LECTURE No. 11. Kidney diseases in children. Classification

1. Classification of kidney diseases in children

I. Hereditary and congenital nephropathies:

1) anatomical anomalies in the structure of the kidneys and urinary organs:

a) malformations of the kidneys: quantitative (agenesis, aplasia, accessory kidneys), positional (dystopia, nephroptosis, rotation), formal (horseshoe-shaped s- and l-shaped kidneys);

b) malformations of the ureters;

c) anomalies in the structure of the bladder and urethra;

d) anomalies in the structure and location of the renal vessels, including the lymphatic system;

e) anomalies of the innervation of the urinary system with the syndrome of neurogenic bladder;

2) impaired differentiation of the renal structure:

a) with cysts;

b) without cysts;

3) hereditary nephritis (without hearing loss, with hearing loss);

4) tubopathies;

5) dysmetabolic nephropathy with crystalluria (oxalaturia, uraturia);

6) nephro- and uropathy in chromosomal diseases;

7) amyloidosis;

8) embryonic tumors.

II. Acquired diseases of the kidneys and urinary organs:

1) glomerulonephritis;

2) interstitial nephritis;

3) pyelonephritis;

4) urinary tract infection;

5) kidney tumors;

6) injuries of the kidneys and urinary organs;

7) urolithiasis;

8) secondary kidney disease in acute infections, diabetes, burn disease.

2. Pyelonephritis

Pyelonephritis is a nonspecific infectious disease of the kidneys that affects the renal parenchyma, predominantly with damage to the interstitial tissue. Causes: infection, impaired urodynamics, impaired immunity.

Etiology. Most often, pyelonephritis is caused by Escherichia coli, Enterococcus, Proteus, staphylococci, streptococci. In some patients with acute pyelonephritis and in 2/3 of patients with chronic pyelonephritis, the microflora is mixed. During treatment, the microflora and its sensitivity to antibiotics change, which requires repeated urine cultures to determine adequate urinary antiseptics.

Pathogenesis. The development of pyelonephritis largely depends on the general condition of the macroorganism and a decrease in its immunobiological reactivity. The infection penetrates into the kidney, pelvis, then into its calyces by hematogenous or lymphogenous route, from the lower urinary tract along the wall of the ureter, along its lumen - in the presence of retrograde reflux. Of particular importance in the development of pyelonephritis are urinary stasis and disturbances of venous and lymphatic outflow from the kidney. According to the current, acute and chronic pyelonephritis are distinguished; by period: period of exacerbation, period of partial remission, period of complete clinical and laboratory remission.

Clinic. The disease begins acutely, with an increase in body temperature to 40 ° C, chills, sweating, pallor of the skin and mucous membranes, pain in the lumbar region, severe pain in the costovertebral angle, general malaise, thirst, dysuria or pollakiuria, painful urination. Additional headache, nausea, and vomiting indicate rapidly increasing intoxication. Pasternatsky's symptom is usually positive. With bilateral acute pyelonephritis, signs of renal failure often appear. Acute pyelonephritis can be complicated by paranephritis and necrosis of the renal papillae.

Diagnosis put on the basis of an anamnesis indicating a recent acute purulent process or the presence of chronic diseases, clinical and laboratory data. In the blood test, neutrophilic leukocytosis, anemia, aneosinophilia, and an increase in ESR are noted. In the analysis of urine - leukocyturia, pyuria with moderate proteinuria and hematuria. In the Zimnitsky test - a decrease in the density of urine during the day. In the sample according to Nechiporenko - leukocytosis. In a biochemical study of blood - an increase in the content of sialic acids, creatinine, urea, the appearance of C-reactive protein. On a survey radiograph, an increase in one of the kidneys in volume is detected, with excretory urography - a sharp restriction of the mobility of the affected kidney during breathing, the absence or later appearance of a shadow of the urinary tract on the side of the lesion. prescribe an ultrasound examination of the kidneys, excretory pyelography to detect changes in the pelvicalyceal system. Voiding urethrography reveals anatomical and functional features, the presence of reflux.

