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LECTURE No. 15. PATHOPHYSIOLOGY OF THE KIDNEY Causes causing impaired renal function: 1) disorders of the nervous and endocrine regulation of renal function; 2) impaired blood supply to the kidneys (atherosclerosis, shock); 3) infectious kidney diseases (pyelonephritis, focal

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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) abnormalities 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 neurogenic bladder syndrome;

2) disorders of differentiation of the renal structure:

a) with cysts;

b) without cysts;

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

4) tubopathies;

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

6) nephro- and uropathy due to chromosomal diseases;

7) amyloidosis;

8) embryonal 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 to the kidneys and urinary organs;

7) urolithiasis;

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

Pyelonephritis is a nonspecific infectious kidney disease that affects the renal parenchyma, mainly affecting interstitial tissue. Causes: infection, urodynamic disorders, 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 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 diagnosed on the basis of anamnesis indicating a recent acute purulent process or the presence of chronic diseases, clinical and laboratory data. A blood test reveals neutrophilic leukocytosis, anemia, aneosinophilia, and increased ESR. Urinalysis revealed leukocyturia, pyuria with moderate proteinuria and hematuria. In the Zimnitsky test - a decrease in urine density during the day. The Nechiporenko test shows leukocytosis. In a biochemical blood test - an increase in the content of sialic acids, creatinine, urea, and the appearance of C-reactive protein. A survey X-ray reveals an increase in volume of one of the kidneys; excretory urography reveals a sharp limitation of the mobility of the affected kidney during breathing, the absence or later appearance of a shadow of the urinary tract on the affected side. Ultrasound examination of the kidneys and excretory pyelography are prescribed to identify changes in the pyelocaliceal system. With voiding urethrography, anatomical and functional features and the presence of reflux are revealed.

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, with 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.

Chronic pyelonephritis can be a consequence of untreated acute pyelonephritis, that is, it can occur without acute symptoms 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 diagnosed on the basis of medical history, clinical and laboratory data. A blood test reveals neutrophilic leukocytosis. In a urine analysis, the predominance of leukocytes over other formed elements of urine is determined in the urine sediment. 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 100,000, then it is necessary to determine their sensitivity to antibiotics and chemotherapy. 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 concentrating ability of the kidneys is impaired early, while the nitrogen excretory function is maintained for many years. With infusion urography, a decrease in the concentrating ability of the kidneys, delayed release of a radiopaque substance, local spasms and deformations of the calyces and pelvis are initially determined. Subsequently, the spastic phase is replaced by atony, the calyces and pelvis dilate.

At 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), 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 vasorenal hypertension.

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

In case of ineffectiveness of these drugs or exacerbations of the disease, broad-spectrum antibiotics are used. The prescription of an antibiotic should each time be preceded by determining the sensitivity of the microflora to it.

Glomerulonephritis, an immunoallergic disease with predominant damage to the glomerular vessels, occurs 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 urinary syndrome;

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

Acute glomerulonephritis is a cyclical infectious-allergic kidney disease that often develops 1 to 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.

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, enlarged 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, hypertensive 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 suffered 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 can be 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. Rehberg and McClure-Aldrich tests are 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 to 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.

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 smaller 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.

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 to 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 excretory function of the kidneys (this stage may be accompanied by severe urinary syndrome, but sometimes it is latent for a long time, manifested only by slight albuminuria or hematuria);

2) renal decompensation, characterized by insufficiency of nitrogen excretory 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 for a long time by nephrotic syndrome, and only later does glomerulonephritis itself progress with impaired nitrogen excretory 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 can 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 the 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.

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

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

TECHNOLOGICAL DISCIPLINE MAP: “Pediatrics with childhood infections”. TOPIC: “Pyelonephritis in children”. OBJECTIVES: educational: to provide the necessary knowledge about the characteristics of the course of diseases of the urinary system in children; causes, pathogenesis, clinic, diagnosis, treatment of acute pyelonephritis in children, rehabilitation, medical examination, sanatorium and resort treatment of children who have suffered pyelonephritis. LECTURE TYPE: introductory, current. TYPE OF LECTURE: informational, multimedia. VENUE: Yelets Medical College. INTER-SUBJECT RELATIONS: anatomy, pharmacology, fundamentals of nursing, therapy, Latin, skin and venereal diseases, a healthy person and his environment, infectious diseases. EQUIPMENT: lecture notes, glossary. HOMEWORK: lecture notes.

1. 2. 3. 4. Plan Definition of pyelonephritis, etiology, main clinical manifestations. Principles of treatment of pyelonephritis, features of caring for a sick child. Diet therapy. Diagnostics, prognosis. Basic measures to prevent relapse of the disease.

Pyelonephritis is classified as an infection of the upper urinary tract, characterized by the development of a nonspecific inflammatory process in the pyelocaliceal system, interstitial tissue and renal tubules. A characteristic feature of pyelonephritis is that the inflammatory process can be one-sided.

Etiopathogenesis Pyelonephritis is a polyetiological pathology: bacteria, viruses, mycoplasma, fungi of the genus Candida, chlamydia, ureaplasma, etc. The leading role in infection belongs to E. coli. Less common: Proteus, enterococci, Klebsiella, Pseudomonas aeruginosa, staphylococcus, streptococcus or associations of pathogens.

Routes of infection of the urinary tract and kidney: Ø ascending, Ø hematogenous. The main role is played by the ascending pathway: predominantly gram-negative bacteria of the intestinal flora. Factors contributing to the development of the inflammatory process: § high virulence of bacteria, § impaired passage (outflow) of urine, § weakening of protective immune mechanisms.

Risk factors for developing the disease. congenital anomalies of the kidneys and urinary tract (promoting stagnation of urine); acute respiratory and intestinal infections, vulvovaginitis; constitutional anomalies (allergic diathesis); decreased immunity; metabolic disorders, increased excretion of salts (oxalates, urates, phosphates); chronic foci of infection; frequent hypothermia.

The mechanism of development of pyelonephritis. With a decrease in immunity, under the influence of provoking factors and a massive and quite active infection, an inflammatory process occurs in the interstitial tissue of the kidneys. Ascending infection of the kidneys is usually associated with reflux (reverse flow). Reflux is a pathological phenomenon that occurs as a result of anatomical defects (more than 100 of them have been described), which create an obstacle to the natural flow of urine and lead to disturbances in urodynamics.

A certain role in the mechanism of development of pyelonephritis is given to immunopathological processes. Ascending infection and interstitial inflammation primarily damage the renal medulla (the part that includes the collecting ducts and part of the distal tubules). The death of these segments of the nephron also disrupts the condition of those sections of the tubules that are located in the cortex of the kidney. The inflammatory process, moving to the cortex, disrupts the function of the glomeruli for the second time, and then renal failure may develop.

