Treatment of acute renal failure in children. Acute renal failure in newborns

Acute renal failure in children is a clinical and laboratory syndrome caused by impaired filtration in the kidneys. The main symptom is the retention of water and metabolic products in the body with further intoxication and multiple organ failure.

Acute renal failure in children is a clinical and laboratory syndrome manifested by impaired renal function. It is based on damage to the renal tubular system with subsequent tissue swelling and deterioration of the organ.

Kidney failure in children has two types: functional disorder and organic structural damage.

Reasons

The main causes are the same for both types of disease:

damage to the renal vessels;
the result of previous infections (sore throat, pneumonia);
inflammatory kidney diseases;
rheumatological diseases;
genetic predisposition;
congenital anomalies of organ development;
oncological processes;
poisoning with medications or other chemical compounds;
urinary system injuries;
severe dehydration of the body.

In the functional form of the disease, the damage is reversible and is compensated by intensive therapeutic actions. Organic pathology is always more severe.

Clinic

Acute renal failure in children has three forms: perirenal, renal, postrenal.

Acute renal failure in a child goes through four successive stages: pereduric, anuric, polyuric, recovery. They are characterized by certain clinical and laboratory parameters.

In the beginning, the only symptom is a decrease in the child's urine output.

This may be a consequence of both an insufficient amount of water in the body (relative) and impaired filtration of water by the kidneys with sufficient intake (absolute oligoanuria).

At the first stage, edema syndrome develops. Hyaline and granular casts are found in the urine. The level of nitrogen and urea in the blood increases. This indicates a violation of filtration in the kidneys. The water-electrolyte and acid-base balance is disturbed. Water retention syndrome occurs in the body, followed by total tissue swelling.

Acid metabolic products accumulate in the blood - metabolic acidosis. The oligoanuric stage lasts mainly from 2 to 15 days. The child becomes weak and inactive. His consciousness is depressed as a result of the beginning of cerebral edema. The skin is pale, swelling is visible on the face. Hemorrhages on the skin are possible. Subsequently, the swelling spreads from head to toe. On palpation, the swelling is warm to the touch. There is a strong smell of acetone coming from the child's mouth. There may be other symptoms: palpitations, increased heart rate, increased blood pressure, shortness of breath.

Sometimes, against the background of edema, a child may experience seizures.

The polyuric stage has the following symptoms of renal failure in children - diuresis gradually increases, urination becomes excessive. This condition is called polyuria. Due to excessive diuresis, dehydration occurs and hypokalemic syndrome develops. The main manifestations are flatulence, lethargy, a feeling of numbness in the limbs, and increased heart rate. During the examination, changes are noted on the ECG.

The specific gravity of urine is reduced and ranges from 1.005-1.001. Filtration and excretion of sodium, urea and creatinine are reduced. The accumulation of these compounds leads to intoxication of the body. At the same time, potassium excretion increases and hypokalemia worsens. At this stage, systemic dialysis is performed to correct disorders.

The next stage is recovery. Its duration ranges from 4 to 6 months. There is a gradual restoration of normal function of the kidneys, major organs and systems.

Diagnostics

The first sign of pathology is a decrease in the amount of urine. There is a clear order of examination here.

History taking and clinical examination.
Assessment of laboratory parameters of kidney function.
Level and nature of deviations in normal vital signs.
Carrying out differential diagnosis.

If there are signs of disease, it is necessary to carefully evaluate the basic urine parameters. The perirenal form of insufficiency has the following characteristics and is based on the following approaches:

anamnestic data (vomiting, diarrhea, trauma, blood loss, cardiovascular pathology);
clinic (dehydration, decreased blood pressure, presence of edema, decreased central venous pressure);
identification of hyaline and granular casts in the urine;
decrease in the amount of sodium, water;
the ratio of urine nitrogen and plasma creatinine is more than 20;
the ratio of urea urine/plasma is more than 10, creatinine urine/plasma is above 40;
renal failure index less than 1%.

