The causes of renal failure in children. Acute renal failure in newborns

Date: 19.10.2019

(Surge arrester) - clinical syndrome of various etiology, 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 arrester);
Renal (organic arrester);
Postrenal arrester.

Prerenal(functional surge arrester).
The main reason is hypovolemia (centralization of blood circulation and renal ischemia). Develop functional disorders kidney (no organic changes). With the timely elimination of kidney ischemia, their function is fully restored. If ischemia is prolonged (prolonged), then secondary organic damage to the renal parenchyma may develop.

A functional surge arrester develops when:

Hypovolemia (dehydration, intoxication,);
Violation of central hemodynamics (myocarditis, cardiac tamponade, myocardial infarction);
Violation of peripheral hemodynamics (, sepsis);
Renal vascular occlusion.

Renal(organic surge arrester).

There are three types of renal arrester:

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

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

The 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 - toxic factor and indirect - circulatory.

The kidneys are characterized by a high intensity of blood circulation. 92.5% of the total amount of blood flows through the kidneys. In the kidney, there are 2 functional circles of blood circulation. Large circle - cortical and small circle - juxtamedullary. The blood circulation can switch from a large circle to a small one (shunting 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 arrester:

The period of action of the etiological factor... Duration from several minutes to hours;
Oligoanuria period(may last up to 21-28 days). It is characterized by the development of oliguria or anuria. Uremic intoxication develops. Oliguria - a decrease in urine output of less than 0.5 ml / kg per hour. Anuria - 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 (pneumonia, pleurisy are possible);
Liver (kidneys and liver are interconnected, in case of impaired renal function, the liver takes over part of its functions);
The blood system (anemia may develop due to inhibition of blood formation, as well as a decrease in renal excretion - erythropoietin);
Violation of the water-electrolyte balance (hyper K, Na, Mg develops). An increase in potassium to 6.5 mmol / L is critical;
Bone system (development of osteodystrophy, osteomalacia);
Endocrine system (increased glucose tolerance).

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

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

Diagnostics (surge arrester):

1) The rate of urine output.

Minimum urine output:

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

Even with normal amount diuresis may be renal failure. You also need to be guided by the indicators - urea and creatinine.

2) Indicators of urea and creatinine:

Urea is not only a marker of renal failure, but also an indicator of liver catabolism (also characterizes liver function).
With an increase in catabolism in the body, lipids and proteins are destroyed. Formed a large number of ammonia (lipophilic compound, toxic), which is poorly excreted by the kidneys. A cycle of urination occurs in the liver. With ammonia, urea is formed (a hydrophilic compound, non-toxic), which is well excreted by the kidneys.
Creatinine is the most important 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 mmol / l, or 0.11 - 0.17 mmol / l. An increase in creatinine up to 0.4 μmol / L characterizes functional ARF. An increase in creatinine greater than 0.4 μmol / l - organic ARF.

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

3) Osmolarity of urine (important criterion).

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

4) Concentration of sodium in urine.

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

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

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

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

Definition by urine analysis of anatomical lesion of the kidney:

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

Treatment.

1) Treatment of functional ARF.
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 is administered 1-4 mg / kg. 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 μg / kg / min).

2) Treatment of organic acute renal failure.

Liquid calculation:

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

It is imperative to control body weight 2 times a day. The increase in body weight 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 administrations. If there is no effect, no need to increase the dose.
Osmodiuretics. In the absence of glomerular filtration, osmodiuretics cannot be used.
Mannitol test. The therapeutic dose is 1 g / kg, for the sample - 0.5 g / kg (half the dose). If this dose leads to an increase in the rate of diuresis, then the same dose is re-administered for confirmation. If the effect has not come, the introduction of manit is contraindicated. Manit acts on the proximal tubule;
Eufillin - increases the rate of glomerular filtration (dose 4 mg / kg per day). Acts on intact nephrons. Not assigned in the organic stage.

