Kidney failure symptoms in a child. Chronic renal failure in children. Renal failure - therapeutic measures

Zhemoytyak V. A. – Associate Professor, Candidate of Sciences honey. sciences

Definition

Acute renal failure (ARF) is a nonspecific, clinical and laboratory syndrome of various etiologies that occurs due to the acute loss of all homeostatic functions of the kidneys.

surge arrester – clinical syndrome, developing most often as a result of acute kidney damage with impaired renal function, accompanied by an increase in the level of creatinine in the blood within 48 hours of more than 25 qsho1/1 or more than 50% of the initial value and/or a decrease in diuresis of less than 0.5 ml/kg hour for more than 6 hours.

AKI is always a critical condition that occurs when renal blood flow is disrupted, renal tissue hypoxia, tubular damage, and the development of interstitial edema, which leads to disruption of basic renal functions: glomerular filtration, tubular reabsorption and secretion.

The syndrome is manifested by electrolyte imbalance, impaired ability to excrete water, acidosis, increasing azotemia, disruption of the heart, respiratory system, liver, central nervous system and other organs and systems.

Synonyms for the diagnosis of acute renal failure are: in English literature – “acute renal failure”, in French – “acute tubular necrosis”, in German – “necronephrosis”.

Epidemiology

In children, renal failure is observed relatively often due to exposure to pathogenic factors or the development of a progressive pathological process against the background of insufficient morphological and functional maturity of the kidneys and high lability of water-mineral metabolism, high frequency kidney abnormalities and urinary tract, high frequency of hereditary and acquired nephropathies.

On average, acute renal failure occurs in 3 children per 1,000,000 population, of which infants are children. AKI accounts for 8–24% of all admissions to the neonatal intensive care unit. Between the ages of 6 months and 5 years, the incidence of AKI is 4–5 children 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 on the prevalence of diseases of the glomerular apparatus of the kidneys and is 1 per 100,000 children.

Etiology

For reasons of development, depending on the level of exposure to the damaging factor, the following forms of acute renal failure are distinguished:

1. prerenal

2. renal

3. postrenal

Prerenal acute renal failure (the result of a sharp decrease in renal perfusion).

Causes

1. Hypovolemia:

Dehydration – losses through the gastrointestinal tract: vomiting, diarrhea (including gastroenteritis), surgical drainage; fluid loss through the kidneys: diuretics, osmotic diuresis in diabetes mellitus, adrenal insufficiency, diuretics, tubulopathies);

Fluid loss into the “third space”: postoperative, burns, intestinal obstruction, acute pancreatitis, peritonitis, extensive trauma, edema due to protein loss - severe hypoalbuminemia (nephrotic syndrome, malabsorption syndrome), liver disease, combined liver and kidney diseases;

Blood loss: due to trauma, surgery, obstetric complications.

2. Reduced cardiac output not associated with hypovolemia - diseases of the heart muscle, valves and pericardium, cardiac arrhythmias, heart failure, pulmonary embolism, high-pressure ventilation.

3. Impaired pressure in the renal vessels: dilation of blood vessels: collapse, shock, including septic, anaphylaxis, pharmacological effects (antihypertensive drugs - vasodilators), spasm of the renal arteries (hypercalcemia, norepinephrine, adrenaline, cyclosporine, tacrolimus, amphorerricin B), liver cirrhosis with ascites (hepatorenal syndrome).

4. Renal hypoperfusion with impaired autoregulation: cycloxygenase inhibitors, angiotensin convertase inhibitors, angiotensin receptor blockers.

5. Syndrome of increased blood viscosity - histiocytosis, erythremia.

6. Obstruction renal vessels(unilateral or bilateral) – stenosis of the renal arteries (as a consequence of thrombosis, systemic vasculitis), dissecting aortic aneurysm, obstruction of the renal veins (as a consequence of thrombosis or compression from outside).

7. Mixed causes: septicemia, disseminated intravascular coagulation syndrome, hypothermia, hypoxia (pneumonia, RDS), aortic cross-clamping.

Most common reasons prerenal acute renal failure in children are dehydration due to acute intestinal infections and losses in the “third space”.

With timely elimination of the cause of the disease, prerenal acute renal failure quickly undergoes reverse development

Prerenal acute renal failure not recognized and corrected in a timely manner (more than 24 hours) turns into renal

Renal acute renal failure caused by damage to the renal parenchyma due to various kidney diseases, including inflammatory, vascular, toxic effects:

1. Ischemic lesion kidneys (if the causes are not eliminated!).

2. Diseases of the kidney parenchyma: immune glomerulopathies - post-streptococcal glomerulonephritis (GN), lupus, membranous proliferative, idiopathic rapidly progressive, hereditary nephritis, GN with Henoch-Schönlein purpura, Goodpasture syndrome.

3. Vasculitis:

Vascular lesions in periarteritis nodosa, systemic lupus erythematosus, serum sickness, Wegener's granulomatosis, Hashimoto's disease.

Microangiopathies: HUS, disseminated intravascular coagulopathy, thrombotic thrombocytopenic purpura, hemorrhagic vasculitis.

4. Toxic damage to tubules:

Nephrotoxins that cause primary tubular damage - interstitial nephritis (TIN): phenacetin, non-steroidal anti-inflammatory drugs, antibacterial drugs, ampicillin, methicillin, sulfonamides, rifampicin, etc., heavy metal salts, sublimate.

Infiltrative ( malignant tumors, Beck's sarcoidosis).

5. Mixed: hemolytic-uremic syndrome, renal vein thrombosis, hemoglobinuria, myoglobinuria, tumors, infection, uric acid nephropathy, developmental abnormalities (polycystic, hypoplasia/dysplasia/aplasia of the kidneys).

Renal causes depend on age. In newborns and young children, the leading causes are unresolved prerenal causes, HUS. In preschoolers and schoolchildren, immune glomerular diseases, vasculitis, and interstitial nephritis prevail.

Postrenal acute renal failure

Her reasons:

1. Urethral (urethral strictures, ureterocele, urethral valves, phimosis).

2. Bladder (neurogenic bladder).

3. Ureteral: bilateral stenosis of the ureteric orifice, hydronephrosis due to narrowing of the ureters, retroperitoneal fibrosis, radiation injuries, surgical (ligation).

Acquired obstructive uropathy also includes: vesicoureteral reflux, stones, blood clots, tumors, inflammatory diseases urinary tract.

Unlike adults, postrenal oliguria is extremely rare in children.

Table 69 – Frequency of causative factors in age groups (%)

The most common causes of acute renal failure in children of different ages are the following factors:

1. In newborns

Prerenal:(approximately 80–85% of cases. Ischemic injury is the most common cause of acute renal failure. Necrosis and apoptosis may develop as a result of renal ischemia).

Intrauterine dehydration.

Bleeding.

Asphyxia.

Congenital heart defects.

Congestive heart failure.

Renal:

Thrombosis of the renal vessels.

Iatrogenic effects in the ante- and postnatal periods.

Renal dysgenesis.

Renovascular injuries.

Postrenal:

Malformations of the urinary system.

Renal vein thrombosis.

Infections.

Blockage of the urinary tract by salt crystals (urolithiasis can develop even in newborns, especially premature infants with hypercalciuria).

2. 1 month – 3 years:

Hemolytic-uremic syndrome.

Primary infectious toxicosis.

Anhydremic shock in acute intestinal infections.

Heavy electrolyte disturbances(hypokalemia, metabolic alkalosis) of various origins.

3. 3–7 years:

Viral and bacterial kidney damage (yersiniosis, influenza).

Drug-induced and interstitial nephritis (poisoning).

4. 7–14 years:

Systemic vasculitis (systemic lupus erythematosus, etc.).

Subacute malignant glomerulonephritis.

Shock (burn, septic, traumatic, transfusion).

Pathogenesis

AKI develops over a period of several hours to several days. The leading pathophysiological links in the development of symptoms of acute renal failure are fluid and electrolyte disturbances, metabolic acidosis, accumulation of carbon dioxide, increased ventilation, lung damage and pathological breathing.

AKI syndrome is rarely isolated. Most often it develops as part of multiple organ failure.

A feature of the course of acute renal failure is its cyclical nature with the possibility of complete restoration of impaired renal functions.

The basis of pathomorphological changes in the kidneys:

1. Mainly affected proximal parts nephron, since they are especially sensitive to damaging factors due to the high activity of metabolic processes.

2. AKI develops when at least 70% of the tubules are affected.

3. Tubulo-epithelial lesions. Glomeruli are usually intact or minimally changed (except for acute renal failure in glomerulonephritis). Tubular changes: ischemia of the renal tissue leads to acute tubular necrosis with mechanical obstruction of the tubules by desquamated epithelium. A distinction is made between tubulonecrosis (necrosis of the epithelium while maintaining the basement membrane) in toxic nephropathies and tubulorhexis (in addition to necrosis of the epithelium, the basement membrane is also destroyed). Observed: interstitial edema, disorganization of connective tissue, congestion of the glomerular capillaries, interstitial edema and mesangial expansion. The preservation of the tubular basement membrane indicates a possible toxic etiology of acute renal failure. Children often experience microthrombosis of capillaries, renal corpuscles, and sometimes segmental or total necrosis of the renal cortex.

