Signs of acute renal failure in children. Kidney failure in children

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

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

At untimely treatment persistent intoxication develops, leading to convulsions. In rare cases, the child begins to lose weight quickly and anemia occurs. Bones become brittle. Ultimately, the affected kidney fails and becomes necrotic, leading to death.

Classification

The causes of the first type of damage are shock, toxic effects of substances, drugs or poisons, diseases of infectious etiology, urolithiasis disease, pyelonephritis. ARF begins with pronounced symptoms characteristic of it. All disorders in the kidney completely disappear after 1-2 months with timely treatment.

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

Stages of the disease

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

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

Causes

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

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

Symptoms

Skin

Pale in color.

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

Respiratory

Shortness of breath, accumulation of fluid in the bronchi.

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

Cardiovascular

Pain in the heart, increased blood and venous pressure.

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

Digestive

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

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

Osteoarticular

Delayed bone growth, brittle bones.

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

Neuropsychic

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

Hiccups, convulsions, headaches, fainting, mental retardation.

Acute urinary retention, pain in the lumbar region.

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

Hematopoietic

Anemia, decreased blood clotting.

Diagnostics

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

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

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

Laboratory diagnostics include general analysis blood test (BAC), conducting its biochemistry and general urinalysis (UCA):

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

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

Treatment

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

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

For infants up to one year old, to ensure sufficient calorie intake, the pediatrician introduces formulas with a high content of carbohydrates, fats and a low protein content.

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

Prevention

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

Timely detected pathology initial stages can be treated without significant consequences for the body.

Forecast

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

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

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

Chronic renal failure (CRF) is pathological condition organism, which 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 the 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.

Causes of kidney failure

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

• pyelonephritis, interstitial nephritis;
• scleroderma, periarteritis nodosa, systemic lupus erythematosus;
• kidney amyloidosis;
• renal artery stenosis, essential arterial hypertension;
• tubulopathies, 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 cervix Bladder) urinary tract.

An interesting fact is that in children under 3 years of age, the development of chronic renal failure is caused by severe structural anomalies urinary tract, hereditary tubulopathies and dysplasias of renal tissue. In this case, kidney function long time may remain compensated.

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

I would like to note children who are at risk for developing chronic renal failure:

• with sclerosing glomerulonephritis;
• children with impaired intrauterine development of the urinary system and, as a consequence, 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 disease, what should you pay attention to?

Suffering from chronic renal failure emotional sphere child: he becomes irritable, often capricious and cries, for which he is unfairly punished.

Parents need to know Clinical signs of this disease, in order to promptly suspect and immediately, only with the help of a doctor, begin therapeutic measures. The main symptoms are determined by a violation of water-electrolyte balance, peripheral circulation, the state of the cardiovascular system, central and peripheral nervous system, the nature of 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 observed, which is combined with a decrease in muscle tone, and thinning of the subcutaneous fat layer. The child’s emotional sphere also suffers: there is excessive aggressiveness and tearfulness, which on the part of parents is assessed as pampering and only leads to a worsening of the relationship with the child and unfair punishments.

2. Kidney dysfunction inevitably leaves its mark on the skin. In the initial stages, the skin becomes dry, then itching and flaking appear, and it acquires a yellowish tint. Pale skin is explained by the development of anemia and intoxication. In the terminal stage, the skin becomes yellowish-earthy in color, with elements on the trunk and limbs hemorrhagic rash(small or large bruises in the form of dots, spots, stripes from purple to scarlet, which do not disappear or change color when pressed). As chronic renal failure progresses, nails may also suffer - they become brittle and leukonychia (white stripes or spots inside the nail) appear.

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

4. Bone damage manifests itself as stiffness in the knees, ankle joints, sacral region, pain in bones and joints at night. X-ray changes bone tissue No. For older children characteristic manifestations are inflammation of the joints due to deposits uric acid and its salts in synovial fluid.

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

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

7. Signs of defeat gastrointestinal tract are a coated tongue, pain in the epigastric region (epigastric region), symptoms of gastritis, enterocolitis, intestinal bleeding. As chronic renal failure progresses, these signs become more severe.