Treatment. Treatment objectives: elimination and reduction of the microbial inflammatory process in the renal tissue and urinary tract; normalization of metabolic disorders and functional state of the kidneys; stimulation of regenerative processes; reduction of sclerotic processes in interstitial tissue. In the acute period, table No. 7a is prescribed, consumption of up to 2 liters of liquid per day. A balanced diet is prescribed to reduce the load on the tubular transport systems and correct metabolic disorders. Then the diet is expanded, increasing its protein and fat content. Proper organization of the general and motor regime is carried out, ensuring a reduction in the functional load on the kidneys and improving the elimination of metabolic products from the body. Early sanitation of foci of infection that contribute to the occurrence and progression of the disease is carried out. Restoration of urine passage, blood and lymph circulation in the renal tissue.

To improve local blood circulation and reduce pain, thermal procedures (warming compresses, heating pads, diathermy of the lumbar region) are prescribed. If the pain does not subside, then antispasmodics are used. Antibacterial therapy is carried out with nalidixic acid (nevigramon, negram), the course of treatment of which should last at least 7 days (0,5-1 g 4 times a day), nitroxoline (5-NOK), prescribed at 0,1 - 0,2 g 4 times a day for 2-3 weeks, nitrofuran derivatives (furadonin 0,15 g 3-4 times a day, course of treatment 5 - 8 days). The use of these drugs should be alternate. Nalidixic acid and nitrofuran derivatives should not be prescribed simultaneously, as this weakens the antibacterial effect. Combined treatment with antibiotics and sulfonamides is effective. The selection of antibiotics is carried out depending on the sensitivity of the microflora to them. Penicillin group drugs (ampicillin, aminoglycoside drugs, long-acting sulfonamides), and herbal medicine are prescribed. Symptomatic and replacement therapy is carried out when signs of renal failure develop.

3. Chronic pyelonephritis

Chronic pyelonephritis may be the result of untreated acute pyelonephritis, i.e., it can proceed without acute events from the onset of the disease.

Clinic. Unilateral chronic pyelonephritis is manifested by dull, constant pain in the lumbar region on the side of the affected kidney. There are no dysuric phenomena in most patients.

Diagnosis put on the basis of anamnesis, clinical and laboratory data. In the blood test, neutrophilic leukocytosis is noted. In the analysis of urine in the urine sediment, the predominance of leukocytes over other formed elements of urine is determined. The relative density of urine remains normal, one of the symptoms of the disease is bacteriuria. If the number of bacteria in 1 ml of urine exceeds 100, then it is necessary to determine their sensitivity to antibiotics and chemotherapy drugs. Arterial hypertension is a common symptom of chronic pyelonephritis, especially a bilateral process. The functional state of the kidneys is examined using chromocystoscopy, excretory urography, and clearance methods.

In chronic pyelonephritis, the concentration ability of the kidneys is disturbed early, while the nitrogen excretion function persists for many years. With infusion urography, a decrease in the concentration ability of the kidneys, a delayed release of a radiopaque substance, local spasms and deformations of the cups and pelvis are first determined. Subsequently, the spastic phase is replaced by atony, the calyxes and pelvises expand.

RџSЂRё differential diagnosis with chronic glomerulonephritis, the nature of the urinary syndrome (the predominance of leukocyturia over hematuria, the presence of active leukocytes, significant bacteriuria in pyelonephritis), and excretory urography data are of great importance. Nephrotic syndrome indicates the presence of glomerulonephritis. In case of arterial hypertension, differential diagnosis is carried out between pyelonephritis, hypertension and renovascular hypertension.

Treatment should be carried out for a long time. Treatment should begin with the appointment of nitrofurans (furadonin, furadantin, etc.), 5-NOC, nalidixic acid (negram, nevigramone), sulfonamides (urosulfan, atazol, etc.), alternating them alternately. At the same time, it is advisable to treat with cranberry extract.

With the ineffectiveness of these drugs, exacerbations of the disease, broad-spectrum antibiotics are used. The appointment of an antibiotic each time should be preceded by a determination of the sensitivity of the microflora to it.