If there is no effect of 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 the 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 energy balance of the body (parenteral nutrition);
Dialysis therapy - the sooner the better;
(with renal failure, they die from bacterial complications, sepsis). Prescribed in courses of 5 days in a half dose, a break of 2 days between courses. The drugs of choice are oxacillin, erythromycin (they are excreted by the biliary route). You can enter - cefobit. Nephrotoxic antibiotics (aminoglycosides, methicillin, tetracyclines, 1st generation cephalosporins) are contraindicated. If extracorporeal detoxification is performed, the usual doses of antibiotic are administered.

We transfuse solutions depending on the osmolarity of the plasma:

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

To maintain the colloidal-osmolar pressure, stabizol is introduced to reform. With anuria, protein preparations, solutions containing potassium (trisol, ascesol, potassium chloride, Ringer's solution) are contraindicated.

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

Calcium gluconate 10% - 0.2 ml / kg;
Glucose solution 20% - 4-5 ml / kg with insulin (1 unit for 5 g of glucose);
A solution of sodium bicarbonate 4% - 2-4 ml / kg (cannot be combined with calcium gluconate in one syringe);
An osmotic laxative (xylitol, sorbitol) is prescribed internally.

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;
The 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);
The 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 the right and timely treatment of acute renal failure, using all methods, the prognosis can be favorable with full recovery.

Renal failure is dangerous pathological condition, characterized by partial or complete disruption of the kidneys and their excretory function. It is mainly found in adults, rarely diagnosed in children. The disease can be congenital or acquired.

In a sick child, urine excretion is sharply reduced, or its outflow stops completely. As a result, toxic substances accumulate in the body (which are not excreted in the urine), the acid-base and water-salt balance is disturbed. In the absence of full, adequate medical care, the child may die. Therefore, it will be important for parents to know more about the manifestations of this disease.

Let's talk in more detail about the symptoms of renal failure in children and the treatment of pathology.

Common signs in children of renal failure

Exists characteristic signs developing disease, which should alert parents and encourage them to show the child to a specialist. These include:

Decreased urine output.

Intoxication symptoms: weakness, fatigue, headache, as well as nausea, vomiting and diarrhea.

Feeling unwell, fever.

Yellowish skin tone.

Swelling of the face and limbs.

Examination reveals an increased level of protein in the urine, the formation of sand and calculi in the kidneys. A striking sign of kidney failure in children is nephrotic syndrome, which almost never occurs in adults.

Symptoms of Acute Renal Failure

It occurs due to poisoning of the body with toxic substances that accumulate due to the termination normal work kidneys.

It is developing rapidly. In the first days of the onset of the disease, it manifests itself with pronounced symptoms of intoxication - feeling unwell, weakness, nausea, vomiting, etc. Further, uremia is added, nitrogenous toxins penetrate into the blood. There is a violation of the water-electrolyte balance, diuresis is observed, the child's body weight sharply decreases.

However, with the onset of the last, fourth stage, the manifestation of negative symptoms of insufficiency decreases, the so-called "clinical recovery" occurs, after which the disease can return again.

If the child has symptoms acute form renal failure, you should immediately call an ambulance or take the patient to the hospital.
Self-medication in this case, threatens with dangerous consequences.

Chronic renal failure

This form can be congenital, acquired, hereditary. However, it most often develops due to untreated chronic diseases urinary system. Can develop long time and as a result lead to complete failure of the kidneys.

Doctors distinguish four stages of this pathology: latent, compensated, as well as intermittent and terminal.

At the slightest suspicion of a malfunction of the urinary system, the child should be shown to the pediatrician. The doctor will prescribe an examination and give a referral to a specialist nephrologist.

Kidney failure treatment

In the treatment of acute renal failure, first of all, measures are taken to detoxify the body, restore normal blood circulation in the renal tissue. Prescribe drugs from several groups: diuretics, vasodilators, anti-shock agents and blood thinners.

Children under 1 year of age are usually prescribed hemodialysis procedures. In case of complications such as hyperglycemia, hypertension, pulmonary edema or cerebral edema, the patient will need an apparatus " artificial kidney».