The main clinical manifestations of pyelonephritis are symptoms of intoxication: hectic fever (39 -40°C), chills, headache, sleep disturbance, weakness, lethargy, increased fatigue, decreased appetite; pain syndrome: pain and muscle tension in the lumbar region and along the ureters; positive Pasternatsky symptom (in older children);

dysuric syndrome: painful frequent urination, frequent urge (sometimes unsuccessful) to urinate, which is often accompanied by itching of the perineum or a burning sensation (urinary incontinence is often noted in young children); urinary syndrome: impaired urine clarity (cloudy with sediment and flakes), high leukocyturia (leading symptom), bacteriuria (more than 50-100 thousand microbial bodies in 1 ml of urine), proteinuria (from traces of protein to 2 mmol/l).

Features of the course of pyelonephritis in newborns and children in the first months of life: acute onset, severe course, high fever (sometimes reaching 39 -40°C), rapidly increasing symptoms of intoxication; meningeal symptoms are possible; dyspeptic syndrome: nausea, vomiting, sometimes loose stools; dysuric phenomena are mild.

Laboratory and instrumental diagnostic methods: 1. Clinical blood test (moderate anemia, increased ESR, leukocytosis). 2. General urine analysis (leukocyturia, bacteriuria). 3. Urinalysis according to Nechiporenko (leukocytes more than 2,000 per 1 ml). 4. Urinalysis according to Addis-Kakovsky (leukocytes more than 2,000 per day). 5. Increased titer of serum antibodies to bacteria isolated from urine.

6. Immunofluorescence bacterioscopy (if urine microbes are surrounded by antibodies, then this is a reliable sign of pyelonephritis). 7. Zimnitsky test (decreased ability for osmotic concentration - maximum urine density below 1020). 8. Ultrasound of the kidneys. 9. Contrast urography. 10. Renoscintigraphy.

Basic principles of treatment of pyelonephritis. 1. Bed rest for the period of fever. 2. Diet therapy (milk-vegetable without irritating and extractive dishes, in the first days with a moderate restriction of protein and salt to 2-3 g per day). 3. Monitor the administration of a sufficient amount of fluid, recommend drinking cranberry and lingonberry juice and herbal infusions in the intervals between taking medications.

4. Antibiotic therapy: ampicillin, carbenicillin, tseporin, chloramphenicol or their combinations (taking into account the nephrotoxicity of the drugs and the sensitivity of the urine microflora to them). In case of persistent and severe cases, they resort to the prescription of aminoglycosides (gentamicin), the course is from 10 to 14 days. 5. Preparations of the nitrofuran series (furagin, furadonin), nalidixic acid (nevigramon, negram), oxolinic acid (gramurin), nitroxoline (5-NOK) for 10-14 days, uroseptic or sulfonamide drugs, courses of treatment for 5-7 days.

6. Herbal medicine: infusions of herbs and berries that have diuretic, antiseptic, and anti-inflammatory effects. 7. Vitamin therapy. 8. During the period of remission, sanatorium treatment is indicated. 9. Sanitation of chronic foci of infection. Prognosis of the disease. Pyelonephritis, if it is not associated with congenital pathology, can be treated successfully. With congenital pathology, the disease is characterized by a relapsing course. However, timely surgical correction can lead to recovery.

Prevention. 1. Compliance with hygienic rules for caring for children (especially girls). 2. Prevention of acute respiratory viral infections and intestinal diseases. 3. Prevention and treatment of helminthic infestation. 4. Timely sanitation of chronic foci of infection. 5. General strengthening measures (hardening, massage, exercise therapy, rational regimen). 6. Conducting urine tests after any infectious disease. 7. “D” observation for 3 years from the beginning of clinical and laboratory remission, to prevent relapses of the disease, monitor the state of kidney function, urine tests, dietary regimen and physical activity.

Questions for self-study: 1. Define pyelonephritis. 2. What are the causative factors for the development of pyelonephritis? 3. What are the main clinical manifestations of pyelonephritis? 4. What are the features of the clinical course of 5. pyelonephritis in newborns and young children 6. of age? 7. What are the basic principles of treatment of pyelonephritis? 8. What is the prognosis for pyelonephritis? 9. What measures need to be taken to prevent relapse of diseases?

Diseases of the kidneys and urinary tract are detected in 3-4% of children. In addition to the high proportion in the structure of diseases, the pathology of the urinary system attracts attention due to the seriousness of the prognosis. Delayed recognition of the disease and late treatment often underlie the progression of the pathological process and the development of chronic renal failure, which leads to retarded growth and development of the child, disability, and reduced life expectancy. Diseases of the urinary system in adults are often a continuation of an illness that began in childhood.

All diseases of the urinary system in children can be divided into 2 large groups: the first is hereditary and congenital diseases, the second is acquired pathology.

Nephropathies of the first group are of great importance in pediatrics: they are registered more often in children than in adults (due to the short life expectancy of patients). The most common findings include structural anomalies in the development of the kidneys and urinary tract, anomalies in the structure and location of the renal vessels, as well as the innervation of the organs of the urinary system with neurogenic bladder syndrome.

Of the variety of nephropathies of the second group observed in children, urinary infection predominates. In terms of frequency, it ranks second in the structure of childhood diseases, second only to respiratory tract infections (WHO data).

URINARY INFECTION

Urinary infection is an inflammatory process caused by microorganisms and localized in any part of the mucous membrane of the urinary tract (in the urethra, bladder, pelvis, calyces) or throughout its entire length.

The diagnosis of “urinary infection” is valid in young children, since due to their lack of maturity and differentiation

kidney tissue (and all urinary tract), as well as reduced immunity (age-related physiological feature), the inflammatory process is not limited to one part of the urinary tract. Children 1.5-2 years old do not have only urethritis, cystitis or pyelitis. At this age, cystopyelonephritis is diagnosed in acute cases. In older children, the term “urinary infection” is used as a temporary diagnosis at the time of examination, and after determining the level of damage to the urinary tract, the diagnosis is replaced with another, more specific one.

Urinary infections are especially common in children under 3 years of age. The second peak of the disease occurs over the age of 20 years. Among newborns and children in the first months of life, boys and girls get sick with the same frequency, which confirms the hematogenous route of infection and emphasizes the role of developmental anomalies of the urinary system, developing with equal frequency in both sexes. At older ages, mostly girls are affected.

Most often, acute urinary infection occurs in the form of pyelonephritis (primary non-obstructive and secondary obstructive) or cystopyelonephritis. Less commonly observed are its forms such as cystourethritis and cystitis.

Etiology

The most common inflammatory process in the organs of the urinary system is caused by Escherichia coli (uropathogenic strains), the sources of infection are the intestines (especially in children with dysbacteriosis) and the periurethral area. The emergence and further development of infection is facilitated by helminthic infestations and inflammatory diseases of the external genital organs. Microorganisms, due to the presence of fimbriae on their surface, are fixed on the mucous membrane of the urinary tract, which prevents their elimination with the urine stream. The most pathogenic for the urinary tract are E. coli that have a capsule (C-Ag). It is assumed that C-Ags have low immunogenicity, so the human immune system does not recognize them actively enough, which leads to long-term persistence of bacteria.