The renal failure index is the main sign that allows you to determine the degree of damage. It is based on the assessment of 3 main criteria: the amount of urine sodium, the amount of urine creatinine and plasma creatinine.

In the renal form, the following criteria are met:

anamnestic data (previous kidney disease);
exceptions: obstruction of the urinary tract;
increased amount of sodium and water;
renal failure index above 1%;
the ratio of urine creatinine to plasma creatinine concentration is less than 20.

The main differential diagnosis of these two forms is based on comparison and assessment of the filtration function. In the renal form it is sharply reduced.

The postrenal form is established on the basis of anamnesis (defects of the genitourinary system, trauma), palpation examination (presence of formations and a full bladder).

Scintigraphy and sonography of the organ are performed, and if the serum creatinine level is less than 0.46 mmol/l, excretory urography is indicated.

Treatment

Main principles of treatment:

improvement of peripheral microcirculation;
restoration of fluid loss;
carrying out detoxification;
prevention of infectious complications;
elimination of acidosis.

When renal failure has already developed in children, the mainstay of treatment is intravenous administration of solutions. Apply 0.9% NaCl, 5% glucose solution, Ringer's solution. The volume of infusions is determined by the decrease in circulating blood volume.

Hyperkalemia is corrected intravenously by administering a 10% calcium gluconate solution and a 40% glucose solution.

Correction of changes in the acid-base state is carried out with a 4% sodium bicarbonate solution under the control of blood parameters. In infancy, the patient receives the same treatment, but the drugs are administered in a lower dose

Corticosteroid therapy is indicated for the infectious-allergic nature of the disease.

Prednisolone and dexamethasone are used in therapeutic doses and according to age classification.

Diuretics are used to improve kidney function and correct blood electrolytes. Depending on the parameters of plasma electrolytes, osmotic diuretics (mannitol), saluretics () are used. Antibacterial therapy is carried out if there are complications caused by infection. Drugs are selected taking into account the sensitivity of bacteria to them.

A necessary component of therapy is diet. Limit the protein content to 1 gram per kilogram of body weight while maintaining the calorie content of the diet. Diet therapy reduces blood nitrogen and corrects acidosis.

Urgent Care

Emergency care is determined by the cause of the deficiency.

The main drugs are:

0.9% NaC solution intravenously;
mannitol and furosemide intravenously;
dopamine and furosemide;
anti-shock measures to compensate for hypotension - epinephrine, norepinephrine;
10% calcium chloride and 5% glucose + 40-50 units of insulin to correct hyperkalemia.

If emergency care is provided, after stabilization of hemodynamics and vital signs, the patient is given further treatment. All actions are aimed at restoring homeostasis.

RENAL FAILURE . It is characterized by a violation of homeostatic constants (pH, osmolarity, etc.) due to significant impairment of renal function and is an outcome or complication of diseases conventionally divided into renal (glomerulonephritis, pyelonephritis, etc.), prerenal (hypovolemia, dehydration, etc.) and postrenal (obstructive uropathy, etc.).

Acute renal failure (ARF). It manifests itself as a sudden disruption of homeostasis (hyperazotemia, acidosis, electrolyte disorders) as a result of an acute violation of the basic functions of the kidneys (nitrogen excretion, regulation of the metabolic balance, water-electrolyte balance). In childhood, acute renal failure can develop in diseases accompanied by hypotension and hypovolemia (burns, shock, etc.) with a subsequent decrease in renal blood flow; DIC syndrome in septic shock, HUS and other pathologies; for GN and PN; with cortical necrosis of the kidneys (in newborns), as well as with difficulty in the outflow of urine from the kidneys. Morphological changes in the kidneys depend on the cause and period of acute renal failure in which the kidney biopsy was performed (initial, oligoanuria, polyuria and recovery). The changes in the tubules are most pronounced: their lumen is expanded, the epithelium is degenerated and atrophied, the basal membrane has areas of rupture. The interstitial tissue is edematous, with cellular infiltration; there may be minimal changes in the glomeruli due to tubular necrosis (effect of nephrotoxin), as well as characteristic signs of glomerulo- or pyelonephritis (PN), complicated by acute renal failure. Depending on the cause of acute renal failure, regeneration of the tubular epithelium and a gradual decrease in other morphological changes occur in the polyuric stage.