For children over 10 years old, blood filtration is additionally carried out, that is, plasmapheresis is prescribed.

To reduce the risk of infection, treatment for kidney failure is supplemented with antibacterial drugs. To maintain the body, the patient is prescribed potassium preparations, glucose and electrolyte mixtures.

With CPO, a complex therapy of a diseased kidney and associated diseases is carried out. With progressive uremia, the child is prescribed hemodialysis procedures. After improvement of the condition, drug treatment is carried out.

According to indications, antacids, calcium preparations, vitamins D, group B are prescribed. They are used to reduce the level of phosphorus. In the case of hypertension (a common symptom of the chronic course of the pathology), drugs are prescribed to reduce blood pressure.

In order to increase urine output, diuretics are prescribed. In the presence of anemia, iron supplements.

In severe cases of renal failure, a stable remission can be achieved only with the help of organ transplantation.

Folk recipes

This fortified drink will help support kidney health: mix equal amounts of finely broken raspberry sprigs, crushed rose hips and crushed black currant leaves. Brew 1 tablespoon for half a liter of boiling water, let the child drink a little, but every day.

To normalize the water-salt balance, doctors recommend drinking fresh pomegranate juice. Adults - 50 ml, twice a day. It is better for children to dilute the juice with clean water. The course of regular admission is 2 months.

It is useful to drink a decoction of crushed pomegranate peel and crushed rose hips mixed in equal amounts. The mixture must be poured with boiling water and boiled for 5 minutes. Then let it brew and strain. You can not cook, but use a thermos. You need to pour boiling water over the ingredients, leave for a couple of hours. Strain and drink a little throughout the day.

In conclusion, we note that impaired kidney function is not a sentence for a child. But, for this it is very important to recognize the first symptoms in time and quickly apply for medical help... You should also promptly treat any existing diseases of the genitourinary system, because any infection can give an impetus to the development of this serious pathology. Be healthy!

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

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

Reasons for the development of renal failure

The reasons for the development of chronic renal failure include congenital, acquired or hereditary, often chronically occurring, diseases of the urinary system. Glomerulonephritis takes the leading position, followed by:

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

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

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

I would like to note the children who are at risk for the development of chronic renal failure:

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

To suspect this ailment, what should you pay attention to?

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

Parents need to know Clinical signs this disease, in order to promptly suspect and immediately, only with the help of a doctor, start therapeutic measures... The main symptoms are determined by a violation of water and electrolyte balance, peripheral circulation, condition of cardio-vascular system, central and peripheral nervous system, the nature of the damage to internal organs.

So, in order.

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

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

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

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

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

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

7. Signs of damage to the gastrointestinal tract are lining of the tongue, soreness in the epigastric region (epigastric region), symptoms of gastritis, enterocolitis, intestinal bleeding. As chronic renal failure progresses, these signs worsen.

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

9. The most characteristic and dangerous are violations in water-electrolyte metabolism, which in turn determine a specific clinical picture. Increased formation and excretion of urine (polyuria) with insufficient fluid intake is accompanied by thirst, decreased skin turgor, blood thickening due to increased hemoglobin. These signs are for children early age are very dangerous and can be fatal due to dehydration. Children complain of fatigue, drowsiness, thirst is accompanied by dryness of the tongue, reduced urine production, muscle twitching appears, and body temperature rises. leads to a violation on the part of all body systems. With the accelerated excretion of sodium from the body, patients are characterized by an asthenic state, accompanied by muscle hypotension, decreased pressure, decreased body temperature, and decreased urine output. In this case, there is no thirst, on the contrary, vomiting develops, the tongue is coated with a bloom, but moist, migraine develops, joint pain, myalgia, and sometimes convulsions. The above symptoms depend on the pathogenetically determined type of dehydration (intracellular or extracellular dehydration), but they are rare in isolation.

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

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

The level of magnesium in this pathology is increasing. The heart muscle also suffers from this - bradycardia (various types of blockade due to a violation of the conduction of electrical impulses through the conducting system of the heart).