Regardless of the cause of acute renal failure, the microscopic picture is the same.

Nephronecrosis - swelling is visible within 10–15 minutes after kidney damage, and necrosis is visible after 48 hours. The proximal tubules are most affected.

Dilation of the tubules and cessation of water reabsorption leads to increased pressure in the tubules, their sudden swelling and rupture of convoluted tubules

Cortical necrosis is the most severe form of glomerular damage (irreversible).

Despite the variety of etiological factors of organic acute renal failure, its pathogenesis consists of the following main pathological processes:

1. renal vasoconstriction causing tissue ischemia;

2. decreased permeability of glomerular capillaries, leading to a drop in glomerular filtration rate (GFR);

3. obstruction of the tubules by cellular detritus;

4. transepithelial return flow of filtrate into the peritubular space;

5. thrombotic microangiopathy of the glomerulus of the kidney – characteristic hemolytic-uremic syndrome (HUS), the leading cause of acute renal failure in children.

The hemodynamic factor plays a dominant role in the pathogenesis of acute renal failure syndrome. It is described by a well-known phenomenon (tubuloglomerular feedback), the essence of which is damage to the epithelial cells of the proximal tubules due to the influence of any factors leading to a decrease in the reabsorption of salts and water in the initial part of the nephron. The increased intake of Na ions and water into the distal parts of the nephron serves as a stimulus for the release of vasoactive substances (renin) by the juxtaglomerular apparatus. Renin causes and maintains spasm of the afferent arterioles with redistribution of renal blood flow, neglect of arterioles and a decrease in GFR. All this leads to a decrease in the excretion of salts and water. The feedback signal provided by the tubules to reduce blood flow and GFR in conditions of excess excretion of solutions is called tubuloglomerular feedback. Under physiological conditions, it provides a safety mechanism to limit GFR when tubular capacity is overloaded. However, in acute kidney injury, activation of this mechanism further reduces renal blood flow, limiting delivery nutrients and exacerbating tubular damage. When renal blood flow decreases to 30%, glomerular filtration is not detected.

In the oliguric stage of acute renal failure, the hemodynamic factor no longer plays a dominant role. Attempts to increase renal blood flow when renal damage has already occurred do not significantly increase GFR and do not improve the course of AKI.

Subsequently, significant damage to the reabsorption capacity of nephrons, changes in the normal corticomedullary osmotic gradient in conditions of decreased filtration rate leads to an increase in fractional or absolute excretion of water. This explains the development of the polyuric stage of acute renal failure.

During the recovery stage, the role of the hemodynamic factor again comes to the fore. Increased renal blood flow simultaneously increases GFR and increases diuresis. The duration of the recovery stage is determined by the residual mass of active nephrons, and the rate of renal recovery is directly dependent on renal blood flow in the recovery phase.

Currently, timely use of conservative methods of detoxification and renal replacement therapy makes it possible to interpret acute renal failure syndrome as a reversible condition.

Figure 11 – Pathogenesis of oliguria in acute renal failure (according to N.P. Shabalov, 1993)

Clinic and course of acute renal failure

Since acute renal failure is characterized by a rapid or sudden decrease in glomerular filtration, clinically this is manifested by a decrease in diuresis, impaired nitrogen excretory function, water-electrolyte and other metabolism, and pathological damage to almost all systems and functions.

OPN is a cyclic process, classically going through 4 successive stages:

1. initial;

2. oligoanuric;

3. restoration of diuresis and polyuria;

4. outcome (recovery?).

Stage I of acute renal failure – initial (shock, pre-uric)

Duration – from 6 to 24 hours. The clinical picture is dominated by signs of the underlying disease, which caused acute renal failure and decreased diuresis. Clinically manifested depending on the cause of acute renal failure (a picture of acute infection or poisoning, severe hemodynamic disorders characteristic of shock and collapse; with glomerulonephritis, blood pressure may be increased).

Often observed:

1. anxiety;

2. confusion;

3. high temperature,

5. pain in the abdomen, lower back,

6. increasing decrease in diuresis and urine density (!).

It should be remembered that:

1. Oliguria – decreased diuresis rate ‹ 0.5 ml/kg*hour (in children 1 year of age – ‹ 1.0 ml/kg*hour).

2. Daily diuresis is less than 300 ml/m2/day or 10–12 ml/kg/day.

3. Anuria – decreased diuresis rate ‹ 0.3 ml/kg*hour (in children 1 year of age ‹ 0.5 ml/kg*hour).

4. Daily diuresis is less than 60 ml/m2/day or less than 50 ml/day.

5. Polyuria – increased diuresis rate › 2.5 ml/kg*hour.

The concepts of “oliguria” and “acute renal failure” cannot be equated - they are not synonyms! AKI is the loss of homeostatic functions of the kidneys. Oliguria may be a protective physiological reaction of the kidneys to a decrease in renal blood flow in response to dehydration, hypovolemia, arterial hypotension, hypothermia, etc. If the degree of decrease in renal blood flow affects the state of the filtration function of the kidneys and leads to moderate development of azotemia (increase in serum creatinine by 20–50 %), it is legitimate to talk about the development of prerenal renal failure. In cases where functional disorders lead to structural changes in the renal parenchyma, oliguria reflects the development of renal acute renal failure and is always accompanied by severe azotemia.

Stage II – oligoanuric

The most typical, it exhibits all the signs of acute renal failure. Duration - from several days to weeks.

In the clinical picture, damage to almost all organs and systems becomes obvious: uremic intoxication increases, hyperhydration against the background of decreased diuresis (up to 50–100 ml per day), hyperkalemia. The general condition of the patient is serious.

Signs characteristic of damage to various systems are:

1. Nervous system:

Fatigue, weakness;

Lethargy;

Drowsiness;

Prostration;

Delirium;

Sleep disturbance;

Strong headache;

Muscle twitching.

Oligoanuria, overhydration: peripheral, abdominal and visceral edema, pulmonary and cerebral edema with coma and convulsions, weight gain.

Azotemia:

Smell of ammonia from the mouth;

Skin itching;

Aversion to food.

2. Skin and mucous membranes:

Pallor, icterus sclera and skin;

Hemorrhagic petechiae, ecchymoses;

Dry mouth, stomatitis, cracks in the mucous membrane of the mouth and tongue.

3. Respiratory system:

Dyspnea (acidotic breathing - deep and noisy);

Congestive wheezing in the lungs;

Interstitial pulmonary edema “Fluid lung” (a characteristic feature on the radiograph is the location of the edema in the center of the lungs in the form of a “butterfly”, while the periphery of the lungs is free from edema);

An increased content of medium-molecular uremic toxins (oligopeptides) leads to shunt-diffusion respiratory failure, shock lung, and decompensation of systemic hemodynamics.

4. Cardiovascular disorders:

Signs of heart failure;

Expansion of the boundaries of the heart;

Deafness of heart sounds;

Tachycardia;

Systolic murmur becomes rougher as intoxication and anemia increase;

Arrhythmias;

Arterial hypotension or hypertension;

Pericarditis;

ECG changes (including ventricular fibrillation);

5. Gastrointestinal tract:

Anorexia;

Nausea, vomiting;

Stomach ache;

Enlarged liver;

Intestinal paresis;

Gastritis; uremic enterocolitis.

6. Urinary system:

Urine is cloudy, dark, appears bloody, specific gravity is low, red blood cells, white blood cells, cylinders, clumps of hemoglobin;

Lower back pain;

Pain when tapping the lower back.

Electrolyte disturbances and acid-base imbalances.

Clinical signs of infectious disease or reinfection.

Laboratory indicators of homeostasis change:

1. Urea 25–35 mmol/l;

2. Creatinine 0.3–0.5 mmol/l. The creatinine content increases faster than urea. With increasing azotemia, multiple organ toxic changes occur (including enterocolitis, aggravating water and electrolyte disorders).

3. Water and electrolyte disturbances (hyperkalemia › 6–7 mmol/l, hyperphosphatemia › 4–5 mmol/l, hypermagnesemia – 2–3 mmol/l, decreased sodium, calcium, blood protein (albumin!). Hyperkalemia is especially dangerous (result tissue breakdown and retention of potassium excreted by the kidneys): bradycardia, extrasystole, asystole..., myocarditis may develop, less often - endocarditis, heart failure. These disorders are a common cause of death in patients in this phase.

4. Glomerular filtration decreases to 10–15 ml/min.

5. Basic acid base – metabolic acidosis with a decrease in reserve alkalinity.

6. In the blood: high ESR, leukocytosis, anemia.

The oligoanuric stage accounts for more than 70% of deaths from acute renal failure.