Clinical picture. There are 4 periods of surge arrest:

1. The initial period is characterized by symptoms of the underlying disease (poisoning, shock, etc.).

2. The oligoanuric period is manifested by a rapid (within several hours) decrease in diuresis to 100-300 ml/day with a low relative density of urine (no more than 1012), lasts 8-10 days, is accompanied by a gradual increase in weakness, anorexia, nausea, vomiting, itching skin. With unlimited administration of fluid and salt, hypervolemia and hypertension occur; Pulmonary edema and peripheral edema may develop. A rapid increase in hyperazotemia (up to 5-15 mmol/day urea and creatinine more than 2 mmol/l), severe acidosis (pH up to 7.2), hyperkalemia (up to 9 mmol/l), hyponatremia (below 115 mmol/l) cause uremic to whom. Hemorrhages, gastrointestinal bleeding appear, hemoglobin is below 30 units, leukocytes up to 2.0 10 9 / l. Urine is red due to gross hematuria, proteinuria is usually small - reaches 9% or more in patients with GN complicated by acute renal failure. Some patients have uremic pericarditis; Kussmaul breathing may persist during the first dialysis sessions. Cases of neo-liguric acute renal failure that developed as a result of mild necronephrosis have been described.

3. The polyuric period is observed with a favorable outcome of acute renal failure, lasts up to 2-3 weeks, is characterized by the restoration of diuresis (within 3-5 days) and its increase to 3-4 l/day, an increase in glomerular filtration (from 20 to 60-70 ml /min), elimination of hyperazotemia and signs of uremia; reduction of urinary syndrome, improvement of renal concentration function.

4. The recovery period can last up to 12 months, characterized by a gradual restoration of renal functions. When using peritoneal dialysis and hemodialysis in complex therapy of acute renal failure, lethal outcomes decreased to 20-30 %, the outcome in chronic renal failure, as well as the development of acute renal failure against the background of chronic renal failure, is rarely observed.

Differential diagnosis must be made with oligoanuria without a violation of homeostatic constants, which is observed with obstruction of the urinary organs, AGN, accompanied by oliguria and normal relative density of urine, the absence of hyperazotemia; with chronic renal failure, which, unlike acute renal failure, develops gradually, from the polyuric stage and ends with an oligoanuric irreversible period.

Treatment. It comes down to eliminating the cause of acute renal failure, correcting the resulting homeostatic disorders, and preventing various complications. If hypovolemia is present, an isotonic sodium chloride solution (0.7 %) and glucose (5 %), Ringer's solution in a volume that ensures the restoration of bcc under the control of hematocrit, sometimes administered up to 1.5 l/day liquids. In the oligoanuric stage, the broad mechanism of action of each of the therapeutic measures is explained by the close relationship between the signs of acute renal failure (for example, acidosis maintains hyperkalemia). Therefore, restriction of protein in the diet (up to 0.8-1.0 g/kg per day) and high caloric intake help reduce not only hyperazotemia, but also acidosis, reducing tissue hypercatabolism. Hyperkalemia (dangerous due to cardiac arrest) above 6 mmol/l is corrected by sharp restriction of potassium in food, intravenous administration of 10% calcium gluconate solution, 10-20 ml, 20-40% glucose solution, 100-200 ml ( drip). The amount of sodium bicarbonate administered is calculated based on the deficiency of standard blood bicarbonates (in a 3-4% solution, 100-150 ml). Blood transfusions are carried out according to indications. Corticosteroid drugs are used for acute renal failure that develops against the background of infectious and allergic diseases. In case of pulmonary edema, cardiovascular failure, eclampsia, generally accepted measures are taken. Depending on the osmolarity of the plasma, in the first 2-3 days from the onset of oligoanuria, osmotic diuretics (15-20% solution of mannitol or polyglucin, 200-400 ml for 40-120 minutes), as well as saluretics (Lasix up to 1 g per day) can be administered etc.) If antibacterial therapy is necessary, drugs with minimal nephrotoxicity are administered in a dose corresponding to half the age. In the polyuric stage of acute renal failure, a diet is prescribed in accordance with age, fluid is administered in accordance with diuresis, and sufficient amounts of potassium, sodium and calcium are prescribed to prevent dehydration and electrolyte disorders. If there is no effect from conservative drugs, peritoneal dialysis or hemodialysis is used, which is prescribed for the serious condition of patients, indomitable vomiting, signs of incipient pulmonary edema, etc.; with hyperkalemia over 7 mmol/l, severe acidosis and hyperazotemia. In acute renal failure, the use of renal decapsulation and perinephric novocaine blockade is not justified.