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

An imbalance between phosphorus and calcium leads to osteodystrophy and soft tissue calcification. Elevated level calcium can lead to neuromuscular disorders: tremors of the fingers, muscle twitching, periodically there is vomiting.

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

What do you need to diagnose?

The main methods for diagnosing chronic renal failure are analyzes of urine, blood and ultrasound of the retroperitoneal organs.

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

When a child is found to have a lag in physical development, dry flaky skin, pallor of the skin, bags under the eyes, especially in the morning, nausea, complaints of fatigue, low-grade fever, thirst (the child drinks 2-3 liters or more), night urination, a thorough nephrological examination is necessary.

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

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

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

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

Organic kidney damage, accompanied by anuria, in the recent past in 80% of cases ended in the death of patients. At present, due to the widespread introduction of efferent methods of therapy (dialysis, hemofiltration, etc.) into clinical practice, it has been possible to significantly reduce mortality. According to A.S. Doletsky et al. (2000), today with acute renal failure in children it is about 20%, in newborns - from 14 to 73%.

ICD-10 codes

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

Epidemiology of acute renal failure

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

During the neonatal period, the incidence of acute renal failure requiring dialysis is 1 in 5000 newborns. According to official figures, acute renal failure accounts for 8-24% of all admissions to the department intensive care and resuscitation of newborns. At the age of 6 months to 5 years, the incidence of acute renal failure is 4-5 per 100,000 children. In this age group the main cause of acute renal failure is hemolytic uremic syndrome. V school age the frequency of acute renal failure depends, first of all, on the prevalence of diseases of the glomerular apparatus of the kidneys and is 1 per 100,000 children.

Causes of Acute Renal Failure in Children

Back in 1947 I. Tgiya et al. put forward the theory of renal ischemia as the main cause of acute renal failure. They believed that anuria and uremia are caused by prolonged reflex vasospasm of the renal cortex, which contributes to the cessation of glomerular filtration, a slight increase in reabsorption and degenerative-necrotic changes in the distal convoluted tubules and the ascending part of Henle's loop. Truet's vascular shunt as a pathogenetic basis of shock kidney injury later received universal recognition. Oligoanuria at the shock stage of toxic nephropathy is explained by the blood flow bypassing the malpighian glomeruli, and the ongoing hypoxia of the renal tissue, especially its cortex, contributes to the development of autolytic necrosis of the proximal tubules, as well as organic ARF.

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

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

Oliguria and acute renal failure are not synonymous. Patients with an acute decrease in urine output do not necessarily have organic damage to the renal parenchyma. At the same time, oliguria is the main, the most noticeable clinical symptoms of acute renal failure in children.

The main factors damaging the kidney are circulatory hypoxia, disseminated intravascular coagulation and nephrotoxicity, which contribute to:

persistent spasm of afferent (bringing) arterioles, which reduces blood flow to the glomeruli;
violation of intrarenal hemodynamics, primarily due to arteriovenous shunting of blood flow (Truet's shunt), which sharply depletes the blood supply to the renal cortex;
intravascular thrombogenic blockade, especially in the bringing glomerular arterioles;
a decrease in the permeability of the capillaries of the glomeruli due to the collapse of podocytes;
blockade of tubules with cellular detritus, protein masses;
tubulointerstitial changes in the form of dystrophy or necrosis of the epithelium of the renal tubules (membranolysis and cytolysis), tubulorexis (damage to the basement membrane of the tubules), which is accompanied by free reverse suction filtrate (primary urine) through the damaged basement membrane of the tubules into the interstitium of the kidneys;
swelling of the interstitium due to free penetration of primary urine through damaged tubular walls;
alignment of the cortico-medullary osmotic gradient and blockade of the work of the countercurrent-multiplier apparatus of the kidneys to concentrate urine;
an increase in renal hypoxia due to compression of intrarenal vessels by edema and blood shunting in the kidneys;
necrotic changes in the renal cortex (cortical necrosis), in which there is a high probability of death of patients at the height of acute renal failure or the development of subsequent nephrosclerosis and chronic renal failure.