Pathological processes in the urinary tract and kidneys can also be caused by Proteus, Pseudomonas aeruginosa and other gram-negative microorganisms; less commonly, gram-positive microbes become the cause. Among the latter, Staphylococcus aureus is more often found, entering the kidneys hematogenously from inflammatory foci, for example, with purulent omphalitis in a newborn, abscess pneumonia or purulent-inflammatory skin diseases. An etiological role is also assigned to intracellular microorganisms (chlamydia, mycoplasma), which have a high tropism for

epithelial cells of the genitourinary tract. Enterococci and viruses are of some importance. Infection with viruses often contributes to the persistence of bacterial infection.

Pathogenesis

The infectious agent can enter the kidney through the hematogenous and ascending (urinogenic) route, as well as lymphogenously, through the lymphatic vessels coming from the bladder along the ureters (not everyone recognizes the possibility of penetration through this route). The hematogenous route is most typical for newborns and children in the first months of life. In older children, the ascending route becomes of primary importance when infection occurs from the lower urinary tract per continuitatem. Girls are affected more often than boys, since girls have a wider and shorter urethra. Hygienic care for the child is of great importance.

The penetration of infection from the bladder into the overlying parts of the urinary tract and kidney is facilitated by vesicoureteral reflux (reverse reflux of urine), which occurs as a result of insufficiency of the intramural valve mechanism of the ureters or vesicoureteral anastomosis (Fig. 17-1 inset). Neurogenic bladder dysfunction may also be important. The development of pyelonephritis is also facilitated by disturbances in the outflow of urine that accompany some congenital malformations of the urinary system (Fig. 17-2, 17-3, 17-4 on the inset) or urolithiasis. Above the obstacle, under the influence of microorganisms, urea decomposes with the formation of ammonia, which inactivates C4 and other complement components, resulting in a violation of local immunoresistance to infection. At the same time, venous stagnation develops, lymphatic drainage is impaired, intrarenal pressure increases, while renal blood flow decreases, which contributes to a more rapid development of inflammation and dysfunction of the organ.

The development of pyelonephritis is promoted not only by gross structural anomalies in the structure of the urinary system, reflux and stones that interfere with the passage of urine. Predisposing factors may be:

Structural and functional immaturity of the urinary tract and tubular nephron in newborns and children in the first months of life;

Infectious process in the mother during pregnancy, late gestosis;

Severe gastrointestinal disorders with exicosis and hypokalemia; inflammation of the external genitalia (vulvitis,

vulvovaginitis, balanoposthitis); pneumonia; malnutrition; rickets; hypervitaminosis D (in children of the first years of life), helminthic infestations, the presence of foci of chronic infection.

An important role is played by hereditary metabolic disorders, enzymopathies and dysplasia of the epithelium of the tubular nephron. Favorable conditions for the development of the disease are created by metabolic disorders accompanied by increased urinary excretion of oxalates, urates, phosphates, cystine and calcium.

Along with the listed factors, the immunological reactivity of the body and local cellular defense factors are of great importance in the development of pyelonephritis.

The renal cortex and medulla have varying resistance to microbial invasion. Infection of the medulla occurs more often, since the blood flow in it is less intense and local immunological protection is lower (this is where the inactivation of most of the complement C4 fraction occurs). Bacteria multiply faster in the kidney medulla, so inflammation that begins in the interstitial tissue of the kidneys very quickly spreads to the elements of the nephron located there (loop of Henle, collecting ducts). Damage to the tubules in areas of inflammation with a violation of their integrity leads to the entry of microorganisms and leukocytes into the urine. Spreading, the process captures the distal and then the proximal tubules. Gradually it leads to hyalinosis and sclerosis of arterioles and small arteries of the interstitium, and then to the destruction of the nephron. With a urinary tract infection, this is manifested first by a deterioration in tubular function (decreased concentrating ability of the kidney), and then by impaired glomerular function with the development of hyperazotemia. An increase in residual nitrogen, urea and blood creatinine in patients with chronic pyelonephritis indicates advanced structural disorders in the kidneys and chronic renal failure.

Acute pyelonephritis

Acute pyelonephritis is an acute nonspecific exudative inflammation of the kidney tissue and pyelocaliceal system with severe fever, pain, pyuria and impaired renal function.

Clinical picture

The leading syndromes of the disease in older children in the acute period are reflected in Table. 17-1.

Table 17-1.Leading syndromes of acute pyelonephritis in older children

Features of the clinical picture of acute pyelonephritis in young children, in particular the predominance of extrarenal symptoms, are due to the morphological immaturity of the urinary system and the tendency to generalize the inflammatory process. The disease begins with hyperthermia, increasing signs of toxicosis and exicosis. A rapid onset is especially typical for children with posthypoxic encephalopathy. The excitement characteristic of the first days of illness quickly gives way to adynamia. Phenomena of meningism are possible. The child’s body weight decreases due to severe anorexia, persistent regurgitation and vomiting, and loose stools. Dyspeptic symptoms may prevail over dysuric ones. Sometimes, if you carefully observe your child, you may notice anxiety before or during urination. In general, the clinical picture of acute urinary infection in young children resembles sepsis and is accompanied by changes not only in the kidneys, but also in the liver, adrenal glands and central nervous system.

Remitting fever, sometimes with chills and sweating, lasts about a week. Over the next 1-2 weeks, all manifestations gradually disappear. If the disease drags on for more than 3 months or recurs, the diagnosis of acute pyelonephritis should be reconsidered in order to exclude an exacerbation of the chronic process.

Complications.Complications include sepsis, apostematous nephritis (interstitial nephritis, characterized by the formation of multiple purulent foci, especially in the renal cortex), renal carbuncle, paranephritis, pyonephrosis and necrosis of the renal papillae. Complications are more common in young children.

Laboratory research

Pathological inclusions in the urine are most characteristic of pyelonephritis. It often becomes cloudy and may contain a small amount of protein. The sediment contains many leukocytes, sometimes leukocyte casts, a large number of epithelial cells, there may be red blood cells, possible hematuria (with papillary necrosis) or clots of fresh blood, indicating an acute inflammatory process in the bladder. Leukocytes are usually represented by neutrophils. Almost always, a large number of microorganisms are detected (50,000-100,000 microbial bodies in 1 ml, taken from the average portion of excreted urine - a reliable sign of a bacterial inflammatory process in older children, 10,000 microbial bodies in 1 ml - in the younger age group ).