Chronic renal failure (CRF). It is diagnosed in children with diseases of the urinary organs if their glomerular filtration rate remains less than 20 ml/min for 3-6 months and the level of serum creatinine and urea increases. More than 50 diseases that manifest as kidney damage can result in chronic renal failure, which, unlike acute renal failure, is characterized by progression and irreversibility.

Etiology. The cause of development is acquired and hereditary diseases of the urinary organs, factors determining the development of acute renal failure and its outcome in chronic renal failure. With progressive kidney diseases, their size gradually decreases due to sclerosis. A mosaic pattern of morphological changes is characteristic: the presence of sclerotic glomeruli and tubules along with hypertrophied glomeruli and dilated tubules, with areas of fibrosis of interstitial tissue. The process of formation of chronic renal failure depends on its etiology and the age of the patients. In infants, chronic renal failure progresses against the background of structural and functional immaturity of the kidneys; in urolithiasis, as a result of kidney destruction, hydronephrosis and pyelonephritis. There are a number of general provisions regarding the relationship between the clinical manifestations of chronic renal failure and its biochemical and other manifestations: 1) with sclerosis of 75-80% of the nephrons, the rest lose the ability to further hypertrophy, which causes minimal reserve capabilities, clinically manifested by a decrease in tolerance to sodium, potassium intake, rapid decompensation of chronic renal failure in stressful situations; 2) clinical manifestations of chronic renal failure are associated with a direct deterioration of excretory and other renal functions, with the influence of so-called secondary factors aimed at compensating for primary disorders (for example, removal of calcium from the bones to compensate for acidosis), as well as with lesions of other organs (pericarditis, etc. .), caused by disruption of their vital functions in conditions of changes in homeostatic constants (acidosis, hyperazotemia, etc.).

Clinical picture. CRF is characterized by the gradual development of weakness, pale skin, and anorexia. Blood pressure is often normal in the initial, or polyuric, stage; in the oligoanuric, or uremic, stage, hypertension is usually observed. In the polyuric stage of chronic renal failure (diuresis reaches 2-3 l/day), which can last for years, hyperazotemia is moderate, glomerular filtration is 20-30 ml/min, the relative density of urine is equal to or lower than the relative density of blood plasma (1010-1012). Acidosis may be absent. Urinary syndrome, mild in congenital nephropathy (proteinuria up to 1 g/day), can manifest itself in varying degrees of proteinuria, hematuria and leukocyturia in chronic renal failure due to glomerulo- and pyelonephritis. In the oligoanuric stage, which lasts 1-4 months, a sharp deterioration in the condition is caused by the addition of hemorrhagic syndrome, cardiovascular failure, etc. as a result of increasing metabolic changes. Children with chronic renal failure due to congenital tubulointerstitial kidney diseases (nephronophthisis, etc.) often experience severe symptoms of renal rickets (bone and muscle pain, bone deformities, growth retardation), which is associated with insufficient production of the biologically active metabolite of vitamin D - 1.25( OH)2Oz with sclerotic kidneys, as well as with the influence of iatrogenic factors (diet with limited protein and calcium, treatment with prednisolone, etc.). During this period, anemia and hyperkalemia increase, and renal function in osmotic dilution is impaired, which leads to the rapid development of hypervolemia with inadequate fluid administration. The life expectancy of children with chronic renal failure largely depends on its cause: patients with tubulointerstitial pathology live longer (up to 12 years or more) than patients with glomerulopathies (2-8 years) without dialysis and kidney transplantation in complex therapy.