4. Glomerulonephritis

Glomerulonephritis, an immunoallergic disease with a predominant lesion of the glomerular vessels, proceeds as an acute or chronic process with repeated exacerbations and remissions. Variants of glomerulonephritis:

1) nephritic - manifested by hematuria, proteinuria, hypertension, oliguria, cylindruria, leukocyturia, hypovolemia, hypocomplementemia, encephalopathy;

2) nephrotic - high proteinuria, edema, hypoproteinemia, possibly arterial hypertension, erythrocyturia, azotemia;

3) mixed - severe nephrotic syndrome, significant hematuria, hypertension;

4) hematuric - hematuria predominates in the urinary syndrome;

5) isolated urinary syndrome, manifested by extrarenal symptoms that are slightly expressed.

5. Acute glomerulonephritis

Acute glomerulonephritis is a cyclical infectious-allergic kidney disease that often develops 1-3 weeks after an infectious disease (usually of streptococcal etiology). Acute glomerulonephritis can develop at any age, but most patients are under 40 years of age.

Etiology, pathogenesis. The disease most often occurs after tonsillitis, tonsillitis, upper respiratory tract infections, scarlet fever, etc. 12-β-hemolytic group A streptococcus, pneumococcus, respiratory viruses, parasitic infestation, hypothermia, and trauma play a major role in the occurrence of glomerulonephritis. It may occur under the influence of a viral infection, after the administration of vaccines and serums (serum, vaccine nephritis). Cooling causes reflex disorders of the blood supply to the kidneys and affects the course of immunological reactions. The generally accepted idea is that glomerulonephritis is an immune complex pathology. The appearance of symptoms after an infection is preceded by a long latent period, during which the body’s reactivity changes and antibodies to microbes or viruses are formed.

Antigen-antibody complexes, interacting with complement, are deposited on the surface of the basement membrane of capillaries, mainly glomeruli.

Clinic. Clinical manifestations of glomerulonephritis in children:

1) extrarenal:

a) neurovegetative syndrome (malaise, anorexia, lethargy, nausea, vomiting, poor appetite, headache);

b) cardiovascular syndrome (hypertension, muffled heart sounds, murmurs and accents of heart sounds, enlargement of the liver);

c) edematous syndrome, manifested by pastosity, limited or generalized edema;

2) renal manifestations:

a) urinary syndrome (oliguria, proteinuria, hematuria, cylindruria, transient lymphocytic-mononuclear leukocyturia);

b) pain syndrome. Manifested by pain in the lumbar region or undifferentiated abdominal pain;

c) renal failure syndrome (azotemia is manifested by three main symptoms - edematous, hypertonic and urinary).

Diagnostics. Protein and red blood cells are found in the urine. The amount of protein in the urine usually ranges from 1 to 10 g/l, but often reaches 20 g/l or more. Slight proteinuria may be present from the very beginning of the disease, and in some periods it may even be absent. Small amounts of protein in the urine of patients who have had acute nephritis are observed for a long time and disappear only after 3-6, and in some cases even 9-12 months from the onset of the disease. Hematuria is a mandatory sign of acute hepomerulonephritis. There are macrohematuria and microhematuria, sometimes the number of red blood cells may not exceed 10-15 in the field of view. Cylindruria is not a necessary symptom of gpomerulonephritis. Leukocyturia is insignificant, but sometimes 20-30 or more leukocytes are found in the field of view. At the same time, there is always a quantitative predominance of erythrocytes over leukocytes, which is better revealed when counting the formed elements of urine sediment using the Addis-Kakovsky and Nechiporenko methods. Oliguria (400 - 700 ml of urine per day) is the first symptom of acute nephritis. In a blood test, the hemoglobin content and the number of red blood cells decrease, an increase in ESR is determined, and there is slight leukocytosis. A Rehberg, McClure - Aldrich test is performed. The function of the proximal convoluted tubules is examined, excretory urography, ultrasound examination of the kidneys, and radioisotope renography are prescribed.

There are two forms of acute glomerulonephritis.