With successful therapy, the process enters the recovery stage.

Stage III – stage of restoration of diuresis and polyuria

It is characterized by: increased diuresis with a tendency to hypoelectrolythemia.

The patient's condition is serious. Conventionally, two periods are distinguished:

Early(diuresis increases, but azotemia persists) and late (nitrogen metabolism normalizes).

Characteristic:

1. Gradual restoration of the water excretory function of the kidneys. Increased amount of urine. Urine density is low. There are two possible course options: a gradual increase in diuresis or a sudden increase in the amount of urine. The excretion of water prevails over the excretion of sodium, which leads to hypernatremia, and significant losses of potassium in the urine lead to hypokalemia. In the early polyuric stage - diuresis is up to 3 liters per day, later (by the 5th-6th day) - up to 2 liters.

2. The resulting dehydration and dyselectrolythemia is manifested by loss of body weight, asthenia, lethargy, lethargy, muscle hypotension, vomiting and hypertension.

3. The nitrogen excretion function gradually normalizes.

4. Infectious pathology is often associated.

The stage of restoration of diuresis accounts for about 30% of deaths from acute renal failure. The most common causes are severe disorders of water and electrolyte balance and infectious complications.

The duration of this stage is 1–3 months.

Stage IV – outcome stage (recovery?)

It begins from the moment the level of nitrogenous wastes normalizes.

Ends: restoration of kidney function or formation of chronic renal failure.

Duration – 6–24 months. There is a slow recovery of partial renal functions (concentration, filtration, acidoammoniogenesis), water levels are normalized electrolyte metabolism and acid-base balance, symptoms of damage to the cardiovascular and other systems are eliminated.

Duration: 6–36 months.

Complications:

Most common:

1. anemia;

2. acute pulmonary and cerebral edema;

3. spicy cardiovascular failure;

4. bleeding and hemorrhage;

5. septic infection, pyelonephritis, interstitial nephritis;

6. formation of chronic renal failure.

The outcome of the disease depends on the cause and extent of kidney damage.

A lethal outcome is observed in 10–50% of patients (young children – 25–40%, in older children – 10–25%).

CRF, as an outcome of acute renal failure, develops in 10–20% of children in the first 3–5 years after renal acute renal failure.

Mortality from acute renal failure: up to 20% with the use of renal replacement therapy (RRT) and up to 40% without RRT.

Diagnostics

The main signs of acute renal failure are: rapid rise creatinine level in the blood or a decrease in hourly diuresis. These signs are independent of each other and one of them is sufficient to make a diagnosis of acute renal failure.

To find out the cause of acute renal failure, it is necessary to have data from the anamnesis, basic and additional methods examinations.

If you suspect acute renal failure:

1. Assess diuresis (reduced absolutely or relatively, less often - polyuria, in stage III - a typical symptom).

2. Determine the density of urine (in most patients with acute renal failure, the density is reduced).

3. Physiological hyposthenuria occurs only with polyuria!

4. Maximum density of urine:

By the end of 1 year of life up to 1015.

At an early age up to 1020.

At older ages up to 1030.

5. Examine urinary sediment (proteinuria, erythrocyturia, hemoglobinuria, leukocyturia, cylindruria are detected).

The characteristics of the sediment are determined by the cause of acute renal failure.

Peripheral blood(UAC) – typical:

1. Anemia (with acute renal failure as a sign of hemolysis or bleeding)

2. Thrombocytopenia

3. Decrease in hematocrit

4. Hemolysis (with HUS)

5. Neutrophilia with a shift to the left

6. Lymphopenia

7. Monocytopenia

8. Eosinopenia

Biochemical blood test (BAC) – typical:

1. Increase in blood urea concentration (normal up to 8.55 mmol/l).

3. The dynamics of increases in creatinine and urea levels depend on the severity of kidney damage and the speed of their manifestation, especially increased in catabolic states.

4. Increase in the level of K + blood (normal 3.7–5.2 mmol/l) ~ 60% of patients, acidosis increases hyperkalemia, alkalosis decreases.

6. Increase in P concentration (normal 0.65–1.62 mmol/l).

7. Decrease in Ca levels (normal 2.3–2.7 mmol/l).

8. Decrease in Cl content (normal 96–107 mmol/l).

9. Moderate decrease in Na concentration (normal 135–145 mmol/l).

All data is given for ages 4–15 years.

Acid-Base State (ABS):

1. Metabolic acidosis.

2. Respiratory alkalosis (as a rule, it does not compensate for acidosis).

Coagulogram:

1. Acceleration of clotting time.

2. Increase in fibrinogen concentration.

3. Increase in fibrin degradation products (FDP).

4. Decreased fibrinolytic activity.

5. ECG signs of electrolyte disturbances.

6. Fundamentally important for treatment is the recognition of prerenal and renal acute renal failure. In most cases, rapid improvement in renal perfusion leads to improvement in renal function. Below are the main signs that help in differential diagnosis, but none of them can be used in cases where acute renal failure occurs against the background of chronic renal failure.

Table 70 – Criteria for differential diagnosis of prerenal and renal acute renal failure

Fractional excretion of sodium (FE Na):

FE Na =U Na/P Na 100%

P Na – plasma sodium concentration, mmol/l;

U сr – concentration of creatinine in urine, mmol/l;

P сr – concentration of creatinine in plasma, mmol/l.

Renal Failure Index (RFI):

IPI =U Na U cr/P cr

U Na – sodium concentration in urine, mmol/l;

U cr – concentration of creatinine in urine, mmol/l;

P cr – plasma creatinine concentration, mmol/l.

– prerenal and renal acute renal failure

Table 71 – Criteria for differential diagnosis of acute renal failure and chronic renal failure

Ultrasound helps in diagnosing postrenal acute renal failure, revealing stagnation of urine in the urinary tract - the collecting pelvis and bladder.

Treatment

If possible, it is desirable to eliminate the cause of acute renal failure and factors that impair kidney function, especially nephrotoxic drugs.

Monitoring fluid balance, monitoring diuresis, weighing the patient.

Frequent monitoring (at least once a day) of creatinine, urea, potassium, sodium and calcium levels in the blood serum, blood morphology, CBS.

Adapting the dose of drugs to the degree of loss of kidney function.

Adequate nutrition.

1. Treatment of prerenal acute renal failure is aimed at restoring renal perfusion and function

The vein is catheterized to administer fluids and medications - under the control of central venous pressure (60–80 mm H 2 O) and the bladder - to control diuresis.

In the absence of heart failure, to restore bcc, isotonic sodium chloride solution is administered intravenously at a dose of 10–20 ml/kg (or FFP, 5% albumin solution at a dose of 3–10 ml/kg) for 0.5–2 hours. In case of acute blood loss - transfusion of washed red blood cells according to the hematocrit.

After stabilization of hemodynamics and normalization of blood volume, furosemide is administered intravenously at a dose of 1–2 mg/kg, which has both therapeutic and diagnostic value. Increased urine output (2 ml/hour) is a sign of prerenal acute renal failure, and the lack of effect may indicate renal acute renal failure. If diuresis has not stopped, continue the infusion in a volume of 5–10 ml/hour (monitor central venous pressure every hour!) and reintroduce furosemide after 2–4 hours. Administration of dopamine at a dose of 1.5–3 mcg/kg/min potentiates its effect. If the cause of acute renal failure is heart failure, dobutamine and other drugs are used pathogenetic therapy SN. For acute renal failure in children with nephrotic syndrome, an albumin solution is used - a 1–25% solution at a dose of 1 g/kg for 2–4 hours, combining its infusion with the administration of furosemide.

2. Treatment of renal acute renal failure of the oliguric stage

It is necessary to maintain fluid balance - fluid administration depending on hydration. After replenishing the BCC during dehydration with persistent oliguria or anuria, the volume of injected fluid is limited to 300–400 ml/m2, or 10 ml/kg/day (imperceptible losses) with the addition of an amount of fluid equal to daily diuresis. If overhydration occurs, stop taking fluids orally. There may be a lack of replenishment of intangible losses. In the presence of pathological losses, fluid is administered in a volume of 300-400 ml/m2 per day, summing up with daily diuresis and pathological losses.

Diuretics are prescribed in the absence of BCC deficiency. Use mannitol in the form of a 20% solution (0.2–0.5 g/kg) for 30–60 minutes. If diuresis increases by more than 0.5 ml/kg/hour, titrate around the clock at a dose of 0.5–1 g/kg/day. To combat overhydration and hyperkalemia, furosemide is administered at a dose of 1–2 – (5) mg/kg intravenously 3–6 times a day. The drug is ototoxic. The rate of intravenous administration should not exceed 4 mg/min. To improve renal blood flow and enhance the effect of furosemide, dopamine (1.53 mcg/kg/min) is prescribed.

To improve regional renal blood flow and, as a result, increase diuresis, euphilin is titrated at a dose of 0.4–0.8 mg/kg/hour.