Blood tests reveal moderate anemia, leukocytosis with a shift in the leukocyte formula to the left, an increase in ESR, C-reactive protein concentration, and dysproteinemia. The parameters of the immune system change: the number of T- and B-lymphocytes, Ig content. An increased titer of serum antibodies to bacteria isolated from urine is determined.

Diagnostics

Diagnosis of acute pyelonephritis is especially difficult in young children. Acute pyelonephritis must be excluded in any child in the first years of life with unmotivated fever, intoxication and dyspeptic symptoms. In older children, in typical cases, they are guided by a combination of signs such as fever, dysuria and pain in the lower back or abdomen. The main symptoms are changes in urine (leukocyturia and bacteriuria). The diagnosis should contain the following information.

Determination of the pathogenetic essence of the process (primary or secondary pyelonephritis) indicating the factors predisposing to its development (developmental anomalies, reflux, stones, metabolic disorders, etc.).

Period of the disease (active, reverse development of symptoms, complete clinical and laboratory remission).

State of kidney function.

The presence or absence of complications.

If pyelonephritis is suspected, an ultrasound of the urinary system is required to clarify the size, position, features of the anatomical structure of the kidneys (doubling, hypoplasia, etc.) and the state of the collecting system, possible detection of stones in the kidneys or bladder, and assessment of renal blood flow.

Differential diagnosis

Acute pyelonephritis is primarily differentiated from acute glomerulonephritis, which occurs not during the acute period of a bacterial or viral disease, but 2-3 weeks after a streptococcal infection. Glomerulonephritis almost always develops against the background of already normal body temperature and is rarely accompanied by dysuric disorders. Swelling or pastiness of tissues, arterial hypertension, observed in most patients with glomerulonephritis, are also not characteristic of pyelonephritis. Oliguria in the initial period of glomerulonephritis contrasts with polyuria, often detected in the first days of acute pyelonephritis. With glomerulonephritis, hematuria predominates, slight leukocyturia (lymphocyturia) is possible, casts are detected in the urine sediment. There is no bacteriuria. A decrease in the concentrating ability of the kidneys (in the Zimnitsky test, the maximum density of urine is below 1.020 with diuresis less than 1000 ml/day), ammoniagenesis and acidogenesis are combined in pyelonephritis with normal creatinine clearance (in glomerulonephritis the latter is reduced).

In addition, it is necessary to carry out a differential diagnosis of acute pyelonephritis with sepsis (if pyelonephritis is not a consequence of sepsis), as well as acute appendicitis, which, with an atypical location of the appendix, can be accompanied by dysuric phenomena in the absence of symptoms of peritoneal irritation. In the latter case, research is of great importance to establish the correct diagnosis. per rectum, allowing to identify a painful infiltrate in the right iliac region, and repeated urine tests. If there is a persistent absence of bacterial flora in the urine, testing for mycobacteria is indicated.

In each case of acute urinary infection, it is extremely important to resolve the question: is the pathological process limited to the lower urinary tract or spreads to the pelvis and tubulointerstitial tissue of the kidneys, i.e. define the disease as pyelonephritis, cystopyelonephritis or cystitis. Pyelonephritis is much more severe than cystitis. In addition, with cystitis, there are no changes in the urine that are considered absolute signs of pyelonephritis: leukocyte casts; high activity of enzymes characteristic of tubular epithelium and high concentration b 2 - microglobulins; the presence of bacteria coated with AT (detected using fluorescence microscopy). Unlike cystitis, pyelonephritis is accompanied by an increase in the titer of antibacterial antibodies in the blood serum, a decrease in the concentrating ability of the kidneys, ammoniagenesis and acidogenesis.

Treatment

Treatment is aimed at combating the infectious process, intoxication, restoring urodynamics and kidney function, and increasing the body’s reactivity.

In the acute period, bed rest is necessary, especially with high body temperature, chills, severe intoxication, dysuric disorders and pain. A diet is prescribed with a limitation of extractive substances excreted by the tubular epithelium and having an irritating effect (pepper, onion, garlic, saturated broth, smoked meats, coffee, etc.). In order to speed up diuresis, it is advisable to include fresh fruits and vegetables with diuretic properties in the diet (watermelons, melons, zucchini, cucumbers). It is recommended to increase fluid intake by 50% compared to the age norm. Transfusion, rehydration and detoxification therapy are indicated for young children, as well as older children with severe disease.

All patients with acute pyelonephritis are prescribed antibiotics. In severe cases of the disease, therapy begins with parenteral administration of antibacterial drugs (preferably bactericidal). For most patients, initial antibiotic therapy is prescribed empirically, since the results of bacteriological examination and determination of the sensitivity of microbial flora can be obtained only after 48-72 hours, and therapy should be started immediately. If there is no effect of treatment, after 3 days of empirical therapy, it is corrected by changing the antibiotic in accordance with the antibiogram. For empirical (starting) antibacterial therapy in the acute period of the disease with severe and moderate course, the following drugs can be used (Table 17-2).

“Protected” penicillins (amoxicillin + clavulanic acid, ampicillin + sulbactam).

II generation cephalosporins (cefuroxime, etc.).

III generation cephalosporins (cefotaxime, etc.).

IV generation cephalosporins (cefpirome, etc.).

Aminoglycosides (amikacin, etc.).

The drugs are administered parenterally, and as the activity of the process decreases, they are prescribed orally. When sepsis develops or to influence intracellular microorganisms (chlamydia, mycoplasma, ureaplasma), combinations of antibiotics and macrolides are used. Fluoroquinolones are allowed to be prescribed, including to children of a younger age group, both as monotherapy and in combination with antibiotics.

Table 17-2.Empirical antibacterial therapy for severe forms of pyelonephritis

Drugs of choice

Protected penicillins + aminoglycosides III-IV generation cephalosporins + aminoglycosides Carbapenems

Piperacillin + tazobactam Ticarcillin + clavulanic acid

Fluoroquinolones*

Vancomycin**+3-IV generation cephalosporins Vancomycin**+amikacin

According to Korovina N.A., 2002; * fluoroquinolones are used for health reasons; ** vancomycin is used for confirmed staphylococcal or enterococcal etiology of the disease.

After a course of antibiotics (7-14 days), uroseptics are prescribed. From the group of nitrofurans, furazidin is most often used at a dose of 5-8 mg/day. When the activity of the process decreases, the drug can be prescribed once a day at night in the amount of half the daily dose. Nalidixic acid (60 mg/kg/day), oxolinic acid (20-30 mg/kg/day), pipemidic acid (15 mg/kg/day), nitroxoline (8-10 mg/kg/day) are also used.

The duration of treatment for acute pyelonephritis is 1-3 months - until the urine is completely sanitized. After antibacterial therapy, you can prescribe herbal teas with antiseptic, regenerative and diuretic properties. Alkaline mineral water is shown (“Smirnovskaya”, “Essentuki 20”, etc.).