8. Normochromic is the leading and most early sign CRF. There is a decrease in the number of red blood cells and the amount of hemoglobin, an increase in the number of old red blood cells with a reduced ability to deform, and the rate of hemoglobin synthesis also slows down due to pathological changes in the intracellular heme pool, in bone marrow young erythroid cells are destroyed prematurely. 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 impact on the skin, gastric and intestinal bleeding in the terminal stage of chronic renal failure.

9. The most typical 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, and thickening of the blood due to increased hemoglobin. These signs are for children early age very dangerous and can be fatal due to dehydration. Children complain of fatigue, drowsiness, thirst is accompanied by a dry tongue, decreased urine production, muscle twitching appears, and body temperature rises. leads to disruption of all body systems. With accelerated excretion of sodium from the body, patients are characterized by an asthenic state, accompanied by muscle hypotension, decreased blood pressure, decreased body temperature, and decreased diuresis. In this case, there is no thirst; on the contrary, vomiting develops, the tongue is coated but moist, migraine develops, joint pain, myalgia, and sometimes there are 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 chronic renal failure, the amount of potassium in the blood serum is reduced. But the development of acidosis leads to hyperkalemia. Clinically we see a decrease in reflexes, muscle weakness, lethargy. Changes in the ECG are also visible, indicating a decrease in the contractility of the ventricles of the heart and expansion of the boundaries of the heart.

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

The level of magnesium in this pathology increases. The heart muscle also suffers from this - bradycardia (various types of blockades due to disruption of the conduction of electrical impulses through the conduction system of the heart).

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

An imbalance between phosphorus and calcium leads to osteodystrophy and soft tissue calcification. Increased level calcium can lead to neuromuscular disorders: tremor of the fingers, muscle twitching, and occasional vomiting.

On different stages Chronic renal failure results in a decrease in cellular and humoral immunity, which causes the addition of bacterial complications.

What is needed for diagnosis?

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 urine test, general blood test, coagulogram, biochemical blood test, urine test according to Nechiporenko, urine test according to Zemnitsky, ultrasound of the kidneys and organs abdominal cavity, ECG, study of the level of hormones of the endocrine glands.

If a child has a delay in physical development, dry flaky skin, pale skin, bags under the eyes, especially in the morning, nausea, complaints fatigue, low-grade fever, thirst (the child drinks 2–3 liters or more), night urination, a thorough nephrological examination is necessary.

Doctors rarely diagnose acute renal failure in children, but pathology still occurs. The disease is quite dangerous for the health and life of the child. The pathology is quite acute and is characterized by impaired kidney function, which cannot cope with its work. As a result, the amount of urine decreases and the body is poisoned by toxins that accumulate. Pathology is often diagnosed in newborns due to congenital anomalies or subsequently complications during childbirth. The disease requires immediate treatment, since delay and delay in treatment leads to complications and death.

Acute, pediatric renal failure

The disease of this form occurs as a result of the shutdown of homeostatic renal functions. This is due to hypoxia of the tissue of the internal organ, then the tubules are injured and swelling occurs. In acute renal failure, an electrolyte imbalance occurs in the child. Doctors diagnose an impaired ability to excrete water.

Without timely treatment acute kidney failure will lead to the death of the child.

Stages of the disease

Symptoms appear depending on the stage at which the pathology is. Doctors distinguish four stages of acute renal failure in children. The initial stage appears on the first day. The main sign of a pathological process of this degree is a decrease in the amount of urine. The second stage is called oligoanuric and is characterized by vivid symptoms. At this stage, injury occurs to most internal organs and systems. child's body. The oligoanuric degree of the disease lasts from 1 day to 3 weeks.

At the recovery stage, the body practically returns to normal functioning, and normal urine excretion is restored. The duration of this stage ranges from 5 to 15 days. We can talk about the last stage of recovery only after at least a year has passed, since before this time it is extremely difficult to fully recover. This stage is characterized by improved adaptation to acute diseases. After an acute pathology, it is difficult to predict the further situation, since often after acute illness Chronic kidney failure occurs.