Cyclic form It starts off stormy. Swelling, shortness of breath, headache, pain in the lumbar region appear, and the amount of urine decreases. Urine tests show high levels of proteinuria and hematuria. Blood pressure rises. The swelling lasts for 2-3 weeks, during the course of the disease a turning point occurs: polyuria develops and blood pressure decreases. The recovery period may be accompanied by hyposthenuria. However, often when patients feel well and have almost completely restored their ability to work, slight proteinuria (0,03 - 0,1 g/l) and residual hematuria may be observed for a long time, for months.

latent form is rare, and its diagnosis is of great importance, since often with this form the disease becomes chronic. This form of glomerulonephritis is characterized by a gradual onset, without any significant subjective symptoms, and is manifested only by slight shortness of breath or swelling in the legs. In such cases, it is possible to diagnose glomerulonephritis only with a systematic examination of urine. The duration of the relatively active period in the latent form of the disease can be significant (2-6 months or more).

Differential diagnosis. Conducted between acute glomerulonephritis and exacerbation of chronic glomerulonephritis. What is important here is to clarify the period from the onset of the infectious disease to the acute manifestations of nephritis. In acute cases, this period is 1-3 weeks, and in case of exacerbation of the chronic process - only a few days (1-2 days). Urinary syndrome may be the same in severity, but a persistent decrease in the relative density of urine (below 1,015) and a decrease in the filtration function of the kidneys are more typical for exacerbation of the chronic process.

Treatment. Hospitalization in a hospital, bed rest and diet are prescribed. A sharp restriction of table salt in food (no more than 1,5-2 g per day) in itself can lead to increased release of water and the elimination of edematous and hypertensive syndromes. In the future, watermelons, pumpkins, oranges, and potatoes are given, which provide almost completely sodium-free nutrition. Liquids can be consumed up to 600-1000 ml per day. Long-term restriction of protein intake is not sufficiently justified, since retention of nitrogenous wastes, as a rule, is not observed, and the sometimes supposed increase in blood pressure under the influence of protein nutrition has not been proven. Of the protein products, it is better to eat cottage cheese, as well as egg whites. Fats are allowed in the amount of 50 - 80 g per day. Carbohydrates are added to provide daily caloric intake. Antibacterial therapy is indicated when there is a clear connection between glomerulonephritis and an existing infection, for example, chronic tonsillitis. For chronic tonsillitis, tonsillectomy is indicated 2-3 months after the acute symptoms of the disease have subsided. The use of steroid hormones - prednisone, dexamethasone is possible no earlier than 3-4 weeks from the onset of the disease, when general symptoms (in particular, arterial hypertension) are less pronounced. Corticosteroid hormones are also indicated for the nephrotic form or prolonged course of acute glomerulonephritis. Corticosteroid therapy affects both edema and urinary syndrome. Moderate arterial hypertension is not a contraindication to the use of corticosteroid drugs. Vitamin therapy.

Forecast. Full recovery.

Prevention. It comes down to the prevention and early intensive treatment of acute infectious diseases, elimination of focal infection, especially in the tonsils. Prevention of sudden hypothermia of the body is also of preventive importance.

6. Subacute diffuse glomerulonephritis

Subacute diffuse glomerulonephritis has a malignant course.

Clinic. Rapid onset of the disease, characterized by edema, severe albuminuria (up to 10-30 g/l), as well as severe hypoproteinemia (45-35 g/l) and hypercholesterolemia (up to 6-10 g/l), i.e. signs of lipoid nephrotic syndrome. At the same time, hematuria and oliguria are observed. In urine analysis, the relative density is high only at the beginning, and then it becomes low. The filtration function of the kidneys progressively decreases. Already from the first weeks of the disease, azotemia may increase, which leads to the development of uremia. Arterial hypertension in this form of nephritis can be very high and is accompanied by severe changes in the fundus (retinal hemorrhages, swelling of the optic discs, formation of exudative white retinal spots).

Diagnosis. Taking into account the rapid development of renal failure, severe arterial hypertension is established, often of a malignant type. Subacute glomerulonephritis is indicated by the greater severity of edematous-inflammatory and lipoid-nephrotic syndromes.

Treatment. Treatment with steroid hormones for this form of glomerulonephritis is less effective, and in some cases is not indicated due to high and progressive arterial hypertension (BP above 200/140 mm Hg). Recently, it has been recommended to use immunosuppressants with careful monitoring of the morphological composition of the blood. Treatment with immunosuppressants is more effective in combination with corticosteroid hormones, which are prescribed in lower doses (25-30 mg per day). This combination not only promotes the effectiveness of treatment, but also reduces the risk of complications from both corticosteroids and immunosuppressants (in particular, severe leukopenia).