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

For acute renal failure in children of different ages as the leading are various etiological factors. So, during the neonatal period, fetal hypoxia or asphyxia, pneumopathies, intrauterine infections, sepsis, renal vascular thrombosis, at the age from 1 month to 3 years - HUS, primary infectious toxicosis, anhydremic shock, at the age of 3 to 7 years - viral or bacterial kidney damage, poisoning, traumatic and septic shock, at the age of 7-17 years - systemic vasculitis, glomerulonephritis, traumatic shock.

Pathogenesis of acute renal failure

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

When assessing renal functions, it should be borne in mind that diuresis in a child is the sum of the required and additional fluid loss by the kidneys. Compulsory diuresis is understood as the amount of fluid required to fulfill the entire osmotic load, that is, for the excretion of the volume of urine excreted by the kidneys operating in the maximum concentration mode. At the same time, the maximum osmolarity of urine in an adult is on average 1400 mosm / l, in a newborn - 600 mosm / l, in a child under 1 year old - 700 mosm / l. Consequently, the younger the child, the greater the volume of compulsory diuresis. So, for the allocation of 1 mosm / l, an infant needs a diuresis equal to 1.4 ml, an adult - 0.7 ml. This means that in the absence of organic damage to the nephron, the decrease in diuresis cannot be unlimited and is limited to mandatory, and vice versa, the higher the osmotic load, the higher the diuresis.

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

Symptoms of Acute Renal Failure in Children

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

The most notable and early symptom acute renal failure in children is a decrease in urine output. At the same time, there is a distinction between absolute oliguria, which does not depend on the patient's water regime, and relative oliguria, which is observed with a lack of water in the body. The first of them is related to the surge arrester, the second to the FPN. In some cases, in a patient with acute renal failure, anuria may be absent while the water-excretory function of the kidneys is preserved, however, the volume of the injected fluid will always significantly exceed the volume of diuresis.

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

The study of urine sediment suggests a nosological form that led to impaired renal function. So, hematuria and proteinuria are observed with disseminated intravascular coagulation or intracapillary damage to the glomeruli. The presence of granular and hyaline casts in the sediment indicates renal hypoxia. Leukocyturia (neutrophilic) often occurs with acute inflammation kidney (pyelonephritis, apostematous nephritis). Moderate lymphocyturia, eosinophiluria, proteinuria, cylindruria and microerythrocyturia, as a rule, reflect the development of allergic, metabolic or toxic tubulointerstitial nephritis. Azotemia indicates impaired renal excretory function and a state of homeostasis in sick children. The main marker of azotemia is the concentration of creatinine and urea. An increase in the content of creatinine in the blood (normally no more than 0.1 mmol / l) reflects a violation of renal function. According to the creatinine of blood and urine, taking into account the minute diuresis, the rate of glomerular filtration (clearance of endogenous creatinine) is determined, which is lower than the normal indicator with acute renal failure (75-110 ml / min-1.73 m 2). The concentration of urea (normally 3.3-8.8 mmol / l) reflects not only the state of the excretory function of the kidneys, but also the catabolic processes occurring in the child's body, which are activated during sepsis, burns, severe injuries, etc.

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

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

The preanuric (initial) stage of acute renal failure in children has no special characteristics, but depends on the clinical manifestations of the disease that led to ARF. The main point of diagnosis of the initial period of acute renal failure is progressive oliguria, the rate of development of which can be different:

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

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

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

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

The polyuric stage of ARF is manifested by a gradual increase in urine output. The amount of urine exceeds the normal urine output several times. During this period, it is possible to develop dehydration, hypokalemic syndrome in the form of lethargy, flatulence, transient paresis of the extremities, tachycardia, and typical ECG changes. In children, MT decreases significantly, tissue elasticity and turgor decrease. Low motor activity, decreased appetite in the first days.