Chronic renal failure

Chronic renal failure in children develops against the background of congenital or acquired pathologies. With this form of the disease, the body is gradually poisoned by toxic products. The pathological process is marked by the concentration of electrolytes and changes in the acid-base balance. In medicine, there are four stages of development of chronic disease in children:

1. Compensated;
2. Subcompensated;
3. Decompensated;
4. Terminal or dialysis.

At the initial stage, there are no signs of the disease and pathology can only be detected through laboratory testing. The next stage is marked by slight increases in weight and height. The decompensated degree of insufficiency is marked by extensive symptoms. If the first three stages are identified in a timely manner and the child’s condition is maintained with medicinal procedures and special diets, then it is possible normal development child.

The last stage of chronic failure is the most dangerous and is characterized by uremia.

Swelling occurs on the child's face and body, the child suffers from nausea, loose stool, seizures and other signs of the disease. These symptoms occur due to the accumulation of harmful toxins and fluids in the body. Uremia is marked by the accumulation of water in the lungs, which leads to suffocation. If diagnosed last stage disease, then an internal organ transplant is performed.

Main reasons

Kidney failure in children can be caused by many reasons that are congenital, hereditary or acquired. Most of the causes are associated with abnormal development during intrauterine development, which cannot be avoided. In this case, parents need to support the child’s condition with the help special diets and preventive procedures.

Causes of pathology in newborns

The source of deficiency in newborns is congenital pathologies. Often the pathology is diagnosed in the absence of both internal organs or in the case abnormal development heart and cardiovascular system. If the fetus has a vascular disease of the arteries of the kidney or veins of the organ clogged with blood clots, then Great chance development of deficiency.

Often, impaired patency of the urinary tract and an infectious blood disease leads to pathology of an acute or chronic nature. The cause of the pathology may be dehydration of the newborn as a result of intrauterine infection. If there was a difficult birth with complications and bleeding, the risk of pathology in the newborn increases.

In children under one year old

In a baby pathological process occurs against the background of congenital or acquired diseases, as a result of which a large number of cellular blood elements die. Often pathologies in children under one year of age are preceded by infectious diseases in the intestines. In some cases, the pathology is provoked metabolic disorders, which are especially clearly expressed.

In older children

In older children (over 3 years old), the source of the disease may be infectious lesions of the body, which occur in an acute form. Often the pathology is diagnosed after a child has been poisoned by nephrotoxic drugs or medications. Due to injury or dangerous situations, such as sepsis, burns or bleeding, kidney failure occurs. Often, adult children have urolithiasis or a malignant tumor that has led to blockage of the urinary tract. As a result, kidney failure occurs.

Symptoms of pathology

Symptoms of kidney failure in children may not appear for a long time. The most striking symptoms occur in the second stage, when it begins. In case of renal failure, impaired urine excretion occurs, which is the first sign of the disease. In children of different ages, the symptoms of deficiency do not differ from the manifestations of the disease in adults. With pathology, the following symptoms occur:

• weakness and constant fatigue;
• increased excretion of urine;
• formation of kidney stones;
• low muscle tone;
• yellowing of the skin;
• increased body temperature;
• nausea and vomiting;
• swelling on the face and limbs.

In case of renal failure laboratory research protein will be detected in urine.

Often, children of different ages experience tremor and nephrotic syndrome, which is not so clearly manifested in adults during the disease. In some cases, mucus and blood can be found in a child’s urine, which is associated with damage to the mucous membrane of the internal organs of the urinary system. Parents should immediately contact their pediatrician if the above symptoms are detected.

The chronic form of the disease develops gradually as a result of irreversible disturbances of homeostatic renal functions with severe progressive disease that occurs in its final stage. Acute ophthalmic failure in children is acute condition, in which the filtration capacity of the kidneys is reduced to 25% of normal, and creatinine in the blood exceeds 0.176 mmol/l. TO this state lead to various toxic factors.

Symptoms of the development of kidney failure in children

Typical symptoms of this disease are:

complaints of fatigue,

decreased performance,

appetite,

headache.

Sometimes noted bad taste in the mouth, nausea and vomiting.

The skin of children is pale, dry, flabby.

Muscle tone reduced, minor muscle twitching, tremors of the fingers and hands are observed, pain in the bones and joints rarely appears.

There is arterial hypertension, which is often caused by underlying kidney disease.

Changes in the cardiovascular system: the boundaries of the heart are expanded, sounds are muffled, changes are detected on the ECG.