CRF must be differentiated from acute renal failure, which is characterized by a sudden onset from the oligoanuric stage and reverse development in most cases; from neurohypophyseal diabetes insipidus, in which there is no hyperazotemia and other signs of chronic renal failure; from anemic syndrome in other diseases (hypoplastic anemia, etc.), in which there are no symptoms of chronic renal failure.

Treatment. Aimed at reducing hyperazotemia and correcting water-electrolyte and other metabolic disorders. The basic principles are the same as in the treatment of acute renal failure (see). However, in case of chronic renal failure, corrective measures are used for a long time, the Giordano-Giovanetti diet (protein limitation to 0.7 g/kg per day and high calorie content) - in the presence of severe hyperazotemia. Currently, chronic peritoneal dialysis and hemodialysis are prescribed in preparation for kidney transplantation, as well as in the presence of contraindications to kidney transplantation. In children with chronic renal failure accompanied by renal rickets, complex treatment includes vitamin D and its metabolites, including 1,25(OH)2D3 at 0.25-1.0 mg/day, la(OH)D3 at 0.5-2.0 mg/day for 3-6 months in repeated courses under the control of serum calcium (possible development of nephrocalcinosis). The kidney dialysis-transplantation program remains the most promising in the treatment of children with chronic renal failure, as it helps patients return to normal life in a family environment. Indications for this program are the lack of effect from conservative therapy, an increase in serum creatine levels to 0.6 mmol/l (6 mg%) and potassium in the blood above 7 mmol/l.

(AKI) is a clinical syndrome of various etiologies, which is characterized by a pronounced and rapid decrease in glomerular filtration 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 acute renal failure).
The main reason is hypovolemia (centralization of blood circulation and renal ischemia). Functional kidney disorders develop (no organic changes). With timely elimination of renal ischemia, their function is completely restored. If ischemia is prolonged (prolonged), then secondary organic damage to the renal parenchyma may develop.

Functional surge arrester develops when:

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

Renal(organic OPN).

There are three types of renal acute renal failure:

Cortical necrosis.
Causes: hypovolemia, hypoxia, shock, hemolysis, endotoxins;
Necrotizing 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 flow of urine below the renal pelvis is impaired. Causes: urolithiasis, tumor, neurogenic bladder, traumatic injury to the ureters during gynecological operations.

Pathogenesis of acute renal failure.

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

The kidneys are characterized by high blood circulation intensity. 92.5% of the total 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 (bypass occurs).

Approximate schemes for the development of surge arresters:

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:

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

During this period, complications may occur in other systems:

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

3. Period of polyuria(duration 5-8 days). Characterized by an increase in diuresis and a decrease in azotemia. This period is dangerous, just 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. Low urine density (1002-1004) persists for a long time.

Diagnostics (OSN):

1) Rate of diuresis.

Minimum diuresis:

In adults – 30 ml/hour;
In children under 1 year – 1.5 ml/kg/hour
In children under 5 years old – 1 ml/kg/hour;
In children over 5 years old – 0.5 ml/kg/hour.

Even with a normal amount of urine output, kidney failure can occur. You also need to focus on indicators - urea and creatinine.