Lack of effect is an indication for renal replacement (dialysis) therapy (RRT).

Table 72 - Indications for emergency dialysis in acute renal failure (A. V. Sukalo, 2002)

Indications for dialysis: (N.P. Shabalov, 2004).

Level in blood serum: urea - more than 24 mmol/l, potassium - more than 7 mmol/l (with edema of the brain, lungs - more than 6.5 mmol/l), phosphorus - more than 2.6 mmol/l, blood pH - less 7.2 and base deficiency - more than 10 mmol/l, as well as daily increase in plasma urea - more than 5 mmol/l, potassium - more than 0.75 mmol/l, creatinine - more than 0.18 mmol/l, anuria - over 2 days, severe hyponatremia (less than 120 mmol/l), fluid overload with pulmonary or cerebral edema. Not all of these signs may be present in one patient, but as an indication for hemodialysis, two are sufficient.

Table 73 – Advantages and disadvantages of modern methods of renal replacement therapy (RRT)

To correct acidosis, a 4% sodium bicarbonate solution containing 1 mmol of the substance in 1 ml is slowly introduced.

Correction of electrolyte disorders:

1. Hyperkalemia. Treatment measures should be started when potassium levels rise above 5.5 mmol/l. Diet – exclude foods rich in potassium (potatoes, juices, fruits). Stop prescribing potassium-containing drugs to patients. For hyperkalemia (potassium content over 6 mmol/l):

Calcium gluconate 10% solution 0.5 ml/kg intravenously for 5–10 minutes 3–4 times a day;

Sodium bicarbonate 8.4% solution 2–3 mol/kg in 10% glucose solution in a ratio of 1 to 2 intravenously for 20–30 minutes;

Infusion of glucose at a dose of 0.5 g/kg over 30 minutes with insulin (1 unit of insulin per 4 g of glucose).

2. Correction of phosphorus-calcium balance. Limit the intake of phosphorus from food. In case of tetany against the background of hypocalcemia, it is necessary to administer 0.5–1.0 ml per kg of body weight intravenously of a 1% solution of calcium gluconate.

3. Hyponatremia with reduced diuresis, it is corrected by limiting fluid. A decrease in serum sodium below 120 mmol/l leads to cerebral edema and hemorrhages, which are manifested by vomiting, convulsions, and encephalopathy. Treatment is water restriction and dialysis. In case of hyponatemia, caused by increased losses in urine, its correction is necessary.

4. Hypertensive crisis– a sudden pronounced rise in blood pressure with signs of encephalopathy or circulatory disorders – is treated with nifedipine in a single dose of 0.05–0.5 mg/kg (0.2–0.5–1.0 mg/kg per minute) sublingually or intravenously. They also use intravenous drips of sodium nitroprusside (0.5–8.0 mcg/kg per minute), furosemide 1–2–5 mg/kg intravenously, clonidine 2–6 kg/kg (half the dose intramuscularly, the other half intravenously). For arterial hypertension, drugs are used for continuous use in a daily dose (in 3 divided doses): propranolol 1–5 mg/kg, nifedipine 0.3–1 mg/kg, captopril 0.5–5 mg/kg, furosemide 1–5 mg /kg, hydrochlorothiazide 0.5-2 mg/kg, spironolactone 1-3-5 mg/kg.

5. Convulsive syndrome . Elevated position of the upper half of the body for optimal cerebrospinal fluid dynamics. Diazepam is administered intravenously or rectally at a dose of 0.2–0.3 and 0.5–0.7 mg/kg, respectively.

6. Combating protein catabolism. The main task is to maintain calorie content at the minimum age requirement. Due to the impossibility of complete enteral nutrition due to the presence of edema and dyspeptic symptoms, the prescription of partial parenteral nutrition is indicated. They use concentrated solutions (since fluid limitation is necessary) of glucose with insulin in combination with amino acids and fats.

7. Fight anemia. Transfusion of washed red blood cells when the hematocrit decreases below 0.25 and the hemoglobin level below 70/l. To raise the hemoglobin level by 10 g/l, it is necessary to transfuse washed red blood cells at a dose of 1.5 ml/kg.

Prevention infectious complications indicated in the presence of foci of bacterial infection. Doses of antibacterial and antifungal agents are 30–50% of age.

Treatment of acute renal failure in the stage of polyuria

Change the water regime and electrolyte load. Expand the diet, increasing caloric intake. Liquid and salt are not limiting. Additionally, potassium supplements are prescribed, fat soluble vitamins, membrane protectors.

Prevention of acute renal failure

Required:

1. timely correction of the decrease in blood volume;

2. adequate measures aimed at combating shock, hypoxic-ischemic damage to organs and systems;

3. exclusion of nephrotoxic drugs;

4. monitoring surgical patients in the postoperative period in terms of preventing the development of DIC syndrome and infectious complications;

5. performing an ultrasound of the kidneys in children from the first months of life to exclude congenital anomalies development of the urinary system organs.

Medical examination of patients who have suffered acute renal failure

Home regimen for 3–6 months.

Good nutrition, walks.

Avoid contact with infectious patients.

Limit:

1. visiting preschool institutions;

2. carrying out preventive vaccinations;

3. prescription of gamma globulin for up to a year.

The child is examined after 1.3, then 6 months for 5 years, with monitoring of blood tests: erythrocytes, leukocytes, Hb, ESR, urea, creatinine, electrolytes; glomerular filtration, Zimnitsky test, general urine analysis. X-ray examination - 1.5–2 years after recovery. Ultrasound of the kidneys every 6–12 months to monitor the size and echogenicity of the renal parenchyma.

Acute renal failure in children (ARF) is a disorder of the homeostatic functions of the kidneys, manifested by increasing azotemia, metabolic acidosis, electrolyte imbalance and impaired ability to excrete water.

– acute clinical and laboratory syndrome with potentially reversible disorders of all renal functions, leading to severe disorders of homeostasis.

The main clinical sign of acute renal failure is a decrease in urine volume and an increase in plasma creatinine levels.

The incidence of acute renal failure among newborns ranges from 8 to 24%, mortality – from 51 to 90%.

Etiology.

It is generally accepted to distinguish three groups of causes of acute renal failure: prerenal– 85% associated with insufficient blood supply to the kidneys due to hypoperfusion, renal– 12% caused by damage to the renal parenchyma, postrenal– 3%, due to impaired urine outflow (urinary tract obstruction).

These factors ( ischemic, nephrotic, iatrogenic) contribute to kidney damage and the development of acute renal failure.

Ischemic factors leading to renal hypoperfusion include: asphyxia, hypothermia, dehydration, RDS (respiratory distress syndrome), respiratory failure, polycythemia, DIC (disseminated intravascular coagulation) syndrome, persistent fetal blood flow, heart failure, septic, cardiogenic, posthemorrhagic, posthypoxic shock, use of respiratory care in the treatment of RDS with high positive end-expiratory pressure.

Nephrotic factors associated with generalized neonatal and intrauterine infections, massive tissue damage and hemolysis.

Iatrogenic factors associated with inadequate volumes of administered fluid, electrolytes, and the use of nephrotoxic drugs.

Pathogenesis.

The pathogenesis of prerenal acute renal failure (acute renal failure in children) is determined by damage to kidney tissue, primarily due to hypoxia. Hypoxia causes a complex of neuroendocrine changes ( hypercatecholaminemia, hyperaldosteronism, increased secretion of renin, antidiuretic hormone, etc..), which ultimately lead to vasoconstriction and impaired renal perfusion. The process is aggravated by metabolic acidosis and DIC (disseminated intravascular coagulation) syndrome. As a result of these disorders, the patient develops oligoanuria with metabolic disorders.

Diagnostics.

The general diagnostic algorithm for acute renal failure (acute renal failure in children) is:

• exclusion of the postrenal nature of acute renal failure;
• carrying out differential diagnosis of prerenal and renal acute renal failure.

The main criteria for the differential diagnosis of renal and prerenal acute renal failure are fractional excretion of sodium (FENa) and renal failure index.

Prerenal acute renal failure (functional).

The most common factors for the development of acute renal failure in the neonatal period are:

• systemic hypovolemia ( congenital heart defects and great vessels, shock);
• acute hypoxia and hypercapnia;
• hypothermia.

Clinical picture.

Clinically, renal hypoperfusion in the first hours of life ( initial stage) manifests itself:

• pale skin;
• weakness of the peripheral pulse;
• symptom " white spot"(more than 3 s);
• arterial hypotension (less than 55–50 mm Hg, mean blood pressure less than 30 mm Hg);
• history of blood loss (fetal, placental, postnatal);
• decreased GFR (glomerular filtration rate), tubular reabsorption of water and sodium, hyperazotemia.

Doppler ultrasound shows signs of hypoperfusion along with decreased cardiac output and contractile function myocardium. The severity of the newborn’s condition at this stage is caused by pathological (critical) conditions complicated by kidney damage.