Stages of pediatric renal failure

Stages of disease development chronic form:

latent;

azotemic;

uremic.

Chronic kidney disease can last from 2 to 10 years or more before kidney failure develops. They go through a number of stages, the identification of which is necessary for proper planning of treatment of the disease.

When glomerular filtration and tubular reabsorption are maintained at normal level, the underlying disease is in a stage not accompanied by disorders renal processes. Over time, glomerular filtration becomes lower than normal, the ability of the kidneys to concentrate urine decreases, and the disease progresses to the stage of impaired renal processes. At this stage, homeostasis is maintained.

With a further decrease in the number of active nephrons and the glomerular filtration rate below 50 ml/min in the blood plasma, the levels of creatinine (more than 0.02 g/l) and urea (more than 0.5 g/l) increase. At this stage, conservative treatment of chronic renal failure in children is required. When filtration is below 10 ml/min, azotemia and other disturbances of homeostasis increase, despite conservative therapy, and the terminal stage of the partial form of the disease occurs, in which the use of dialysis is necessary.

With the gradual development of renal failure, homeostasis slowly changes - the level of creatinine, urea, sulfates, phosphates and other metabolites in the blood increases.

When diuresis is maintained (polyuria is observed), water is excreted in sufficient quantities, and the levels of sodium, chlorine, magnesium and potassium in the plasma do not change. Hypocalcemia associated with impaired vitamin D metabolism and calcium absorption in the intestine is constantly observed. Polyuria leads to hypokalemia. Often develops metabolic acidosis. In the terminal stage (when oliguria occurs), azotemia rapidly increases, acidosis worsens, hyperhydration increases, hyponatremia, hypochloremia, hypermagnesemia and hyperkalemia develop. The combination of these humoral disorders causes the symptoms of chronic uremia.

Stages of development of acute renal failure:

initial or shock,

oligoanuric,

restoration of diuresis,

recovery.

Diagnosis of pediatric renal failure in a child

The diagnosis is established on the basis of anamnesis data about chronic disease kidneys, clinical and laboratory data.

Blood tests for symptoms of renal failure in children include anemia, leukocytosis and bleeding. Conservative therapy makes it possible to regulate homeostasis, and general state the patient allows him to work, but an increase in physical activity, errors in diet, mental stress, restriction of drinking, infection, surgery can lead to a deterioration in kidney function. When glomerular filtration is below 10 ml/min, conservative correction of homeostasis is impossible.

In children with end-stage renal failure, emotional lability(apathy gives way to excitement), night sleep disturbances, daytime sleepiness, lethargy and inappropriate behavior, decreased appetite. The face is puffy, gray-yellow in color, the skin is itchy, there are scratches on the skin, the hair is dull and brittle. There is an ammonia smell from the mouth. Arises aphthous stomatitis, the tongue is coated, the stomach is swollen, vomiting, regurgitation, and sometimes diarrhea are repeated, fetid, dark-colored stools. Dystrophy increases, hypothermia is characteristic. Anemia is increasing hemorrhagic syndrome, muscle twitching becomes frequent and painful.

At long term uremia, pain in the arms and legs, brittle bones are observed, which is explained by uremic neuropathy and renal osteodystrophy. Noisy breathing is often due to acidosis, pulmonary edema, or pneumonia. Uremic intoxication is complicated by fibrinous pericarditis, pleurisy, ascites, encephalopathy and uremic coma.

Differential diagnosis renal failure in children is carried out with encephalopathy. Renal failure differs from an attack of encephalopathy in acute glomerulonephritis in its gradual development, not always accompanied by deep coma, small convulsive twitching of individual muscle groups, noisy breathing, while in renal eclampsia there is an acute onset, accompanied by complete loss of consciousness, dilated pupils, large convulsions and asphyxia.

Diagnostics acute failure kidneys in children

The diagnosis is made on the basis of clinical and laboratory data; this is a sudden decrease in diuresis, an increase in azotemia and other typical disorders of homeostasis.