Forecast

The prognosis for life is favorable, recovery occurs in 80% of cases. Lethal outcomes are rare, mainly in young children with the development of complications such as sepsis, apostematous nephritis, renal carbuncle, and inflammation of perinephric tissue. All children who have suffered acute pyelonephritis are monitored at a dispensary for at least 3 years with a monthly control urine test.

Chronic pyelonephritis

Chronic pyelonephritis is a progressive inflammation of the tissue and tubules of the kidneys, causing destructive changes in the pyelocaliceal system and wrinkling of the kidney. The disease is characterized by a long latent or recurrent course.

Chronic pyelonephritis usually develops as an outcome of an acute process. The transition of acute pyelonephritis to chronic is facilitated by factors leading to urostasis (dysplasia of the renal parenchyma, vesicoureteral reflux), cystitis, vulvovaginitis, altered reactivity of the child’s body and inadequate treatment of acute pyelonephritis. In some cases, chronic pyelonephritis develops gradually and does not have a clearly defined onset (primary chronic pyelonephritis).

Clinical picture

Clinical manifestations of the disease are less pronounced than in acute pyelonephritis, and depend both on the etiology and pathogenetic essence of the pathological process (primary, secondary), and on the characteristics of the course (manifest with relapses or latent).

In the manifest course of chronic pyelonephritis with relapses, periodically recurring episodes of exacerbations alternate with more or less long asymptomatic periods. Relapses are often triggered by intercurrent diseases (usually ARVI). During relapse, symptoms of the disease and laboratory parameters are similar to acute pyelonephritis. Outside of exacerbation, the symptoms are quite sparse. Some children experience rapid fatigue, headache, pallor of the skin and visible mucous membranes, and asthenia, which reflects chronic intoxication. Changes in urine during this period become less distinct, the number of leukocytes in the sediment decreases significantly, and bacteriuria is often absent.

In the latent course of chronic pyelonephritis, there are no clinical manifestations, but changes in the urine (leukocyturia, bacteriuria) are detected. The diagnosis is made by accidental detection of leukocyturia, and sometimes bacteriuria, in children undergoing examination for preventive or other purposes. However, even in such cases, careful observation of the child makes it possible to detect signs of chronic intoxication.

Beginning in childhood, chronic pyelonephritis sometimes lasts for decades, manifesting itself in frequent or isolated rare episodes during certain periods of life (for example, during pregnancy). The rest of the time, these individuals consider themselves healthy. However, persistent infection in the renal tissue, slowly developing structural changes and nephrosclerosis ultimately lead to chronic renal failure and hypertension. In most observations, the process becomes apparent in adulthood, with advanced and already irreversible changes in the kidneys. In children, arteri-

Real hypertension as one of the signs of pyelonephritis is observed only in 1.5% of cases (for example, with already developed chronic renal failure). In adults, an increase in blood pressure occurs in 10-25% of cases already at the initial stage of the disease.

According to the European Association of Hemodialysis and Kidney Transplantation, chronic pyelonephritis ranks third as a cause of chronic renal failure in children, inferior in frequency to glomerulonephritis, hereditary and congenital nephropathies.

Diagnostics

Diagnosis of chronic pyelonephritis is often difficult, especially in cases of its latent course. Due to the paucity of changes in urine sediment, analyzes must be repeated using quantitative methods for calculating formed elements (Kakovsky-Addis, Nechiporenko tests). If necessary, they also resort to provocative tests (for example, use a prednisolone test). X-ray and radiological methods of examining patients are very informative.

With the help of excretory urography, it is possible to clarify the size, contours, location and mobility of the kidneys, the condition of the collecting system, ureters, bladder, as well as calculate the renocortical index and determine the correspondence of the kidney area to the child’s age.

Victory cystourethrography allows you to exclude or confirm the presence of reflux, intravesical obstruction and gives an idea of ​​the shape and size of the bladder, the condition of the urethra, the presence of diverticula and stones.

Cystoscopy determines the nature of changes in the mucous membrane of the bladder, anomalies of its development, the location and shape of the orifices of the ureters.

Radioisotope nephrography reveals predominantly unilateral disturbances in the secretion and excretion of the isotope by the proximal tubules and a decrease in renal plasma flow.

Dynamic nephroscintigraphy allows you to obtain information about the state of the functioning renal parenchyma. It is promising to examine urine for the presence of antibodies fixed to bacteria using RIF. Taking into account the possibility of developing chronic pyelonephritis as a complication of metabolic disorders or hereditary tubulopathy, the excretion of amino acids, phosphorus, oxalates and urates should be determined in each patient.

The diagnosis of chronic pyelonephritis (as well as acute) reflects the primary or secondary nature of the disease, the nature of the course

(recurrent, latent), period (active, partial or complete clinical and laboratory remission), functional state of the kidneys (preserved or impaired functions), stage of the disease (compensation, chronic renal failure). For this purpose, kidney function tests are carried out, acid-base balance, sodium, potassium, urea, and creatinine concentrations are determined in the blood.

Differential diagnosis

Differential diagnosis is carried out primarily with chronic cystitis. Due to the insignificant changes in urinary sediment in the asymptomatic course of chronic pyelonephritis, it is necessary to differentiate it from inflammation of the external genitalia (vulvitis, vulvovaginitis, balanoposthitis), for which a consultation with a pediatric gynecologist and urologist is prescribed, as well as examination of vaginal and urethral smears.

Great difficulties arise when distinguishing between chronic pyelonephritis in the terminal stage and chronic glomerulonephritis. In this case, it is necessary to exclude interstitial nephritis, which develops under the influence of nephrotoxic substances, kidney tuberculosis, tumors, especially with unilateral pyelonephritis. Data from the medical history, tuberculin tests, clinical and x-ray examination of the patient, and the results of a urine test for Mycobacterium tuberculosis are taken into account.

Treatment

In case of exacerbation of chronic pyelonephritis, hospitalization is indicated. Bed rest and diet are the same as for acute pyelonephritis (see section “Acute pyelonephritis”). Treatment measures for exacerbation of chronic pyelonephritis are the same as for the treatment of acute pyelonephritis. Drug therapy is aimed at eliminating the bacterial inflammatory process. It is carried out over a long period of time, systematically. In severe cases of pyelonephritis, combination antibacterial therapy is often used to expand the spectrum of antimicrobial action. Treatment is carried out until the pathogen is completely suppressed, with a change of antibiotic in case of ineffectiveness every 10-14 days. In case of chronic renal failure, the age-specific dose of the drug used is reduced by half or a third. After courses of antibiotic therapy, treatment is continued with uroseptics (see section “Acute pyelonephritis”), sometimes up to 6 months. Against the background of maximum activity of pyelonephritis, accompanied by a syndrome of endogenous intoxication, infusion therapy is indicated. The effectiveness of treatment of pyelonephritis developing against the background of metabolic disorders depends on timely correction

rations of nutrition, prescribing an appropriate drinking regime, and the use of means that normalize metabolic processes.