2) Urea and creatinine indicators:

Urea is not only a marker of renal failure, but also an indicator of liver catabolism (also characterizes liver function).
With an increase in catabolism in the body, lipids and proteins are destroyed. A large amount of ammonia (a lipophilic compound, toxic) is formed, which is poorly excreted by the kidneys. The urine cycle occurs in the liver. Ammonia produces urea (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 to 0.4 µmol/l characterizes functional acute renal failure. An increase in creatinine more than 0.4 µmol/l – organic acute renal failure.

The important ratio is blood urea/blood creatinine (in mmol/l). Normal = 20-40. If more than 40, urea production increases (catabolism increases); if less than 20, it indicates renal failure.

3) Urine osmolarity (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 specific gravity of urine. B N = 540-670 mOsmol/l.
With functional acute renal failure, urine osmolarity will be higher than normal. In organic acute renal failure, urine osmolarity is below 540 mOsmol/L. (destructive changes in the proximal tubules, no reabsorption).

4) Sodium concentration in urine.

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

5) Creatinine clearance– absolute criterion of surge arrester. It means purification of a certain volume of liquid of a given compound in 1 minute.
The norm is 80-180 ml/min.
A decrease in creatinine clearance indicates renal failure:

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

6) Presence of urinary lysozyme in urine analysis.
Lysozyme is a protein synthesized in leukocytes and should not be present in the urine. If it is present in the urine, it indicates necrosis of the renal tubules.

Determination of anatomical kidney damage by urine analysis:

Glomeruli – the presence of red blood cells, fat, blood cylinders in urine analysis, proteinuria (++++);
Renal tubules - the presence of epithelial cells of the renal tubules, the cylinders are granular, pigmented;
Interstitium - the presence of leukocytes, eosinophils, renal casts;
Renal vessels (diabetic nephropathy) – low content 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, then 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: aminophylline, dopamine (1-4 mcg/kg/min).

2) Treatment of organic acute renal failure.

Fluid calculation:

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

Be sure to monitor body weight 2 times a day. Body 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 doses. If there is no effect, there is no need to increase the dose.
Osmodiuretics. In the absence of glomerular filtration, osmodiuretics cannot be used.
Manitol test. Therapeutic dose is 1 g/kg, for the test – 0.5 g/kg (half the dose). If this dose leads to an increase in the rate of diuresis, then the same dose is administered again to confirm. If the effect does not occur, the administration of manitol is contraindicated. Manit acts on the proximal tubules;
Eufillin – increases the glomerular filtration rate (dose 4 mg/kg per day). Acts on intact nephrons. Not prescribed in the organic stage.

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, use Sodium thiosulfate or Unithiol;
Improve tissue respiration – cytochrome C;
Syndromic therapy without polypharmacy;
Ensuring the body's energy balance (parenteral nutrition);
Dialysis therapy - the sooner the better;
(with renal failure they die from bacterial complications, sepsis). Prescribed in courses of 5 days at half the dose, with a break of 2 days between courses. The drugs of choice are oxacillin, erythromycin (they are excreted through the biliary route). You can enter - cephobit. Nephrotoxic antibiotics (aminoglycosides, methicillin, tetracyclines, first generation cephalosporins) are contraindicated. If extracorporeal detoxification is performed, the usual doses of antibiotic are administered.

We transfuse solutions depending on plasma osmolarity:

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

To maintain colloid-osmolar pressure, Refortam and Stabilizol are administered. For anuria, protein preparations, solutions containing potassium (Trisol, Ascesol, potassium chloride, Ringer's solution) are contraindicated.

In case of threatening hyperkalemia (above 6 mmol/l), the following is administered:

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

Indications for emergency hemodialysis:

Overhydration with the development of cerebral edema or pulmonary edema;
The urea level is more than 25 mmol/l, or the daily increase in urea is more than 6-8 mmol/l;
Serum creatinine level is more than 0.5 mmol/l, or the daily increase in creatinine is more than 0.18 mmol/l;
Blood potassium 6.0-6.5 mmol/l, sodium less - 120 mmol/l;
Severe blood acidosis (pH less than 7.2);
Increase in body weight per day is 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 complex 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 complete recovery.