To combat edema and arterial hypertension, antihypertensive drugs, hypothiazide (50-100 mg/day), etc. are used. If signs of heart failure appear, diuretics and digitalis preparations are prescribed.

7. Chronic diffuse glomerulonephritis

Chronic diffuse glomerulonephritis is a long-term (at least a year) immunological bilateral kidney disease, in which changes in the urine persist without significant changes for over a year or edema and hypertension are observed for over 3-5 months. This disease ends (sometimes after many years) with the shrinking of the kidneys and the death of patients from chronic renal failure. Chronic glomerulonephritis can be either the outcome of acute glomerulonephritis or primary chronic, without a previous acute attack.

Etiology, pathogenesis. See Acute glomerulonephritis.

Clinic. As with acute glomerulonephritis: edema, arterial hypertension, urinary syndrome and impaired renal function. During chronic glomerulonephritis, two stages are distinguished:

1) renal compensation, i.e. sufficient nitrogen excretion function of the kidneys (this stage may be accompanied by a pronounced urinary syndrome, but sometimes it is latent for a long time, manifesting only a slight albuminuria or hematuria);

2) renal decompensation, characterized by insufficiency of the nitrogen-excreting function of the kidneys (urinary symptoms may be less significant; high arterial hypertension is observed, edema is often moderate; at this stage, hypoisosthenuria and polyuria are expressed, which end in the development of azotemic uremia).

The following clinical forms of chronic glomerulonephritis are distinguished.

1. Nephrotic form - the most common form of primary nephrotic syndrome. This form, in contrast to pure lipoid nephrosis, is characterized by a combination of nephrotic syndrome with signs of inflammatory kidney damage. The clinical picture of the disease can be determined by the nephrotic syndrome for a long time, and only later does the progression of glomerulonephritis itself occur with a violation of the nitrogen excretion function of the kidneys and arterial hypertension.

2. Hypertensive form. Arterial hypertension predominates among the symptoms, while urinary syndrome is less pronounced. Occasionally, chronic glomerulonephritis develops according to the hypertensive type after the first violent attack of glomerulonephritis, but more often it is the result of the occurrence of a latent form of acute glomerulonephritis. Blood pressure reaches 180/100-200/120 mm Hg. Art. and may be subject to large fluctuations during the day under the influence of various factors. Hypertrophy of the left ventricle of the heart is broken, an accent of the second tone is heard over the aorta. Hypertension does not become malignant; blood pressure, especially diastolic blood pressure, does not reach high levels. Changes in the fundus of the eye in the form of neuroretinitis are observed.

3. Mixed form. In this form, there are simultaneously nephrotic and hypertensive syndromes.

4. latent form. This is a fairly common form; It usually manifests itself only as a mild urinary syndrome, without arterial hypertension and edema. It can have a very long course (10-20 years or more), later leading to the development of uremia. The hematuric form should also be distinguished, since in some cases chronic glomerulonephritis can manifest as hematuria without significant proteinuria and general symptoms (hypertension, edema). All forms of chronic glomerulonephritis can periodically produce relapses that resemble or completely repeat the picture of the first acute attack of diffuse glomerulonephritis. Exacerbations are often observed in autumn and spring and occur 1-2 days after exposure to an irritant, most often a streptococcal infection. In any course, chronic diffuse glomerulonephritis passes into the final stage - a secondary wrinkled kidney.

Diagnosis. It is established on the basis of a history of acute glomerulonephritis and the clinical picture. However, in the latent form, as well as in the hypertensive and hematuric forms of the disease, its recognition can be difficult. If the history does not have specific indications of acute glomerulonephritis, then with moderately severe urinary syndrome, differential diagnosis is carried out with one of many unilateral or bilateral kidney diseases.