The presence of vesicoureteral reflux, which often underlies chronic pyelonephritis, requires lengthening the period of active treatment to 10-12 months. After this, if conservative therapy is unsuccessful, the question of surgical elimination of reflux is raised. If the symptoms of concomitant cystitis are pronounced, special treatment is prescribed (intravesical instillation of drugs, forced urination every 2.5-3 hours, physiotherapeutic procedures on the bladder area). In the intervals between taking medications, it is recommended to drink cranberry and lingonberry fruit drinks, and herbal medicine.

In case of a long-term recurrent course of chronic pyelonephritis, torpid to the therapy, when there is a suspicion of immunological failure of the macroorganism, it is necessary to include in the treatment complex drugs that affect the immune status. These include lysozyme and interferon alpha preparations.

Since pyelonephritis causes damage to cell membranes, the administration of antioxidants is justified. Vitamins A, E, B 6 and other drugs are used that help normalize lipid peroxidation. For chronic pyelonephritis, the use of antisclerotic agents (drugs of the aminoquinoline series) is indicated.

During the period of stable clinical and laboratory remission, children are prescribed hardening procedures (rubbing, swimming in indoor pools), massage, therapeutic exercises, and sanatorium-resort treatment.

Prevention

Prevention of infectious inflammation in the urinary system involves, first of all, compliance with hygienic care measures for children, especially girls. It is unacceptable for them to remain in diapers and diapers contaminated with feces for a long time. It is also important to prevent acute intestinal infections, helminthic infestations, as well as the elimination of chronic inflammatory foci and strengthening the body's defenses. It should be remembered that every child after any infectious disease must be given a urine test. In order to prevent the development of chronic pyelonephritis, acute urinary infection should be adequately treated.

All children suffering from chronic pyelonephritis are subject to constant medical supervision. Goals of clinical examination: prevention of relapses, monitoring urine tests and the state of renal functions, determining the dietary regimen and volume

physical activity, as well as the timing of preventive vaccinations. Examinations by an otolaryngologist and dentist are required once every 6 months. If an intercurrent disease occurs, anti-relapse treatment is prescribed.

Forecast

Recovery occurs in 25-33% of children with primary chronic pyelonephritis; in the rest, the pathological process persists. Arterial hypertension appears in children with an increase in nephrosclerotic changes, i.e. with the development of chronic renal failure (this occurs rarely, as a rule, with pyelonephritis with obstructive uropathy or dysmetabolic disorders). Exacerbations of the disease caused by intercurrent infections contribute to the progression of pyelonephritis, more rapid development of chronic renal failure and arterial hypertension.

GLOMERULONEPHRITIS

Glomerulonephritis is a heterogeneous group of acquired kidney diseases, different in etiology, clinical and morphological manifestations, course and outcome, predominantly of the nature of immune inflammation with primary damage to the glomeruli and secondary involvement of the renal tubules and interstitium in the pathological process. There are acute, rapidly progressive and chronic glomerulonephritis.

Etiology

Glomerulonephritis is divided into primary and secondary, developing with systemic diseases (SLE, Henoch-Schönlein purpura, polyarteritis nodosa, rheumatism, etc.).

Pathogenesis

The pathogenesis of glomerulonephritis involves reactions of humoral and cellular immunity, as well as non-immune mechanisms.

Immune complexes consisting of Ags and antibodies synthesized against them can form in the patient’s blood and then become fixed on the glomerular basement membrane. Another option is possible: Ag penetrates through the glomerular basement membrane by diffusion, followed by Ab, and immune complexes arise locally in situ. The resulting immune complexes activate the complement system in a classical or alternative way; the C3 component occupies a central place in the reaction. As a result, damage to the endothelium of the glomerular capillaries occurs, which leads to exudative-proliferative changes, platelet aggregation, activation of the coagulation and kallikrein-kinin blood systems, the development of local hypercoagulation and microthrombosis.

Cellular immune reactions also take part in the development of glomerulonephritis. T-lymphocytes secrete lymphokines that act in many parts of the immunopathological chain; a large number of inflammatory cells and activated complement components appear in the glomeruli (at the site of damage). Cells involved in the immune response release damaging factors: free radicals, proteases, platelet activating factor, vasoactive substances (for example, endothelial relaxing factor), IL1, TNF, platelet-derived growth factor, transforming growth factor, stimulating the proliferation of the glomerular intrinsic cells (mesangial cells). , endothelial, epithelial cells and podocytes). Simultaneously with proliferation, the synthesis of the extracellular matrix increases, which ultimately leads to the development of sclerosis - the morphological basis of chronic renal failure.

In some cases, glomerulonephritis develops when the body synthesizes autoantibodies against modified components of the glomerular basement membrane cells, i.e. The disease changes from an immune complex to an “autoantibody” one.

Non-immune mechanisms of glomerular damage include hemodynamic (systemic and intraglomerular hypertension) and metabolic disorders.

Several mechanisms are involved in the development of arterial hypertension in kidney disease.

Water-electrolyte imbalance (sodium and water retention).

Activation of pressor hormonal systems (renin-angiotensin aldosterone system).

Inhibition of depressor hormonal systems (renal Pg and kinins, endothelial relaxing factor). Metabolic disorders are caused by changes in lipid

metabolism, which is manifested by an increase in the content of total cholesterol, triglycerides, low-density lipoproteins, and non-esterified fatty acids. The nephrotoxic effect of lipids is associated with their deposition in the structures of the kidney, which causes proliferation of mesangial cells and promotes glomerulosclerosis.

Acute poststreptococcal glomerulonephritis

Acute glomerulonephritis is usually identified with the most studied post-streptococcal glomerulonephritis. Poststreptococcal glomerulonephritis is an immunocomplex disease with a cyclic course, etiologically associated with group A β-hemolytic streptococcus, clinically characterized by acute nephritic syndrome. Acute post-streptococcal glomerulonephritis is most often diagnosed at the age of 5-12 years, as well as in adolescents and young adults. Boys get sick more often than girls.

Etiology

The disease occurs after a streptococcal infection: tonsillitis, scarlet fever, acute respiratory tract infection. It is possible to develop acute post-streptococcal glomerulonephritis after otitis media, osteomyelitis or skin lesions (for example, impetigo, erysipelas). The disease is caused by nephritogenic strains of β-hemolytic streptococcus of group A, as evidenced by the high level of ASLO-O, antistreptohyaluronidase, antistreptokinase, and antibody titer to streptococcal M-protein in patients.