In the absence of adequate therapy, the initial stage of acute renal failure (acute renal failure in children) passes into the oligoanuric stage, which is caused by an increase in circulatory failure of the kidney and is characterized by a decrease in diuresis, excessive weight gain, adynamia, refusal to eat, decreased tissue turgor, edematous syndrome, hepatomegaly, bloating.

Renal Failure Index (RFI) is less than 3 (1), fractional excretion of sodium (FENa) is less than 3% (1–2.5). If pronounced prerenal oliguria persists for more than a day, and possibly earlier, ischemic changes in the glomeruli and tubules develop in the kidney, which in turn is manifested by a decrease in glomerular filtration rate (GFR), azotemia, hypoproteinemia, hyperkalemia, magnesemia, phosphatemia, hyponatremia, calcemia, chloremia, anemia, thrombocytopenia. This is the state of A.G. Antonov et al. (2000) proposed to consider it as ischemic nephropathy (IN) of newborns. Depending on the degree of renal dysfunction, there are three degrees of severity of ischemic nephropathy in newborns.

• INI (initial form of acute renal failure):
• lack of clear clinical manifestations;
• the presence of critical conditions accompanied by signs of cardiovascular disorders, weight loss and dehydration;
• short-term oliguria, proteinuria;
• plasma creatinine (89–130 µmol/l);
• plasma urea (8–16.7 mmol/l);
• moderate decrease in GFR and tubular reabsorption of sodium and water.

The doctor requires dynamic monitoring of renal functions and blood flow, and, if necessary, normalization of renal hemodynamics, adjustment of doses and frequency of administration of nephrotoxic drugs, and adequate energy supply.

With the continued action of factors unfavorable for the kidney, the degree of renal damage intensifies and progresses to the next.

• INII (non-oliguric form of acute renal failure):
• absence of a specific clinical picture, however, the appearance of sclerema and increased blood pressure may indicate INII;
• the presence of critical conditions with impaired hemodynamics and gastrointestinal function (gastrointestinal tract), hemorrhagic syndrome;
• diuresis is normal or increased or oliguria for no more than 24 hours;
• moderate proteinuria, possible appearance of altered red blood cells (more than 5 in the field of view) and hyaline casts;
• plasma creatinine more than 130 µmol/l and/or urea more than 16.7 mmol/l; expressed by a decrease in GFR (glomerular filtration rate);
• increased K+ excretion;
• decreased reabsorption of H2O and, to a lesser extent, Na+.

Due to the fact that diuresis in this form of acute renal failure does not have significant disturbances, INII often remains unrecognized.

This stage on the part of the doctor requires dynamic monitoring of renal functions and blood flow, normalization of BCC (circulating blood volume) and contractile function of the myocardium, dose adjustment and frequency of administration of nephrotoxic drugs if there is a vital need for their administration, the use of drugs that improve intrarenal hemodynamics, ensuring adequate nutrition and energy supply, timely recognition of DIC (disseminated intravascular coagulation) syndrome and its correction.

• INIII (oligoanuric form of acute renal failure):
• edema syndrome, accumulation of fluid in cavities;
• critical conditions accompanied by hemorrhagic syndrome, purulent-septic diseases;
• an increase in proteinuria, the appearance of altered red blood cells and granular casts;
• oliguria for more than 24 hours;
• plasma creatinine level more than 130 µmol/l and/or
• urea more than 16.7 mmol/l;
• a sharp decrease in GFR;
• metabolic acidosis.

The doctor’s tactics are aimed at limiting the volume of administered fluid (previous diuresis + NP at the rate of 25–35 ml/kg per day), improving renal blood flow, limiting the dose and frequency of nephrotoxic drugs if their use is vital. The duration of the oligoanuric stage is on average 52 hours.

With the transition to the polyuric stage of acute renal failure, the water excretory function of the kidneys increases. Diuresis is 2–3 times higher than age norm, contributing to low urine osmolarity and significant losses of sodium and potassium ions in the urine. In this case, the relative release of sodium ions is less than water, which leads to the transition of hyponatremia to hypernatremia, and hyperkalemia to hypokalemia. Azotemia levels may remain high for some time.

During the recovery stage, diuresis is restored, but a moderate decrease in GFR and tubular reabsorption remains. At this stage, maintenance of euvolemia, correction of possible electrolyte disturbances, and dynamic control are required.

If acute renal failure persists after the end of the 1st week of life, speech, as a rule, it's already underway about renal and postrenal renal failure - organic acute renal failure.

It must be remembered that timely unrecognized and uncorrected prerenal acute renal failure (more than 24 hours) turns into renal acute renal failure.

The real causes of acute renal failure are: congenital (cystic dysplasia, hypoplasia, agenesis or polycystic kidney disease), inflammatory and vascular abnormalities, toxic damage to the tubules by endotoxins (uric acid, hemoglobin, myoglobin) and exotoxins, congenital nephrotic syndrome, acute tubular necrosis (arteries, veins), consumptive coagulopathy, renal poison (amphoterecin B), aminoglycosides, acute course of acquired renal diseases (interstitial nephritis or pyelonephritis).

The causes of postrenal acute renal failure (acute renal failure in children) are urinary tract obstruction (bilateral ureteropelvic, bilateral urethrovesical obstruction, atresia, urethral stenosis or diverticulum, urethrocele large sizes, compression of the urinary tract from the outside by a tumor), which leads to disruption of the outflow of urine. In the early childhood Postrenal causes account for about 1% of all cases of acute renal failure.

Clinically acute renal failure, caused by renal or postrenal causes, first begins to appear at the end of the 1st and during the 2nd week of life.

Treatment.

A newborn child with clinical manifestations of acute renal failure must be placed in an incubator to create a comfortable temperature regime. Every 2–3 hours he should change his body position to avoid the development rhabdomyosis. Preventive measure aimed at preventing the development rhabdomyosis, is to perform a gentle, gentle massage of the body of a newborn baby 3-4 times a day.

The patient is monitored for HR (heart rate), RR (respiratory rate), BP (blood pressure), CVP (central venous pressure) - (normal - 5 cm water column), SaO2, body temperature.

Urine collection is carried out taking into account hourly diuresis (the bladder is catheterized). The newborn baby must be weighed every 8–12 hours. A detailed analysis of blood and urine is carried out at least once a week, ABS (acid-base status) (SB, BB, BE) - at least 4 times a day. It is necessary to monitor the coagulogram (the main indicators characterizing hemostasis).

To determine kidney function, a biochemical analysis is performed blood with determination of the level of creatinine, urea, total protein, cholesterol, sodium, potassium, chlorine, magnesium, calcium in the blood serum and the concentration of creatinine, urea, potassium, sodium, phosphorus, chlorine, calcium in daily urine. Based on the results obtained, indicators characterizing glomerular filtration and tubular reabsorption are calculated. If pathological changes are detected in biochemical blood and urine tests, the studies are repeated once every 3–4 days, and the urea concentration is determined daily.

Ultrasound examination of the kidneys is performed daily. Doppler examination of cardiac, renal and cerebral hemodynamics is indicated in critical conditions in the first hours of life, then to check the adequacy of the treatment or in case of negative dynamics of renal functions.

Before starting drug therapy, it is necessary to determine the causes and stage of acute renal failure.

Treatment during the period of oligoanuria includes the following activities.

• Correction of volemic disorders with a 5% glucose solution or 0.9% saline solution at a rate of 10–20 ml/kg for 0.5–1 hour or infusion of a 5% albumin solution at a rate of 10 ml/kg at a rate of 5–10 ml/hour , 6% infucol solution – 10–15 ml/kg. In the case of hemorrhagic disorders, an infusion of fresh frozen plasma is indicated at the rate of 10–15 ml/kg per 1–2 hours. In this case, it is necessary to constantly monitor central venous pressure and blood pressure. If there is no effect, it is necessary to repeat the administration of a 5% glucose solution or 0.9% saline solution or albumin in the same volumes. Calculation of the volume of further infusion therapy does not include the volume of transfused fluid and is 40–60 ml/kg · day in full-term newborns and 50–80 ml/kg · day in premature newborns. During the infusion, body weight is monitored every 6–8 hours.
• To improve renal blood flow, a 0.5% dopamine solution or a 4% dopmine solution is prescribed at a dose of 0.5–5.0 mcg/kg min.
• When myocardial contractile function decreases, cardiotonic drugs are used - dopamine, dobutamine, dobutrex at a dose of 6-8 mcg/kg min or more (contraindicated in IVH (intraventricular hemorrhage)). In case of vascular insufficiency, they resort to the prescription of glucocorticoids and adrenaline (0.02–1.0 mcg/kg · min) or mesaton (0.2–2.0 mcg/kg · min).

The use of diuretics until the volume of blood volume (BP, CVP) is normalized is contraindicated, and then Lasix is ​​prescribed at a rate of 1–4 (5) mg/kg intravenously (prolonged).