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

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

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

Diagnosis of acute renal failure in children

The main points of diagnosis of acute renal failure in children is the detection of decreased urine output in combination with VEO disorders and azotemia. A prerequisite accurate diagnosis oligoanuria is bladder catheterization.

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

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

V differential diagnosis FPN and SPD load tests can be used.

A test with the introduction of vasodilating drugs (pentamin, aminophylline, etc.) promotes an increase in urine output in oliguria due to the centralization of blood flow.
Test with water load and urine alkalization. The patient is injected intravenously for 1-2 hours in a volume equal to about 2% of MT, or 20 ml / kg. Usually, hemodez and 10% glucose solution are used in equal proportions. If the patient has FPN, diuresis increases and OPM decreases within 2 hours. Against the background of metabolic acidosis, an additional 2-3 ml / kg of a 4.2% sodium bicarbonate solution is administered. If the urine is acidic, the likelihood of acute renal failure is high.
The test with the introduction of saluretics is carried out in the absence of dehydration against the background of persisting oligoanuria. The absence of diuresis indicates acute renal failure. It should be remembered that the introduction of a large dose of lasix (> 10 mg / kg) against the background of acute renal failure is dangerous, therefore, it is advisable to divide it into parts and enter it fractionally within 1-2 hours. They usually start with a dose of 2 mg / kg, after 1 hour, if there is no effect, another 3-5 mg / kg is administered. Lasix acts more effectively against the background of continuous infusion of dopamine at a dose of 1-3 μg / (kgmin), preliminary administration of rheoprotectors and sodium bicarbonate at age-specific doses.

Treatment of acute renal failure in children

Treatment of FPN or pre-anuric stage of acute renal failure is almost directly related to the treatment of the underlying disease and correction of its manifestations, contributing to the development of renal failure, "shock" kidney and consists in protecting the kidneys from toxic and hypoxic damage. To do this, you need to as quickly as possible:

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

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

V last years in order to improve renal blood flow, dopamine infusion is often used at a rate of 2-4 μg / kg per minute (immediately after hemodynamic stabilization for 1-3 days). Mannitol (1 g of dry matter per 1 kg of child's MT) in the form of a 10% solution (intravenously drip quickly - in 40-60 minutes) reduces the spasm of the adducting and excretory arterioles of the renal glomeruli, stimulates the glomerular filtration rate and, due to the high osmolarity of the solution, provides a significant increase in urine output ... During this period, Lasix is prescribed fractionally at a dose of up to 5-10 mg / kg. Pre-alkalinization of urine enhances the diuretic effect of lasix by introducing a 4.2% sodium bicarbonate solution intravenously (at a dose of 2-3 ml / kg).

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

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

The absolute indications for dialysis therapy are:

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

Dialysis is performed daily during the entire period of anuria. The duration of the program dialysis is 4-5 hours. On the 1st day, in order to avoid disequilibration (redistribution of water into the cells due to the slower washing out of urea from them and the creation of a gradient of osmotic pressure), dialysis is best done twice; the duration of the session is about 2 hours with an interval of 6-8 hours. In older children, it becomes necessary to carry out dialysis in the first days of the polyuric stage.

Intestinal, gastric dialysis, exchange blood transfusion are currently practically not used in children with acute renal failure. In the first months of life, if it is not possible to provide venous access, as well as if there is a real danger of hypotensive reactions against the background of hemodialysis, preference is given to peritoneal dialysis. The dialysis membrane during it is the child's own peritoneum, which is washed with dialysis solution introduced into abdominal cavity on special catheters. With this method, blood purification is carried out almost continuously, which avoids dis-equilibration and collapse. In older children, low-flow veno-venous hemofiltration or constant hemodiafiltration is used (in adult patients, when they are used, they are removed per day, followed by adequate replacement of up to 40-60 liters of fluid).