Differential diagnosis. When differentiating hypertensive and mixed forms of chronic glomerulonephritis with hypertension, it is important to determine the time of onset of urinary syndrome in relation to the onset of arterial hypertension. In chronic glomerulonephritis, urinary syndrome long precedes arterial hypertension or occurs simultaneously with it. Chronic glomerulonephritis is characterized by less severe cardiac hypertrophy, less propensity to hypertensive crises (with the exception of exacerbations occurring with eclampsia) and rare or less intense development of atherosclerosis, including the coronary arteries.

In favor of the presence of chronic glomerulonephritis in differential diagnosis with chronic pyelonephritis, the predominance of erythrocytes over leukocytes in the urine sediment, the absence of active and pale leukocytes when stained according to Sternheimer - Mapbin, the same size and shape of the two kidneys and the normal structure of the pelvis and calyces, which is detected by X-ray examination . The nephrotic form of chronic glomerulonephritis should be differentiated from lipoid nephrosis, amyloidosis, and diabetic glomerulosclerosis. In the differential diagnosis of amyloidosis of the kidneys, the presence in the body of foci of chronic infection and amyloid degeneration of another localization is important.

Treatment. It is necessary to eliminate foci of infection (removal of tonsils, sanitation of the oral cavity, etc.). Long-term dietary restrictions (salt and protein). Patients with chronic nephritis should avoid cooling, especially exposure to damp cold, and a dry and warm climate is recommended. If the general condition is satisfactory and there are no complications, sanatorium treatment is indicated. Bed rest is necessary only during the period of significant edema or the development of heart failure, with uremia. For the treatment of patients with chronic glomerulonephritis, diet is of great importance, which is prescribed depending on the forms and stage of the disease. In nephrotic and mixed forms (there is edema), the intake of sodium chloride from food should not exceed 1,5-2,5 g per day, and stop adding salt to food. With sufficient excretory function of the kidneys (no edema), food should contain a sufficient amount of animal protein, rich in complete phosphorus-containing amino acids, which normalizes nitrogen balance and compensates for protein losses.

In the hypertensive form, it is recommended to moderately limit the consumption of sodium chloride to 3-4 g per day with a normal content of proteins and carbohydrates in the diet. The latent form of the disease does not require large restrictions in the diet of patients; it must be complete, varied and rich in vitamins. Vitamins (C, B complex, A) should be included in the diet for other forms of chronic glomerulonephritis. The basis of pathogenetic therapy for this disease is the prescription of corticosteroid drugs. For the course of treatment, 1500-2000 mg of prednisone is used, then the dose is gradually reduced. It is recommended to carry out repeated courses of treatment during exacerbations or small maintenance courses. While taking corticosteroid hormones, an exacerbation of hidden foci of infection is possible, and therefore antibiotics are prescribed simultaneously or after removal of foci of infection (for example, tonsillectomy). A contraindication to the use of corticosteroids in chronic glomerulonephritis is progressive azotemia.

For moderate arterial hypertension (BP 180/110 mm Hg), antihypertensive drugs are added to treatment. In case of high arterial hypertension, a preliminary reduction in blood pressure is required. If corticosteroid therapy is contraindicated or if it is ineffective, the use of non-hormonal immunosuppressants is recommended. These are drugs of the 4-aminoquinoline series - hingamine (delagil, resokhin, chloroquine), hydroxychloroquine (plaquenil). In mixed forms of chronic glomerulonephritis (edematous and severe hypertensive syndromes), the use of natriuretics is indicated, as they have a diuretic and hypotensive effect. Hypothiazide is prescribed 50-100 mg 2 times a day, Lasix 40-120 mg per day, ethacrynic acid (uregit) 150-200 mg per day. It is better to combine saluretics with the aldosterone antagonist aldactone (veroshpiron) - 50 mg 4 times a day, which increases sodium excretion and reduces potassium excretion. The diuretic effect is accompanied by the release of potassium in the urine, which leads to hypokalemia with the development of general weakness, adynamia and impaired cardiac contractility. Therefore, a solution of potassium chloride is prescribed at the same time.

In the treatment of the hypertensive form of chronic glomerulonephritis, antihypertensive drugs used in the treatment of hypertension (reserpine, adelfan) should be prescribed. However, sharp fluctuations in blood pressure and its orthostatic fall should be avoided, which can worsen renal blood flow and the filtration function of the kidneys.

Author: Gavrilova N.V.

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