Sodium and potassium should not be prescribed unless it is necessary to replenish a deficiency resulting from current losses. Potassium replacement should be done with great care to avoid hyperkalemia.

• Hyperkalemia (7.0–7.5 mmol/l) can be eliminated by the following therapeutic measures under ECG monitoring:
• administering a 10% solution of calcium gluconate intravenously slowly at the rate of 0.5–1.0 ml/kg over 5–10 minutes in a 5-fold dilution per saline solution or drip;
• administration of sodium bicarbonate at a rate of 2 mEq/kg intravenously (induced alkalosis promotes the transport of potassium into the cell);
• infusion of a 10% glucose solution at a dose of 0.5–1.0 g/kg with insulin in a ratio of 0.25 units. insulin per 1 g of glucose (improves potassium transport into the cell);
• prescription of sorbents (enterosorption - sonium A, sodium elutite - 1–1.5 g/kg daily orally or rectally, smecta - 1/3 sachet 3 times a day orally);
• using ion exchange resins (resonium, keysolate) – 1 g/kg daily orally;
• gastric lavage 2-3 times a day;
• cleansing enemas up to 4 times a day.

To remove potassium you can use:

• furosemide – 1–4 mg/kg;
• sodium polystyrene sulfonate – 1 g/kg orally.
• Severe acidosis is corrected with sodium bicarbonate to maintain the pH at least 7.3; SB not lower than 20 mmol/l; at VE 10–12 mmol/l sodium bicarbonate may not be administered. The volume of sodium bicarbonate is calculated using the formula

V = VE of the patient · 0.5 · Body weight.

It is most favorable to administer a bolus of 2% sodium bicarbonate solution.

Due to concomitant hyperphosphatemia (more than 2 mmol/l) and hypocalcemia (less than 2 mmol/l in full-term and less than 1.75 mmol/l in preterm), the use of phosphate-binding drugs such as aluminum is indicated to normalize serum phosphate levels hydroxide at a dose of 50–150 mg/kg daily orally or sodium bicarbonate at a dose of 1–2 ml/kg 3 times a day intravenously (in the absence of hypercalcemia). In case of hypocalcemia, correction should be carried out slowly with a 10% solution of calcium gluconate at a dose of 0.5–1.0 ml/kg intravenously in a 5-fold dilution until the clinical manifestations of hypocalcemia disappear.

Protein intake in acute renal failure is limited to 1.5–2.0 g/kg daily. At the same time, it is necessary to ensure that physiological need energy was satisfied from fats (1/3) and carbohydrates. To feed newborns with acute renal failure, mixtures of “SMA” and “PM 60/40” are often used.

In cases of uncorrectable hyperkalemia, persistent metabolic acidosis, and the appearance of increasing heart failure against the background of hypervolemia, it is necessary to include extrarenal cleansing - peritoneal dialysis, hemodialysis - in the treatment complex.

Indications for peritoneal dialysis or hemodialysis:

• anuria for more than 24 hours or oliguria for more than 48 hours, as well as excessive fluid retention (uncontrolled increase
• body weight more than 10%);
• anuria/oliguria and uncontrolled hyperkalemia (7 mmol/l or more) and/or hypocalcemia; hyponatremia (less than 120 mmol/l);
• anuria/oliguria and uncontrolled acidosis (BE less than 15, SB less than 20 mmol/l);
• anuria/oliguria and creatinine over 250–350 µmol/l; anuria/oliguria and urea over 20 mmol/l;
• anuria/oliguria and uncontrollable vomiting, convulsions.

Contraindications to peritoneal dialysis:

• peritonitis;
• respiratory failure (this is a relative contraindication);
• laparotomy performed earlier than two days, the presence of drainages in abdominal cavity, ileostomy, diaphragmatic and inguinal hernias.

The prognosis for acute renal failure in newborns is extremely unfavorable; mortality without timely dialysis is 80%.

The primary “target” of the disease is representatives of the adult population; in rare cases, the syndrome is detected in children. Kidney failure It is more often an acquired pathology, although there are also hereditary risk factors.

It is important for parents to have information about the signs indicating the development of the syndrome in their child.

The primary symptom is a reduction in urine volume or a complete absence of diuresis.

The body cannot function in conditions of constant accumulation of metabolic waste and toxins. It is also unable to maintain acid-base and water-salt balance. Pathology requires prompt medical attention, otherwise there is a risk of death.

Kidney failure - common “childhood” signs

The following pathological manifestations should be a cause for concern and see a doctor:

• a decrease in the volume of diuresis (urine that is excreted from the body);
• severe swelling on the face and in the extremities;
• general and functional disorders similar to the state of poisoning: lethargy, fatigue, headache, diarrhea, vomiting;
• heat;
• the appearance of a jaundiced skin tint.

When visiting a doctor and conducting diagnostics, changes in test parameters are detected:

• proteinuria (the presence of proteins in the urine);
• signs of urolithiasis on various stages(sand or kidney stones).

The development of nephrotic syndrome, characterized by edema, a significant amount of protein in the urine and a decrease in protein in the blood, accompanies renal failure in children, but practically does not occur in adults.

Acute renal failure in children

It is accompanied by intoxication of the body with metabolic wastes that cannot be excreted in the urine due to renal dysfunction.

The symptoms of this form develop quickly. Over the course of several days, symptoms resembling poisoning appear - the child becomes lethargic, nausea occurs, and sometimes vomiting.
Such manifestations are associated with intoxication with nitrogenous metabolites (uremia) and water and electrolyte balance disorders.

Self-medication at this stage is unacceptable!

Afterwards, previously insufficient diuresis increases again, and the child’s body weight may decrease. This is often followed by a stage, sometimes called “clinical recovery,” when signs of intoxication begin to gradually disappear.

However, this may be followed by a relapse - the return of pathological symptoms.

Signs of acute renal failure require immediate medical attention and hospitalization!

Chronic renal failure in children

It can develop as a result of the acute form, or be a consequence of chronic infections of the urinary organs. In some cases, the cause is a burdened hereditary factor.
Pathological changes occur over a long period of time and threaten complete loss of kidney function.

IN clinical medicine There are four diseases:

1. latent (not accompanied by pronounced symptoms);
2. azotemic - a stage characterized by clinical manifestations both general (intoxication) and relating to individual body systems (digestive, nervous, cardiovascular);
3. decompensation – added local inflammation and swelling;
4. terminal - the only options for the patient in this case will be a kidney transplant or hemodialysis.

If your child has minor abnormalities in kidney function or urination, you should immediately contact your pediatrician for advice. If necessary, the doctor will give a referral for examination by a specialist.

Renal failure - therapeutic measures

The main goals in the treatment of acute renal failure are measures to cleanse the body of toxic substances accumulated in it and restore normal blood flow in the tissues of the organ. For this purpose, drugs of various groups are used: diuretics, antishock drugs, as well as vasodilators and medications that reduce blood viscosity.

Babies under 1 year hemodialysis procedures are carried out. Using an “artificial kidney” blood filtering device will help eliminate complications such as swelling of the brain and lung tissue, high blood pressure, and the presence of sugar in the blood.

For older children (from 10 years old) it is possible to use plasmaphoresis sessions (procedures for purifying blood that occurs outside the patient’s body).

To eliminate existing infections and reduce the risk of secondary infections, antibacterial drugs are included in the treatment of renal failure. Administration of potassium, glucose, and electrolyte mixtures may serve as supportive measures.

Chronic renal failure requires complex treatment of both the damaged kidney and the underlying concomitant pathology.

If the second or later stages occur and intoxication is observed, then hemodialysis sessions will be prescribed. Medications include:

• antacids as symptomatic therapy;
• vitamin and mineral supplements (vitamin D, calcium, B vitamins);
• iron supplements – in case of anemia development;
• drugs that lower phosphorus levels;
• antihypertensive drugs (if chronic renal failure is accompanied by hypertension);
• diuretics - to normalize urine output.

In later stages and severe course disease, the only solution may be a donor kidney transplant.

Traditional medicine recipes for kidney health

Here are some popular methods for preparing natural medicines:

• restorative drink. You will need to mix equal parts of raspberry branches, crushed rose hips and finely chopped black currant leaves. Now pour 1 tablespoon of this mixture with boiling water (about 500 ml). Your child should take this medicine daily. in small portions;
• fresh pomegranate juice. This drink helps stabilize the water-salt balance. It is preferable for a child to take juice diluted with water. Regular use juice for two months will also become a general strengthening measure;
• decoction of pomegranate skin and rose hips. Both ingredients should be crushed and mixed in equal parts. Then add boiling water and cook for 5 minutes. Let the broth cool and strain. You can speed up the cooking process by replacing boiling with infusion in a closed thermos. You need to drink the resulting natural medicine in small portions throughout the day.