In a child, such a severe pathology as renal failure is rare. However, it is much more dangerous for children than for adults and can progress rapidly. It is worth knowing the possible causes and symptoms of the disease in order to prevent the consequences in time.

Kidney failure in children

The disease in childhood can be acute or chronic. Acute renal failure (ARF) is a syndrome that occurs during a sharp decline in kidney function. It is based on oxygen starvation of the renal tissue, damage to the tubules and the occurrence of edema. With this severe pathology, the kidneys lose the ability to secrete fluid, and an acute imbalance of electrolytes and salts occurs in the body. Another name for acute renal failure is acute uremia.

Long-term kidney diseases often lead to persistent disruption of the entire urinary system. In the absence of treatment or in the presence of organic pathologies, chronic renal failure (CRF) may develop.

This syndrome is characterized by the accumulation of nitrogen metabolism products in the body, which disrupts many types of metabolism, leads to increased blood pressure, anemia and changes in the functioning of most organs. The diagnosis of chronic renal failure is made if the decrease in kidney function lasts more than 3 months.

Kidney failure can occur at any age, because there are many reasons for it. Sometimes it is recorded even in the fetus, for example, during intrauterine hypoxia. Previously, the percentage of children surviving after acute renal failure was very low, now the mortality rate has decreased to 20% (in newborns, the mortality rate is still high - up to 50-75%). The incidence of acute renal failure in children under 5 years of age is 4 cases per 100 thousand, of which 30% are children under one year of age. At school age, no more than 1 case of acute renal failure is registered for the same number of people. The statistics of chronic renal failure in children are as follows: 10-50 cases per 1 million population.

Pathogenesis

Acute kidney failure progresses according to the following stages:

Preanuric. Pathogenic factors begin to affect the kidney tissue, and the organs lose their basic functions.
Anuric. The body retains toxins and metabolic products, mineral salts, and water. The acid-base balance shifts towards oxidation (acidosis). Acute poisoning of the body with ammonia and other metabolites occurs.
Polyuric. Diuresis gradually improves, but polyuria develops - an increase in the amount of urine excreted.
Restorative. The kidney vessels restore their function, the permeability of the glomerular capillaries is normalized.

Chronic renal failure, regardless of the cause, is caused by a decrease in the number of active nephrons (kidney cells). They are replaced by connective tissue as the disease progresses. The load on the remaining nephrons increases - the adaptation mechanism turns on. This causes hypertrophy of nephrons, disruption of their structure and further progression of chronic renal failure. As a result, many types of metabolism change pathologically, and the body is in a state of intoxication.

Reasons

Surge arresters can exist in two forms:

Organic (associated with damage to kidney tissue, leads to the accumulation of nitrogen metabolism products in the blood, disrupts electrolyte balance).
Functional (develops against the background of an existing failure of water-salt metabolism or disruption of blood flow, breathing, and is often reversible).

Functional renal failure is typical for severe poisoning, disseminated intravascular coagulation syndrome (sharp increase in blood clotting), intoxication, dehydration, and oxygen starvation. Such conditions reduce blood flow to the glomeruli, and blood flow inside the kidneys is also greatly reduced. This causes the death of nephrons with the development of acute renal failure.

Both organic and functional kidney failure in children can be caused by the following conditions:

In children in the first weeks of life - pulmonary pathologies, sepsis, intrauterine infections, hypoxia and suffocation during childbirth, due to transfusion of incompatible blood, burn disease, renal vein thrombosis.
In children under 3 years of age - infectious intoxication, shock, hemolytic-uremic syndrome.
In preschool children, kidney tissue is damaged by microbes and viruses, sepsis, trauma, poisoning.
Schoolchildren have systemic autoimmune diseases.

AKI occurs against the background of congenital organic kidney lesions - polycystic disease, developmental anomalies, but its share in the overall morbidity structure is low.

Chronic renal failure is rarely observed in children in the first year of life; in children under 3-7 years of age, it often develops against the background of existing congenital kidney disease.

