excretion - erythropoietin);
Violation of water and electrolyte balance (hyper K, Na, Mg develops). Increasing potassium to 6.5 mmol/l is critical;
Skeletal system (development of osteodystrophy, osteomalacia);
Endocrine system (increased glucose tolerance).

3. Polyuria period(duration 5-8 days). It is characterized by an increase in diuresis and a decrease in azotemia. This period is dangerous, like the period of oliguria. The amount of urine excreted increases to 10 liters per day (in adults). This can lead to dehydration, resulting in renal ischemia;

4.Recovery period(duration 1.5-2 years). There is a slow recovery of kidney function. For a long time, low density of urine persists (1002-1004).

Diagnostics (OPN):

1) The rate of diuresis.

Minimum diuresis:

In adults - 30 ml / hour;
In children under 1 year old - 1.5 ml / kg / hour
In children under 5 years old - 1 ml / kg / hour;
In children older than 5 years - 0.5 ml / kg / hour.

Even with a normal amount of diuresis, there may be renal failure. You also need to focus on indicators - urea and creatinine.

2) Indicators of urea and creatinine:

Urea is not only a marker of renal failure, but also an indicator of liver catabolism (it also characterizes liver function).
With an increase in catabolism, lipids and proteins are destroyed in the body. A large amount of ammonia (a lipophilic compound, toxic) is formed, which is poorly excreted by the kidneys. The cycle of urination takes place in the liver. With ammonia, urea is formed (a hydrophilic compound, non-toxic), which is well excreted by the kidneys.
Creatinine is a more significant criterion for acute renal failure. It is synthesized in the muscles and filtered in the renal tubules, completely excreted in the urine (no adsorption). Creatinine characterizes glomerular filtration. Normally 110-170 µmol/l, or 0.11-0.17 mmol/l. An increase in creatinine up to 0.4 µmol/l characterizes functional acute renal failure. An increase in creatinine greater than 0.4 µmol / l - organic acute renal failure.

Important ratio of blood urea/to blood creatinine (in mmol/l). Normal = 20-40. If more than 40, urea production increases (catabolism increases), if less than 20, it indicates kidney failure.

3) Osmolarity of urine (an important criterion).

The osmolarity of urine can be calculated using the formula: Uosm.=26 x (S+6), where S is the last 2 digits of the urine specific gravity. B N \u003d 540-670 mosmol / l.
With functional AKI, the osmolarity of urine will be higher than normal. With organic acute renal failure, the osmolarity of urine is below 540 mosmol / l. (destructive changes in the proximal tubules, no reabsorption).

4) The concentration of sodium in the urine.

With functional OPN -Na is less than 10 mmol / l;
With organic acute renal failure - Na is more than 25 mmol / l.

5) Creatinine clearance- absolute criterion of acute renal failure. Means - purification of a certain volume of liquid of a given compound in 1 minute.
The norm is 80-180 ml / min.
Decreased creatinine clearance indicates renal failure:

80-50 ml / min - borderline;
50-20 ml / min - a mild degree of renal failure;
20-10 ml / min - the average degree of renal failure;
Less than 10 ml / min - severe renal failure.

6) The presence in the analysis of urine - urinary lysozyme.
Lysozyme - a protein synthesized in leukocytes and should not be in the urine. If it is present in the urine, then this indicates necrosis of the tubules of the kidneys.

Definition by urinalysis of the anatomical lesion of the kidney:

Glomeruli - the presence of erythrocytes, fat, blood cylinders in the urine analysis, proteinuria (++++);
Renal tubules - the presence of epithelial cells of the renal tubules, cylinders are granular, pigmented;
Interstitium - the presence of leukocytes, eosinophils, renal cylinders;
Renal vessels (diabetic nephropathy) - a small amount of red blood cells.

Treatment.

1) Treatment of functional acute renal failure.
The main treatment is infusion therapy (). The rate of rehydration in children in the first hour is 20 ml/kg, further 5-10 ml/kg/hour. After the first hour of infusion furasemide 1-4 mg/kg is administered. Furosemide is administered 2-4 times a day.

At this stage, antiplatelet agents can be used to improve microcirculation: dipyridamole, pentoxifylline.

Also used: aminofillin, dopamine (1-4 mcg / kg / min).