Kidney failure is a serious problem that can lead to death or the need for a transplant. However, much more dangerous is the tendency to ignore the child’s symptoms. It should be remembered that a timely visit to a doctor can ensure diagnosis, treatment and a minimum of consequences for the baby’s body. It is also important to follow the pediatrician’s recommendations in the treatment of acute childhood genitourinary infections, which often cause kidney failure.

Zhemoytyak V. A. – Associate Professor, Candidate of Sciences honey. sciences

If acute renal failure is considered to be a reversible process in principle, then chronic renal failure (CRF) is a clinical and laboratory syndrome in which, due to sclerosis of the renal tissue, an irreversible disruption of all homeostatic functions of the kidneys develops.

According to the WHO definition, chronic renal failure is considered a situation when, for more than 3 months:

1. endogenous creatinine clearance below 20 ml/min;

2. serum creatinine concentration above 0.176 mmol/l;

3. Urea level is above 8.55 mmol/l.

Chronic renal failure is characterized by a steadily progressive course.

Etiology

Congenital and hereditary diseases kidneys, tubulopathy, renal dysplasia, glomerulonephritis, pyelonephritis, systemic connective tissue diseases (SLE, periarteritis nodosa, scleroderma), PMR, obstructive uropathy, HUS.

Causes of terminal chronic renal failure in the Republic of Belarus (A. V. Sukalo, 2009):

1. Congenital and hereditary anomalies of the kidneys and urinary tract – 60.8%

2. Chronic glomerulonephritis – 18,5%

3. Nephrosclerosis as an outcome of acute renal failure (HUS, ACI) – 8.9%

4. Unspecified – 7.6%

5. Systemic lupus erythematosus – 2.5%

6. Kidney tuberculosis – 2.5%

7. Chronic pyelonephritis – 1.3%

Pathological anatomy

The development of chronic renal failure is based on sclerosis of the glomeruli, tubular atrophy and interstitial sclerosis. All this leads to a gradual decrease in the size of the kidneys. In the terminal phase of chronic renal failure, all morphological changes are of the same type and are manifested by the replacement of nephrons with connective tissue with the loss of morphological features characteristic of the disease that led to chronic renal failure.

The cause of sclerosis, fibrosis and wrinkling of the kidneys are inflammatory (immune and non-immune) and dystrophic changes glomeruli, tubules, stroma.

Histological examination reveals:

1. cystic dilated tubules, in the lumen of which there is colloid (thyroidization);

2. interstitial sclerosis;

3. when nephrobiopsy specimens are stained with MSB (Marcius scarlet blue), the connective tissue is stained blue;

4. glomerular sclerosis;

5. periglomerular sclerosis;

6. hyalinized glomeruli;

7. atrophy of the nephroepithelium;

8. round cell infiltration in the interstitium;

9. interstitial sclerosis.

Pathogenesis

Based on the fact that the kidneys regulate:

1. arterial pressure

2. metabolism of calcium and phosphorus

3. erythropoiesis

4. excretion of sodium and potassium

5.removal of toxins and water

6. Blood pH – with chronic renal failure, these processes are disrupted, and this is manifested by the syndromes and symptoms given in Table 74.

Table 74 - Syndromes characteristic of chronic renal failure

Table 75 – Stages of chronic renal failure

1. I compensated(impaired function – IF) - The reserve capacity of the kidneys is reduced (detected during stress tests) without violating homeostatic constants. The general condition is not disturbed. There are no clinical symptoms of chronic renal failure, with the exception of moderate hypertension

2. II subcompensated(chronic renal insuficiency - CR I) - Labile hyperazotemia is detected in combination with disorders of partial renal functions (50–75% decrease). Hyperkalemia, acidosis, anemia, acute renal failure (with dehydration) may occur.

3. III decompensated(chronic renal failure -CRF) - All signs of chronic renal failure are clearly manifested - anemia, hypertension, osteodystrophy. The volume of renal functions is less than 25% of normal. There is a violation of CBS and water-electrolyte metabolism

4. IV terminal(uremia) (end stage renal disease - ESRD) - Residual kidney function less than 5%. Oliguria and multiple organ disorders are observed: weakness, anorexia, nausea, heart failure, gastrointestinal bleeding, hypertension, coma. Azotemia, electrolyte disturbances, acidosis, and anemia worsen

Table 76 – Stages of chronic renal failure

Glomerular filtration rate (GFR)

GFR is the most reliable indicator of kidney function.

Depends on:

1. age

3. body surface area (measured GFR is usually referred to the standard body surface - 1.73 m2)

GFR reflects the degree of preservation/loss of the mass of functioning renal parenchyma, or the mass of active nephrons.

A decrease in GFR of less than 60 ml/min/1.73 m2 indicates a loss of more than 50% of nephrons.

Glomerular filtration

Ref = P – (Po+Ps)

Ref – effective filtration pressure

P – hydrostatic pressure in the capillaries of the glomeruli = 45–65 mm Hg.

Po – plasma oncotic pressure 24 mm Hg.

Рс – hydrostatic pressure of the glomerular capsule – 15 mm Hg.

Ref = 6–26 mm Hg.

If blood pressure is low, there is no filtration

Clearance is the volume of plasma cleared in 1 minute.

Normal clearance values:

1. in newborns – 10–25; at 1 year – 65;

2. after a year and in adults – 100±20 ml/min

Calculation of glomerular renal filtration (endogenous creatinine clearance) using the Barrat formula:

1. in young children:

CF=(0.55 body length in cm)/plasma creatinine in mg%

2. in older children:

CF=(0.45 body length in cm)/plasma creatinine in mg%

Note: coefficients 0.45 and 0.55 are selected empirically.

Schwartz formula for the simplest determination of GFR (N. S. Ignatova, N. A. Korovina, 2007)

GFR ml/min/1.73 m 2 =(38 body length (cm))/blood creatinine (µmol/l)

Calculation of glomerular renal filtration (endogenous creatinine clearance) using the Schwartz formula depending on age:

1. in children 1–2 years old:

CF=(40 body length in cm)/plasma creatinine in µmol/l

2. for children from 2 to 12 years old and for girls over 12 years old:

CF=(49 body length in cm)/plasma creatinine in µmol/l

3. for boys over 12 years old:

CF=(62 height in cm)/plasma creatinine in µmol/l

Note: coefficients 40, 49 and 62 are selected empirically.

Tubular reabsorption of water in% = [(C-V)/C] 100

C – ground clearance

V – minute diuresis

Normal tubular reabsorption of water is 97–99%

Table 77 - Characteristics of chronic renal failure (V.I. Naumova, 1991)

Table 78 - Chronic renal failure syndromes, causes of their development and clinical manifestations (M. S. Ignatova, P. Grossman, 1986)

Table 79 – Main pathogenetic factors in the development of chronic renal failure (K. Scharer, H. Utmer, 1987)

CRF clinically manifests itself when the number of active nephrons decreases by 70–80%.

CRF I

1. Manifested by signs of the underlying disease.

2. Renal dysfunction is minor.

3. Fatigue, malaise, loss of appetite.

CRF II

1. Reduction of glomerular filtration by 50%.

2. Increase in creatinine to 0.15–0.35 mmol/l.

3. Polyuria, polydipsia, nocturia, hyposthenuria.

CRF III

1. Reduced glomerular filtration by 75%.

2. Creatinine increased to 0.35–0.5 mmol/l.

3. Hyposthenuria, hypokalemia, hypocalcemia, metabolic acidosis.

Complete and detailed clinical picture of chronic renal failure

CRF III-IV (by organs and systems)

1. CNS – encephalopathy:

Tearfulness;

Irritability;

Sleep disorders;

Headache;

Emotional lability;

Eclampsia;

Polyneuropathy.

2. Leather– Pale skin, subictericity, hypertrichosis, itchy skin.

3. Gastrointestinal tract:

Decreased appetite;

Nausea;

Aversion to food;

Stomatitis;

Gastritis;

Pancreatitis;

4. Cardiovascular system:

Bradycardia;

Muted tones;

Systolic murmur;

Hypertension;

Hypertrophy and dilatation of the left heart;

Left ventricular heart failure;

Pericarditis.

5. Respiratory organs:

Hard breathing;

Strengthening the pulmonary pattern;

Rounded shadows at the root of the lungs;

Cloud-like infiltrates along the periphery;

Uremic catarrh of the upper respiratory tract;

Exudative pleurisy.

6. Hematological signs:

Hemorrhagic syndrome;

Hemorrhages in the pleura, pericardium, brain.

7. Bones phosphorus-calcium metabolism:

Osteopathy;

Osteoporosis;

With alkalosis - tetany.

Treatment

Maintenance therapy:

1. food

2. albumin replacement

4. Anticoagulants

ACE inhibitors (non Fin-major or minor)

Bilater/unilateral. nephrectomy

Kidney transplant (weight › 9kg)

Predialysis therapy for chronic renal failure includes:

1. treatment of the underlying disease;

2. correction metabolic disorders;

3. elimination of secondary changes and complications;

4. general strengthening effects.