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

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

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

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

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

When seizures occur in children with acute renal failure, GHB is used at a dose of 50-100 mg / kg, it is possible in combination with benzodiazepines (seduxen, etc.). If convulsions occur against the background of hypertension (hypertensive crisis, eclampsia), emergency dialysis with ultrafiltration is required. Before dialysis, children with a hypertensive crisis can be prescribed kapoten (under the tongue) at a dose of 1-6 mg / (kg day), apressin (0.1-0.5 mg / kg), a-blockers (prazosin, cardura), less commonly used clonidine (sublingually or intravenously). It is possible to prescribe calcium channel blockers (nifedipine) at a dose of 0.25-0.5 mg / kg or beta-blockers (anaprilin) at a dose of 0.1-0.3 mg / kg, especially in the presence of high diastolic blood pressure (> 100 mmHg . Art.). If there is no effect, sodium nitroprussnd (1-8 μg / kgmin) or perlinganite (0.1-1.0 μg / kgmin) is used intravenously.

With critical indicators (Нb

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

It's important to know!

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

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 conditionally 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 violation of homeostasis (hyperazotemia, acidosis, electrolyte disturbances) as a result of an acute violation of the basic functions of the kidneys (nitrogen excretory, regulation of CBS, 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 with septic shock, HUS and other pathology; with GN and PN; with cortical necrosis of the kidneys (in newborns), as well as with obstruction of 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 most pronounced changes in the tubules: their lumen is dilated, the epithelium is dystrophied and atrophied, the basal membrane with foci of ruptures. The interstitial tissue is edematous, with cellular infiltration, there may be minimal changes in the glomeruli with tubular necrosis (the action of nephrotoxin), as well as characteristic signs of glomerulo- or pyelonephritis (PN) complicated by acute renal failure. Regeneration of tubular epithelium, a gradual decrease in other morphological changes occur depending on the cause of ARF in the polyuric stage.

The clinical picture. There are 4 arrester periods:

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 urine output to 100-300 ml / day with a low relative density urine (no more than 1012), lasts 8-10 days, accompanied by a gradual increase in weakness, anorexia, nausea, vomiting, itching of the skin. With unrestricted administration of fluid and salt, hypervolemia, hypertension occur; pulmonary edema and peripheral edema may develop. A rapid increase in hyperazotemia (up to 5-15 mmol / day of 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, hemoglobin below 30 units, leukocytes up to 2.0 10 9 / l appear. Urine is red due to gross hematuria, proteinuria is usually small - up to 9% or more in patients with GN, complicated by acute renal failure. Some patients have uremic pericarditis; Kussmaul breathing can be maintained during the first dialysis sessions. Cases of neoliguric ARF developed as a result of mild necronephrosis are 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 urine output (within 3-5 days) and its increase up to 3-4 l / day, an increase in glomerular filtration (from 20 to 60-70 ml / min), elimination of hyperazotemia and signs of uremia; a decrease in urinary syndrome, an improvement in the concentration function of the kidneys.

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

Differential diagnosis must be carried out with oligoanuria without violating homeostatic constants, which is observed with obturation of the urinary organs, OGN, accompanied by oliguria and normal relative density of urine, absence of hyperazotemia; with chronic renal failure, which, in contrast to acute renal failure, develops gradually, from the polyuric stage and ends with an oligoanuric irreversible period.

Treatment. It boils down to eliminating the cause of acute renal failure, correcting the arisen homeostatic disorders, preventing various complications. In the presence of hypovolemia, enter isotonic solution sodium chloride (0.7 %) and glucose (5 %), Ringer's solution in a volume that ensures the restoration of the BCC under the control of hematocrit is 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 of signs of acute renal failure (for example, acidosis maintains hyperkalemia). Therefore, the restriction in the diet of proteins (up to 0.8-1.0 g / kg per day) and high calorie intake contribute to the reduction of not only hyperazotemia, but also acidosis, reducing tissue hypercatabolism. Hyperkalemia (dangerous due to cardiac arrest) above 6 mmol / l is corrected by a 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 injected is calculated from the deficiency of standard blood bicarbonates (in a 3-4% solution, 100-150 ml each). Blood transfusions are performed according to indications. Corticosteroid drugs are used for acute renal failure, developed against the background of infectious and allergic diseases. With pulmonary edema, cardiovascular insufficiency, eclampsia, generally accepted measures are taken. Depending on the plasma osmolarity, in the first 2-3 days from the onset of oligoanuria, osmotic diuretics can be administered (15-20% mannitol or polyglucin solution, 200-400 ml for 40-120 minutes), as well as saluretics (lasix up to 1 g per day etc.) If necessary, antibiotic therapy is administered drugs with minimal nephro-toxicity, in a dose corresponding to half of 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, a sufficient amount of potassium, sodium and calcium to prevent dehydration and electrolyte disorders. In the absence of the effect of conservative drugs, peritoneal dialysis or hemodialysis is used, which is prescribed in the serious condition of patients, indomitable vomiting, signs of incipient pulmonary edema, etc.; with hyperkalemia over 7 mmol / l, severe acidosis and hyperazotemia. With acute renal failure, the use of renal decapsulation and perirenal novocaine blockade is not justified.