Renal failure should be differentiated from:

Encephalopathies.
Acute glomerulonephritis.

Treatment

Treatment for acute renal failure should be started as soon as possible. The goals are to restore circulating blood volume, improve blood microcirculation in the kidney tissue, and detoxify the body.

In the early stages of the disease, the following administration gives an excellent effect:

Blood thinners.
Vasodilators.
Diuretic drugs.
Drugs in antishock therapy.

Many young patients under one year old with acute renal failure require urgent treatment on a special device. Without dialysis, it is impossible to save a patient with complications - hyperkalemia, pulmonary and cerebral edema, high blood pressure. For babies under 6 months and newborns, peritoneal dialysis (continuous washing of the peritoneum) is more often recommended.

Older children additionally undergo blood filtration (plasmapheresis). Be sure to perform intensive antibiotic therapy to prevent infectious complications. At the recovery stage, potassium preparations, electrolyte mixtures, glucose, etc. are used.

Chronic renal failure in children requires correction of the activity of many organs and systems.

With the development of chronic renal failure, the following drugs are prescribed (according to indications):

Calcium and vitamin D preparations to prevent calcium metabolism disorders.
Antacids to reduce phosphorus levels in the blood.
Diuretics to increase diuresis.
Medicines for high blood pressure when it is elevated.
Iron supplements for anemia.

If symptoms of uremia increase, the child is treated with hemodialysis. After stabilization of the condition of children under 3-10 years of age, they are most often transferred back to conservative therapy. Blood plasmapheresis courses provide good results. A kidney transplant into a child usually allows for stable remission for many years.

The amount of fluid consumed per day for a child is determined only by a doctor, based on blood and urine parameters. Infants are given mother's milk and adapted formulas. After one year of age, children are required to be prescribed a diet with strict restrictions on salt and protein. A potato-egg-vegetable diet is preferred. In case of acute renal failure, fish, meat, and salt are completely excluded. Children must receive the required set of amino acids from special preparations.

Prognosis and possible complications

In acute renal failure, death can occur from a number of severe complications. In particular, hyperkalemia is dangerous - it often ends in cardiac arrest. Complications of acute renal failure can include uremic coma, sepsis, and multiple organ failure. The prognosis depends on the cause of the pathology and the speed of medical care. Chronic renal failure and other renal diseases, including renal failure, occur in 35% of surviving newborns. In older children, more than 75% of survivors have a good prognosis - organ function is restored.

Latent and compensated stages of chronic renal failure, subject to regular courses of treatment and diet, have a favorable prognosis, recovery is possible, especially if the underlying pathology is corrected. At the intermittent stage, complete recovery is impossible, but it is possible to keep the patient alive through dialysis for a long time. Even in the terminal stage, hemodialysis allows you to live for at least 10 years. A kidney transplant gives a sick child a chance for a long and fulfilling life in 50-80% of cases.

Acute renal failure in children (ARF) is a disorder of homeostatic functions, 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, post-hemorrhagic, post-hypoxic shock, use of respiratory care in the treatment of RDS with high positive end-expiratory pressure.

Nephrotic factors are 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 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;
“white spot” symptom (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 ultrasonography reveals signs of hypoperfusion along with a decrease in cardiac output and myocardial contractile function. 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 myocardial contractile function, 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 the 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 persists. At this stage, maintenance of euvolemia, correction of possible electrolyte disturbances, and dynamic control are required.

When acute renal failure persists after the end of the 1st week of life, as a rule, we are talking 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, large urethrocele, compression of the urinary tract from the outside by a tumor), which leads to impaired urine outflow . In 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. A 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 with determination of the level of creatinine, urea, total protein, cholesterol, sodium, potassium, chlorine, magnesium, calcium in 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.

Photo: tvoelechenie.ru

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 in saline 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. In this case, it is necessary to ensure that the physiological need for energy is satisfied by 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 drains in the abdominal cavity, ileostomies, diaphragmatic and inguinal hernias.