Pathogenesis

When infected with group A β-hemolytic streptococcus, the patient’s body begins to synthesize specific antibodies that interact with streptococcal Ag to form immune complexes. Since there is a similarity between streptococcal Ag and the own Ag structures of the glomeruli of the kidneys, antibodies synthesized in response to the presence of streptococcus also begin to interact with their own Ag. Damage to nephron structures occurs. Direct exposure to streptococcal toxins also leads to damage to kidney tissue and the synthesis of nephrocytotoxic autoantibodies and lymphocytes. The disease changes from immune complex to autoantibody. Pathological

changes in the kidneys characteristic of post-streptococcal glomerulonephritis are the result of immune autoaggression, inflammatory changes and allergic processes.

Pathomorphology

Acute post-streptococcal nephritis is characterized by a picture of endocapillary proliferative glomerulonephritis. According to electron microscopic examination, large deposits (deposits on the basement membrane in the form of humps) are a pathognomonic sign. Immunofluorescence studies detect complement components, mainly C3 and immunoglobulins.

Clinical picture

In typical cases, acute post-streptococcal glomerulonephritis develops 1-3 weeks after a sore throat or other streptococcal respiratory tract infection or 3-6 weeks after impetigo. There are two possible course of the disease: cyclic (typical) and acyclic (monosymptomatic). In typical cases, acute glomerulonephritis occurs cyclically with a successive change of three periods and is manifested by nephritic syndrome, including extrarenal (edema, increased blood pressure, changes in the heart and central nervous system) and renal (oliguria, hematuria, proteinuria, cylindruria) symptoms.

The child becomes lethargic, complains of headache, nausea, sometimes vomiting, pain in the lumbar region caused by stretching of the kidney capsule due to edema of the renal parenchyma. Thirst and swelling appear, and diuresis decreases. In the vast majority of children, urine becomes the color of meat slop, it can be brownish and even the color of black coffee. Sometimes the urine appears unchanged, but even in these cases, urine analysis reveals significant erythrocyturia. An increase in blood pressure (both systolic and diastolic) is almost always detected. Changes in the vessels of the fundus appear, hemorrhages and swelling of the optic disc are possible. Tachycardia is often detected, less often - bradycardia, muffled heart sounds, weakening of the first sound at the apex of the heart, and strengthening of the second sound above the aorta. The boundaries of relative dullness of the heart are expanding. In the first 3-7 days, an increase or stability of clinical symptoms and oliguria is observed, which is referred to as the initial period, or the period of developed manifestations.

The period of reverse development of symptoms: polyuria appears, edema and gross hematuria disappear, blood pressure normalizes. State

patients improve, drowsiness, nausea, and headache disappear, as edema of the central nervous system and spasm of cerebral vessels are relieved.

After about 1.5-2 months (sometimes later), urine values ​​return to normal. A period of complete clinical and laboratory remission begins. However, complete recovery, taking into account the involution of morphological changes in the kidneys, occurs much later - after 1-2 years. If individual clinical symptoms persist for more than 6 months, they speak of a protracted course of acute glomerulonephritis; the duration of symptoms for more than 1 year indicates a transition to chronic nephritis.

The acyclic course of acute glomerulonephritis is characterized by an isolated urinary syndrome, the absence of extrarenal manifestations, or they are so insignificant and short-lived that they go unnoticed.

Complications.With a rapid and severe course of acute nephritis in the initial period, life-threatening complications are possible: renal eclampsia, acute renal failure and acute heart failure.

The most common complication is eclampsia (angiospastic encephalopathy), caused by cerebral vasospasm and edema. Eclampsia manifests itself as tonic-clonic seizures. The attack resembles an epileptic seizure and is always accompanied by an increase in blood pressure. In the absence of timely adequate therapy, death from hemorrhage in the brain is possible.

AKI develops during the hyperergic course of acute glomerulonephritis, accompanied by a sharp reduction or cessation of urination. As a result, water, nitrogenous waste and potassium are retained in the body. Overhydration and metabolic acidosis develop. From the 3-5th day, oligoanuria is accompanied by dyspeptic disorders, hemorrhagic syndrome, signs of damage to the central nervous system and cardiovascular system. Severe anemia and leukocytosis are detected. The child falls into a uremic coma.

Acute cardiovascular failure occurs rarely in children. It is characterized by a sharp increase in the size of the liver, an increase in peripheral edema and the clinical picture of pulmonary edema (usually this is the cause of death of the patient).

Laboratory research

Laboratory examination of urine reveals proteinuria (up to 1-2 g/day, sometimes more), hematuria (from micro to macrohematuria), cylindruria (hyaline, granular and erythrocyte casts); in the first days of the disease, leukocyturia can be detected, pre-

produced mainly by lymphocytes and eosinophils and reflecting the immune inflammatory process in the glomeruli.

A general blood test revealed neutrophilic leukocytosis, possible eosinophilia, increased ESR, and anemia. A decrease in glomerular filtration, a slight increase in the content of nitrogenous wastes, dysproteinemia (an increase in the proportion ofα- and β -globulins), hypocomplementemia, acidosis. Serological blood tests reveal elevated titers of antistreptolysin-O, antistreptohyaluronidase, and antistreptokinase in most patients. In the first week of the disease, CEC and a decrease in the concentration of the C3 fraction of complement are detected. In the blood serum, the concentration of IgG, IgM, and rarely IgA increases.

Disturbances in the blood coagulation system reflect the following parameters: reduction in prothrombin time, increase in prothrombin index, decrease in antithrombin III content, inhibition of fibrinolytic activity, appearance of fibrin and fibrinogen degradation products in blood serum and urine.

Diagnostics

Edema or tissue pastiness, hematuria and arterial hypertension constitute a triad of clinical symptoms that serve as the main criterion for the diagnosis of acute glomerulonephritis. Difficulties in recognizing the disease arise when the disease is monosymptomatic or erased, when only proteinuria and/or microhematuria (isolated urinary syndrome) is detected in the child. In these cases, the diagnosis is helped by anamnesis data (previous diseases), as well as observation of the dynamics of the process and the results of additional studies, including determination of the titer of antistreptococcal antibodies and the concentration of complement components in the blood serum.

When formulating a diagnosis, one should indicate the clinical severity of acute glomerulonephritis (for example, with nephritic, nephrotic, isolated urinary syndrome, or with nephrotic syndrome, hematuria and arterial hypertension), the period of the disease, the state of renal function (impaired, without impairment) and complications.

Differential diagnosis

Acute glomerulonephritis should be differentiated from exacerbation of chronic nephritis, subacute, hereditary nephritis, acute pyelonephritis, renal tuberculosis, nephrolithiasis (radiocontrast examination helps to exclude the latter). To prevent an exacerbation of chronic nephritis from being mistaken for acute nephritis, it is necessary to carefully

It is important to collect an anamnesis, finding out whether the child has previously had edema, changes in urine, or high blood pressure. A decrease in the concentrating ability of the kidneys and changes in the fundus of the eye also speak in favor of exacerbation of chronic nephritis. Sometimes the issue of differential diagnosis is resolved through long-term observation of the child, and in some cases, the basis for diagnosis is a morphological examination of a kidney biopsy.