Mode. Gentle plus exercise therapy, in terminal stage and in case of exacerbations of the underlying disease - bed rest.

Diet.

1. B Stage I Protein may not be limited.

2. In II – reduce by 50%.

3. III – Giovanetti diet (protein – 0.6 g/kg, sodium – 200 mg/day).

4. Sodium intake is controlled by blood levels and blood pressure.

5. Monitoring potassium concentration.

To improve hemodynamics and reduce azotemia, the following drugs are used:

1. aminophylline

2. chimes

3. trental

4. saluretics

5. Lespenefril

6.chophytol

To correct anemia the following are used:

1. iron supplements

3. erythropoietin

4. red blood cell mass

For heart failure, glycosides are used, but the doses should be reduced by 1.5–2 times.

Treatment of infectious complications requires a reduction in doses of antibacterial drugs by 1.5–2 times.

In the absence of effect from conservative therapy, dialysis and kidney transplantation are indicated.

Before transplantation of a compatible kidney, the indications for hemodialysis are decided on a case-by-case basis.

Indications for hemodialysis.

1. glomerular filtration rate below 10 ml/(min 1.73 m2);

2. blood creatinine above 0.7 mmol/l;

3. hyperkalemia above 6.5 mmol/l;

4. “uncontrolled” hypertension;

5. uremic pericarditis.

Contraindications to hemodialysis:

1. multiple developmental defects;

2. mental illness;

3. malignant tumors;

4. low body weight;

5. parents' refusal of dialysis therapy.

Kidney failure- chronic or acute kidney disease, which leads to disturbances in urination, hormone synthesis (erythropoietin, calcitriol) and water-salt balance.

At an early age, the pathology is rare and is characterized by general malaise, chills and nausea. The volume of urine is different from normal. During diagnosis, a pale yellow color of the skin is noted.

If treatment is not timely, persistent intoxication develops, leading to convulsions. In rare cases, the child begins to lose weight quickly and anemia occurs. Bones become brittle. Ultimately, the affected kidney fails and becomes necrotic, leading to death.

Classification

The first type of damage is caused by shock, toxic effect substances, drugs or poisons, diseases of infectious etiology, urolithiasis, pyelonephritis. OPN starts brightly severe symptoms, characteristic of her. All disorders in the kidney completely disappear after 1-2 months with timely treatment.

The causes of chronic renal failure are urolithiasis, endocrine and cardiovascular systems, persistent infectious diseases and diabetes. CRF begins with nonspecific symptoms (weakness, fatigue, drowsiness). Treatment improves the patient's condition, but kidney function is not completely restored.

Stages of the disease

1. Initial - manifested by pain in the abdomen, pallor of the skin and nausea. Duration from the onset of the disease is up to two days.
2. Oligoanuric - manifested by complete urinary retention, renal colic, anemia, nausea, vomiting, anorexia, increased gas formation in the intestines, diarrhea, weakness, increased fatigue, lethargy. From the respiratory system, shortness of breath and accumulation of fluid in the bronchi are noted. Duration from 2 to 11 days.
3. Diuretic - manifested by normalization of urine to 2-4 liters per day, the patient’s condition normalizes. Duration 9-11 days.
4. Full recovery stage - kidney function returns to normal after 6 months.

1. Latent - a meager number of nonspecific symptoms appears.
2. Compensated - manifested by nausea, vomiting, abdominal pain, dry mouth, fatigue.
3. Intermittent - the patient’s condition worsens, persistent disturbances in water-electrolyte and acid-base balances. Without treatment, a transition to the last stage is noted.
4. Terminal - the kidneys completely fail and cannot perform their function. Without dialysis, death is possible.

Causes

1. Traumatic shock - occurs with severe injuries and is characterized by centralization of blood circulation, which impoverishes the blood supply to the kidneys.
2. Diseases infectious nature(glomerulonephritis, pyelonephritis) - the pathogen damages kidney tissue, releases toxins, which leads to impaired renal function.
3. Urolithiasis - a stone obstructs the flow of urine.
4. Intoxication - the effect of medicinal (example: incorrect dose of antibiotic), toxic substances on the kidney leads to its damage.
5. Tissue damage - the slightest damage to the kidney wall leads to serious diseases.

• kidney cysts are round formations filled with fluid;
• tumor - formation in organ tissues;
• vascular thrombosis - closure of the renal vessels, which interferes with the blood supply to the kidney;
• nephropathy - diseases of the glomeruli and renal parenchyma;
• necrosis of kidney tissue - necrosis of kidney tissue due to dystrophy;
• diabetes mellitus - increased levels of sugar (glucose) in the blood impair renal function;
• systemic lupus erythematosus - a connective tissue disease;
• congenital kidney diseases - deviations from the normal form, congenital cysts, renal vascular disorders, hydronephrosis, Fanconi disease;
• absence of one kidney - only one kidney takes on the entire load, which leads to its overload.

Symptoms

Skin

Pale in color.

Pale yellow in color, dry skin, constant unbearable itching, swelling of the subcutaneous fat.

Respiratory

Shortness of breath, accumulation of fluid in the bronchi.

Shortness of breath, accumulation of fluid in the pleural cavity.

Cardiovascular

Pain in the heart, increased blood and venous pressure.

Severe arterial hypertension, hypertrophy of the heart muscle, tachycardia, cardiac asthma develops due to stagnation of blood in the pulmonary circulation.

Digestive

Nausea, vomiting, anorexia, abdominal pain, increased gas formation in the intestines, diarrhea, which turns into constipation.

Loss of appetite, nausea, vomiting, dry mouth, abdominal pain, increased gas formation in the intestines.

Osteoarticular

Delayed bone growth, brittle bones.

Delayed bone growth, brittle bones, development of joint syndrome (pain, limited mobility, deformation in the joint).

Neuropsychic

Foggy consciousness, fatigue, drowsiness, lethargy, headaches, fainting.

Hiccups, convulsions, headaches, fainting, mental retardation.

Acute urinary retention, pain in the lumbar region.

Polyuria (copious amounts of urine excreted), discomfort in the lumbar region.

Hematopoietic

Anemia, decreased blood clotting.

Diagnostics

Objective examination - the child is pale or pale yellow, drowsy, lethargic, there is growth retardation and thinness.

Palpation (palpation) - the kidney is palpable, which indicates its enlargement; pain may occur.

Percussion (tapping) - the boundaries of the kidney are enlarged, Pasternatsky's symptom is positive.

Laboratory diagnostics include a complete blood count (CBC), its biochemistry and a general urinalysis (UCA):

1. LAC - low red blood cell count; if there is inflammation, then ESR (erythrocyte sedimentation rate) and leukocytes are increased.
2. Biochemical blood test - increased urea (up to 32-50 mmol/liter), creatinine (up to 0.5-0.9 mmol/liter), sodium (Na+), potassium (K+), phosphate (PO43-), magnesium (Mg2+ ), calcium content (Ca2+) is reduced.
3. OAM - with acute renal failure, dark urine, low daily diuresis, decreased relative density; with chronic renal failure, the color is light, the volume of urine excreted per day is large, the relative density is reduced.

1. Ultrasound - determines functional state and the size of the kidneys, which are enlarged, the presence of cysts or tumors, the presence of necrotic processes.
2. X-ray of the lungs will help determine the presence of fluid in the bronchi or pleural cavity.
3. CT scan - shows the size of the kidneys, their location and possible abnormalities.

Treatment

With acute renal failure conservative therapy completely restores kidney function. Treatment of chronic renal failure consists of supportive care and regular kidney dialysis.

The child must adhere to a diet that is indicated for both types of pathology. You should avoid fatty, sweet and salty foods. Limit consumption of foods rich in protein. Drink 1 to 2.5 liters of clean still water daily. Teas with rose hips and lingonberries are welcome. The diet must include vegetable fats - oils from corn, olives, flax. Rice porridge is recommended for the patient.

For infants up to one year old, for sufficient calorie intake, the pediatrician introduces mixtures with increased content carbohydrates, fats and a small amount of protein.

If progression of renal failure is observed after treatment, a kidney transplant is performed urgently.

Prevention

Hereditary factors play a role in the occurrence of kidney failure, so during the first days of a baby’s life, doctors check and rule out hereditary pathologies. Timely treatment of other diseases of the urinary and endocrine systems(glomerulonephritis, pyelonephritis, urolithiasis) reduces the likelihood of renal failure. child with high risk the occurrence of the disease must be periodically shown to the attending physician.

Timely identified pathology in the initial stages is treated without significant consequences for the body.

Forecast

It is extremely rare, in 23 cases out of 100, that renal function is not restored, filtration capacity is impaired, and the kidney cannot maintain normal urine concentration. Acute renal failure becomes chronic.

Untreated AKI is fatal due to uremic coma and sepsis. Chronic renal failure remains with the baby forever, it must be monitored and treated in the early stages.