Chronic renal failure (CRF)... It is diagnosed in children with diseases of the urinary organs if they retain for 3-6 months a decrease in glomerular filtration rate of less than 20 ml / min, an increase in the level of serum creatinine, urea. Over 50 diseases manifested by kidney damage can result in chronic renal failure, which, in contrast to acute renal failure, is characterized by progression and irreversibility.

Etiology. The cause of development is acquired and hereditary diseases of the urinary organs, factors that determine the development of acute renal failure and its outcome in chronic renal failure. With progressive kidney disease, there is a gradual decrease in their size due to hardening. Mosaicity of morphological changes is characteristic: the presence of sclerosed glomeruli and tubules along with hypertrophied glomeruli and dilated tubules, with areas of fibrosis of interstitial tissue. The process of CRF formation 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, with 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) during sclerosis, 75-80% of the nephrons 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 CRF 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, removing calcium from bones in order to compensate for acidosis), as well as with lesions of other organs (pericarditis, etc. .), caused by the violation of their vital activity in conditions of changes in homeostatic constants (acidosis, hyperazotemia, etc.).

The clinical picture. CRF is characterized by the gradual development of weakness, pallor of the skin, anorexia. Blood pressure is more 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 moderately expressed, glomerular filtration is 20-30 ml / min, the relative density of urine is equal or lower than the relative density of blood plasma (1010-1012). Acidosis may be absent. Urinary syndrome, mild in congenital nephropathies (proteinuria up to 1 g / day), can manifest itself with varying degrees of proteinuria, hematuria and leukocyturia in chronic renal failure due to glomerulo- and pyelonephritis. In the oligoanuric stage, lasting 1-4 months, a sharp deterioration is caused by the addition of hemorrhagic syndrome, cardiovascular failure, etc. as a result of increasing metabolic changes. Children with CRF due to congenital tubulointerstitial kidney diseases (nephronophthisis, etc.) often have pronounced symptoms of renal rickets (pain in bones and muscles, bone deformities, growth retardation), which is associated with insufficient production of a biologically active metabolite of vitamin D - 1.25 ( OH) 2Os sclerosed kidneys, as well as with the influence of iatrogenic factors (diet with limited protein and calcium, treatment with prednisolone, etc.). During this period, anemia, hyperkalemia increase, renal function by 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 are 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. It is 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 chronic renal failure, corrective measures are used for a long time, the Giordano-Giovanetti diet (protein restriction 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 for kidney transplantation. In children with CRF, accompanied by renal rickets, vitamin D and its metabolites are included in complex treatment, including 1.25 (OH) 2 D 3 at 0.25-1.0 mg / day, la (OH) D 3 by 0.5-2.0 mg / day for 3-6 months by repeated courses under the control of serum calcium (nephrocalcinosis may develop). The dialysis-kidney transplant program remains the most promising in the treatment of children with chronic renal failure, as it helps patients to return to normal life in a family setting. The indications for this program are the lack of effect from conservative therapy, an increase in the level of serum creatine to 0.6 mmol / L (6 mg%) and potassium in the blood over 7 mmol / L.