In the initial period of the disease, symptoms appear due to shock (painful, anaphylactic or bacterial), acute poisoning, hemolysis, infectious disease, and already on the first day a decrease in diuresis is detected (less than 500 ml per day), i.e. a period of oligurianuria develops, and homeostasis is disrupted. In plasma, along with an increase in the levels of urea, creatinine, residual nitrogen, phosphates, sulfates, magnesium, and potassium, the levels of chlorine, sodium and calcium decrease. The combination of these disorders leads to an increase in the symptoms of acute uremia. Adynamia, loss of appetite, nausea, vomiting, and oliguria-anuria are also observed.

With increasing azotemia (urea level increases by 0.5 g/l daily), acidosis, overhydration and electrolyte disturbances drowsiness, retardation of consciousness, muscle twitching appear, shortness of breath increases due to acidosis and pulmonary edema, early stage determined radiographically. Abdominal pain and liver enlargement may occur.

Symptoms of the acute form of the disease are characterized by changes in the cardiovascular system (tachycardia, dull tones, systolic murmur at the apex, expansion of the borders of the heart, arterial hypertension). Rhythm disorders are associated with hyperkalemia: it is especially dangerous and can cause sudden death. With hyperkalemia of more than 6.5 mmol/l on the ECG, the T wave is high, pointed, the QRS complex widens, and sometimes the R wave decreases. Heart block and ventricular fibrillation can result in cardiac arrest. The blood test shows anemia, leukocytosis, which is characteristic of the period of oliguria-anuria. Death in acute renal failure often occurs from uremic coma, hemodynamic disorders and sepsis. If the child exhibits symptoms of acute renal failure, hypoisosthenuria is also detected.

The period of diuresis restoration begins with an increase in diuresis of more than 500 ml per day. Improvement occurs gradually, even after the onset of polyuria and as the level of azotemia decreases and homeostasis is restored. During the period of polyuria, hypokalemia (less than 3.8 mmol/l) with ECG changes (low voltage of the T wave, U wave, decreased ST segment) and extrasystole is possible. The recovery period is observed when the content of residual nitrogen in the blood normalizes. Homeostasis is restored. During this period, renal processes are restored. It lasts up to a year or more. But in some patients, the decrease in glomerular filtration and the concentrating ability of the kidneys remains, and in some, renal failure takes a chronic course, with associated pyelonephritis playing a major role.

Differential diagnosis is carried out with exacerbation of chronic renal failure or its terminal stage, where anamnesis data, a decrease in kidney size in chronic glomerulonephritis and pyelonephritis, or the identification of a chronic urological disease help. In acute glomerulonephritis, high proteinuria is observed.

How to treat renal failure in a child using traditional methods?

Therapy is inseparable from the treatment of kidney disease. In a stage not accompanied by disturbances in renal processes, etiological and pathogenetic therapy is carried out, which can lead to remission and a slower course of renal failure in the child.

At the stage of renal impairment, pathogenetic therapy and symptomatic treatment methods are prescribed ( antihypertensive drugs, antibacterial agents, protein limitation in the daily diet - no more than 1 g per 1 kg of body weight, Spa treatment renal failure in children, etc.). Conservative treatment aimed at restoring homeostasis, reducing azotemia and reducing symptoms of uremia.

The combination of these measures makes it possible to delay the onset of the disease, and periodic monitoring of the level of glomerular filtration, renal blood flow and concentrating ability of the kidneys, the level of creatinine and urea in plasma makes it possible to predict the course of the disease.

How to treat acute renal failure?

Treatment should be aimed at: stopping the action of the damaging factor that caused renal failure, correcting homeostasis disorders, preventing and treating complications.

If acute renal failure is caused by shock, then antishock therapy;

if acute renal failure is caused by acute hemolysis, then a replacement blood transfusion, plasmapheresis, elimination of the agent that caused hemolysis, and administration of large doses of steroids are performed to prevent antibody formation;

if the disease has developed as a result of poisoning, then hemosorption is carried out using antidotes; in case of poisoning with sulfonamides, a 4% solution of Sodium bicarbonate is administered with catheterization of the ureters;

if the child’s insufficiency has developed as a result of kidney disease, antihypertensive drugs are prescribed in combination with diuretics, anticoagulants, plasmapheresis, and extracorporeal dialysis.

If the cause of acute renal failure is bacterial shock, then, in addition to anti-shock measures, antibiotics are prescribed.