2) Treatment of organic acute renal failure.

Liquid calculation:

In adults - diuresis of the previous day + 300 + pathological losses;
In children under the age of 1 -1.5 ml/kg/h + diuresis of the previous day + pathological losses;
In children under 5 years old - 1 ml / kg / hour + diuresis of the previous day + pathological losses;
In children after 5 years, 0.5 ml/kg/h + diuresis of the previous day + pathological losses.

Be sure to control body weight 2 times a day. Weight gain should not exceed 1% per day.

Diuretics:

Lasix acts on the proximal tubules, and if the tubules are damaged, lasix has no effect.
Lasix is used 2-4 times a day at a dose of 2 mg/kg, the daily dose is not higher than 10 mg/kg. Adults 700 mg divided into 3 injections. If there is no effect - do not increase the dose.
Osmodiuretics. In the absence of glomerular filtration, osmodiuretics should not be used.
Manitol test. Therapeutic dose - 1g / kg, for the sample - 0.5 g / kg (half the dose). If this dose leads to an increase in the rate of diuresis, then the same dose is repeated for confirmation. If the effect has not come, the introduction of manit is contraindicated. Manit acts on the proximal tubules;
Eufillin - increases the glomerular filtration rate (dose 4 mg / kg per day). Acts on intact nephrons. In the organic stage is not assigned.

If there is no effect from diuretics, dialysis therapy is performed.

Necessary:

Restore the structure of kidney cells (regeneration). Oligoanuria lasts 21 days. Improve the globular function of the protein (improve disulfide bridges in the protein molecule). For this purpose, apply - Sodium thiosulfate or Unitiol;
Improve tissue respiration - cytochrome C;
Posyndromic therapy without polypharmacy;
Ensuring the energy balance of the body (parenteral nutrition);
Dialysis – the sooner the better;
(with renal failure, they die from bacterial complications, sepsis). They are prescribed in courses of 5 days at a half dose, between courses there is a break of 2 days. The drugs of choice are oxacillin, erythromycin (they are excreted by the biliary route). You can enter - cefobit. Nephrotoxic antibiotics (aminoglycosides, methicillin, tetracyclines, 1st generation cephalosporins) are contraindicated. If extracorporeal detoxification is carried out, the usual doses of antibiotics are administered.

We transfuse solutions depending on the osmolarity of the plasma:

If the osmolarity is above 310 - infusion therapy consists of 5% glucose, dextrants. 10-20-40% glucose cannot be administered during hypoxia due to the development of lactic acidosis;
If the osmolarity is normal 280-310 - infusion with isotonic glucose 5% and saline solutions (NaCl-0.9%);
With hypoosmolarity (below 280), NaCl -7.5% - 4 ml / kg is included in the infusion.

To maintain colloid-osmolar pressure, they are administered - refortam, stabizol. With anuria, protein preparations, solutions containing potassium (trisol, assesol, potassium chloride, Ringer's solution) are contraindicated.

With threatening hyperkalemia (above 6 mmol / l), the following are administered:

Calcium gluconate 10% - 0.2 ml / kg;
Glucose solution 20% - 4-5 ml / kg with insulin (1 unit per 5 g of glucose);
A solution of sodium bicarbonate 4% - 2-4 ml / kg (not together with calcium gluconate in one syringe);
An osmotic laxative (xylitol, sorbitol) is administered orally.

Indications for emergency hemodialysis:

Hyperhydration with the development of cerebral edema or pulmonary edema;
The level of urea is more than 25 mmol / l, or the daily increase in urea is more than 6-8 mmol / l;
Serum creatinine level more than 0.5 mmol / l, or daily increase in creatinine more than 0.18 mmol / l;
Blood potassium 6.0-6.5 mmol/l, sodium less than 120 mmol/l;
Severe blood acidosis (pH less than 7.2);
Increase in body weight per day more than 5%;
Lack of effect from conservative treatment (anuria for more than 2 days).

In conclusion, I would like to note that the treatment of acute renal failure is one of the most difficult problems in pediatrics and requires both conservative treatment and the use of invasive methods of renal replacement therapy.
With proper and timely treatment of acute renal failure, using all methods, the prognosis can be favorable with a complete recovery.