At the beginning of acute renal failure, a 10% solution of Mannitol is administered intravenously at the rate of 1 g per 1 kg of the patient’s body weight. If anuria continues for 2–3 days, treatment with Mannitol is not advisable. In the initial period of oliguria-anuria, diuresis is stimulated with furosemide (160 mg IV 4 times a day).

If diuresis increases, then the use of Furosemide is continued, then therapy is aimed at regulating homeostasis.

The diet for acute renal failure in children (restriction of protein and potassium intake) should be high in calories due to a sufficient amount of carbohydrates and fats. The amount of fluid administered should exceed diuresis, as well as the amount of water lost through vomiting and diarrhea, by no more than 500 ml. This volume includes 400 ml of a 20% glucose solution with 20 units of insulin.

Syndromic therapy: for overhydration, administer hypertonic solutions Glucose in combination with diuretics, Reopoliglucin and other blood substitutes. For hyperkalemia, a glucose solution and a 3-4% sodium bicarbonate solution are administered intravenously.

In case of hyponatremia, perfusion treatment of renal failure in children is carried out, aimed at eliminating overhydration. For hypocalcemia, calcium supplements are administered. For hyperphosphatemia, solutions of Sodium bicarbonate, Cocarboxylase, and B vitamins are administered. Antibiotics are prescribed for prophylactic purposes, but their dose is reduced by 2–3 times. Streptomycin, Monomycin, Neomycin in conditions of anuria have a pronounced ototoxic property and should not be used (for example, Penicillin is prescribed at a dose of 50 mg/kg per day, Oxacillin 200 mg/kg per day, Cefalotin 100 mg/kg per day, Methicillin 200 mg/kg per day).

Drug therapy for chronic renal failure in children

Calcium metabolism disorders and the development of osteodystrophy require long-term use calcium gluconate and vitamin D up to 100,000 IU per day, but the administration of vitamin D in large doses with hyperphosphatemia can lead to calcification of internal organs.

To reduce the level of phosphates in the blood, use Almagel 1 - 2 tsp. 4 times a day. Treatment requires regular monitoring of calcium and phosphorus levels in the blood. For acidosis, depending on its degree, a 5% solution of sodium bicarbonate is administered intravenously. When diuresis decreases, Furosemide (Lasix) is prescribed in doses (up to 1 g per day) that provide polyuria.

To reduce blood pressure, antihypertensive drugs are used in combination with Furosemide. Treatment of anemia is complex and includes the administration of testosterone propionate to enhance erythropoiesis (1 ml of 5% oil solution IM daily) and iron supplements.

When the hematocrit is 25% and below, red blood cell transfusions are prescribed in fractional doses. Antibacterial therapy for renal failure in children should be used with caution: the doses of Penicillin, Ampicillin, Methicillin, Ceporin and sulfonamides are reduced by 2-3 times. Streptomycin, Monomycin, Neomycin, even in reduced doses, can cause neuritis auditory nerve and other complications. Nitrofuran derivatives are contraindicated in chronic renal failure.

In heart failure, glycosides are used with caution, in reduced doses, especially in case of hypokalemia.

When treating pericarditis, small doses of Prednisolone are prescribed, but hemodialysis is more effective.

Hemodialysis and plasmapheresis for renal failure

With persistent oliguria and increasing symptoms of uremia, the patient is transferred to the hemodialysis department, where extracorporeal cleansing is performed using an artificial kidney or peritoneal dialysis. Types of dialysis: intestinal, peritoneal, extracorporeal.

Indications for hemodialysis:

oligoanuria for more than 1 – 2 days,

pulmonary edema,

overhydration with symptoms of cerebral edema,

hypertension,

hyperkalemia,

increasing azotemia,

drug poisoning and chemicals,

plasma urea level is more than 2 g/l, potassium level is 6.5 mmol/l,

decompensated metabolic acidosis

and clinical picture of acute uremia.

Contraindications to hemodialysis: cerebral, gastric and intestinal bleeding, severe hemodynamic disturbances with decreased blood pressure. Contraindications to peritoneal dialysis are recent surgery on the abdominal organs and adhesions in the abdominal cavity.

Hemodialysis may be indicated during exacerbation of the disease, and after improvement of the patient's condition, conservative therapy is carried out for a long time.

Good effect obtained after plasmapheresis. In the terminal stage, if conservative therapy does not have an effect and there are no contraindications, the patient is transferred to hemodialysis treatment. Regular hemodialysis is used when creatinine clearance is below 10 ml/min and its plasma level becomes above 0.1 g/l.

Hemodialysis and kidney transplantation change the fate of patients with renal failure, allowing them to prolong their lives and achieve rehabilitation for years. The selection of patients for these types of treatment is carried out by specialists from hemodialysis and organ transplantation centers.

Diet for kidney failure

The protein content in the daily diet depends on the degree of renal dysfunction. When glomerular filtration is below 50 ml/min and the level of creatinine in the blood is above 0.02 g/l, it is recommended to reduce the amount of protein consumed to 30 - 40 g per day, and when glomerular filtration is below 20 ml/min, a diet with a protein content of no more than 20 is prescribed – 24 g per day. The diet should be high-calorie (about 3000 kcal) and contain essential amino acids (potato-egg diet without meat and fish).

Food is prepared with a limited (up to 2 - 3 g) amount of table salt, and for patients with high hypertension- without salt.

Causes of childhood kidney failure

Causes of chronic disease:

chronic glomerulonephritis,

chronic pyelonephritis,

nephritis in systemic diseases,

hereditary nephritis,

polycystic kidney disease,

diabetic glomerulosclerosis,

kidney amyloidosis,

tubopathies,

chromosomal diseases,

dysmetabolic nephropathies.

Causes of acute renal failure

Kidney damage associated with exogenous nephrotoxins (poisoning with heavy metal salts, poisonous mushrooms, bites poisonous snakes and insects).

Toxic-allergic lesions associated with overdose medicines or the presence of increased sensitivity to them.

Infectious diseases (hemorrhagic fever With renal syndrome, anaerobic sepsis, leptospirosis, hemolytic-uremic syndrome).

Absence of a kidney (agenesis).

Complications of diffuse renal disease (acute glomerulonephritis and acute pyelonephritis, nephritis with hemorrhagic vasculitis, systemic lupus erythematosus).

Postrenal acute renal failure is divided depending on the location of the obstruction of the urinary tract and the cause leading to obstruction (such as a tumor, urolithiasis).

Renal hemodynamic disorders and exogenous intoxications cause 90% of all cases of the disease. The main mechanism of kidney damage in a child is

• anoxia renal tubules,
• development of necrosis of the tubular epithelium,
• swelling and cellular infiltration of interstitial tissue,
• damage to the kidney capillaries (necrotizing nephrosis develops).

More often than not, these damages are reversible.

Risk factors for developing kidney failure in children:

presence in the family of cases and deaths in at a young age from renal failure;

early, torpid onset of pathology with decreased renal function;

detection of signs of disembryogenesis and sclerosing variants of glomerulonephritis during biopsy in renal tissue;

the presence of a persistent hypoimmune state with signs of auto-aggression;

increasing instability of cell membranes in the absence of a family predisposition to dysmetabolic nephropathies.

The pathogenetic mechanism of the disease is a progressive decrease in the number of active nephrons, which leads to a decrease in the efficiency of renal processes and impaired renal function. The morphological picture of the kidney depends on the underlying disease, but replacement of the parenchyma is more often observed connective tissue and kidney shrinkage.

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 disturbance 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; at cortical necrosis kidneys (in newborns), as well as when there is 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 low relative density urine (no more than 1012), lasts 8-10 days, is accompanied by a gradual increase in weakness, anorexia, nausea, vomiting, itchy 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 and is characterized by a gradual restoration of renal functions. When using peritoneal dialysis and hemodialysis in complex therapy of acute renal failure deaths 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 disruption of homeostatic constants, which is observed with obstruction urinary organs, AGN, accompanied by oliguria and normal relative density of urine, 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. In the presence of hypovolemia, administer isotonic solution sodium chloride (0.7 %) and glucose (5 %), Ringer's solution in a volume that ensures the restoration of bcc under the control of hematocrit, sometimes injected 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 administered sodium bicarbonate 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 in serious condition sick, uncontrollable 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 perirenal 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 general provisions in relation to the connection 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 for further hypertrophy, which causes minimal reserve capabilities, clinically manifested by a decrease in tolerance to sodium and 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 setting. 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.