Treatment

Treatment of patients with acute diffuse glomerulonephritis is carried out in a hospital. In the acute period, bed rest, rest, and warmth are necessary to improve blood circulation in the kidneys, lower blood pressure, and reduce proteinuria and hematuria. The regimen is expanded as extrarenal symptoms are relieved (disappearance of edema, decrease in blood pressure). A special diet and dosed fluid intake are recommended. In the first days of illness, with oliguria and arterial hypertension, a salt-free table is prescribed. When blood pressure normalizes and edema disappears, salt is gradually added to food, starting from 0.5-1 g/day. The volume of fluid is calculated based on the urine output of the previous day. Limiting salt and water reduces the volume of extracellular fluid, which helps lower blood pressure. With oliguria and decreased glomerular filtration, protein is limited to 0.5 g/kg/day. Animal protein is significantly limited for children with severe arterial hypertension and widespread edema. Spicy dishes and products containing extractives and allergens are contraindicated. If you have oliguria, you should avoid foods rich in potassium. The total energy value of food should meet the child's needs - mainly due to carbohydrates and fats.

If the focus of streptococcal infection remains active, etiological (antibacterial) therapy is indicated. Preference is given to penicillin antibiotics. In the presence of chronic tonsillitis and/or adenoids, surgical treatment with antibiotics is recommended by the end of the 2nd month of the disease.

It is advisable to prescribe sodium heparin in a daily dose of 100-150 units/kg/day subcutaneously for 2-4 weeks to prevent intravascular coagulation. Antiplatelet agents are used (for example, dipyridamole 5 mg/kg).

Antihypertensive therapy is necessary for severe arterial hypertension. Use ACE inhibitors (captopril, enalapril); calcium channel blockers (nifedipine); intravenous 2.4% solution of aminophylline (aminophylline) in 10-20% glucose solution, followed by infusion of furosemide (1-4 mg/kg/day), clonidine or methyldopa can be used.

For severe edema, signs of heart failure, arterial hypertension and the threat of eclampsia, diuretics are prescribed - usually furosemide at a rate of 1-4 mg/kg/day.

For hematuria that persists for more than 2 months, it is recommended to prescribe 4-aminoquinoline drugs at a dose of 5-10 mg/kg.

Prevention

To prevent acute glomerulonephritis, timely diagnosis and adequate therapy of streptococcal diseases, sanitation of foci of chronic infection, and rational implementation of preventive vaccinations are needed. Dispensary observation of children who have suffered acute post-streptococcal glomerulonephritis is carried out for 5 years after discharge from the hospital.

Forecast

On average, 85-90% of children recover; in the rest, residual changes in urine persist for a long time, which does not allow the child to be considered completely cured. In a small proportion of children, nephritis becomes chronic or subacute. Deaths are rarely recorded. Nephrotic syndrome and prolonged course of nephritis should be considered unfavorable signs with a high probability of transition to chronic glomerulonephritis.

Rapidly progressive glomerulonephritis

Rapidly progressive glomerulonephritis (subacute, malignant, extracapillary, with crescents) is characterized by extremely high activity of the pathological process, a severe progressive course, increasing renal failure with the development of terminal uremia over several weeks or months.

Rapidly progressive glomerulonephritis in children as a variant of primary glomerulonephritis is rarely observed (in 3-5% of cases), mainly in adolescents.

Etiology and pathogenesis

There are several immunopathogenetic types of primary rapidly progressive glomerulonephritis. Secondary rapidly progressive glomerulonephritis can develop with various infectious, systemic diseases and tumors.

There are 3 types of primary idiopathic rapidly progressive glomerulonephritis:

With AT against Ag of the glomerular basement membrane, the cells of which apparently acquire antigenic properties under the influence of viruses and other environmental factors;

Immune complex rapidly progressive glomerulonephritis;

Rapidly progressive glomerulonephritis without immune complexes, but often with antibodies to the cytoplasm of neutrophils.

Pathological anatomy

When examining nephrobiopsy specimens, extracapillary glomerulonephritis is most often detected with the formation of crescents in more than 50% of the glomeruli.

Clinical picture and laboratory data

The clinical picture of the disease is characterized by a general serious condition of the patient, caused by a rapid increase in edema (up to anasarca) and gross hematuria, a significant and persistent increase in blood pressure, oliguria, and decreased renal function. From approximately the 2-3rd week of illness, hyperazotemia with a steady increase in the concentration of urea and creatinine, anemia, hypoproteinemia, and hypercholesterolemia are detected. In the urine sediment, along with red blood cells, leukocytes and casts are found.

Treatment

Due to the extremely high activity of the process in rapidly progressing glomerulonephritis, active therapy should be started immediately. A combination of plasmapheresis and pulse therapy with methylprednisolone at a dose of 20-30 mg/kg/day and/or cyclophosphamide at 12-14 mg/kg/day intravenously every other day or 3 days in a row is used. Subsequently, the patient is transferred to 4-component therapy (glucocorticoids + cytostatics + anticoagulants + antiplatelet agents) in usual therapeutic doses. In the absence of effect from active therapy and the rapid outcome of glomerulonephritis to terminal chronic renal failure, hemodialysis and kidney transplantation are indicated.

Forecast

The prognosis of rapidly progressing glomerulonephritis, even with timely active treatment, is unfavorable. In most children, a few months after the onset of the disease, death occurs from chronic renal failure. With rapidly progressing glomerulonephritis associated with post-streptococcal glomerulonephritis, a favorable outcome in remission with restoration of kidney function and even recovery is possible.

Chronic glomerulonephritis

Chronic glomerulonephritis is a group of heterogeneous primary glomerulopathies characterized by progressive inflammatory, sclerotic and destructive changes with the outcome in chronic renal failure.

Chronic glomerulonephritis is diagnosed at any age; it can be a consequence of untreated acute nephritis, but more often develops as a primary chronic disease.

CLASSIFICATION

In pediatric practice, hematuric, nephrotic and mixed forms of chronic glomerulonephritis are traditionally distinguished. When making a diagnosis, it is necessary to clarify the morphological variant of the disease. In accordance with the morphological classification of chronic glomerulonephritis, the following forms of chronic glomerulonephritis are distinguished.

Minimal changes in the glomeruli.

Focal segmental glomerular sclerosis (hyalinosis).

Membranous glomerulonephritis (membranous nephropathy).

Mesangioproliferative glomerulonephritis.

Mesangiocapillary (membranoproliferative glomerulonephritis).

Fibroplastic glomerulonephritis (final of all types). ETIOLOGY

The cause of the disease cannot be determined in all cases. The role of nephritogenic strains of streptococcus, persistent viruses (hepatitis B, cytomegalovirus, Coxsackie virus, Epstein-Barr virus, influenza, etc.) is suggested; genetically determined characteristics of immunity (for example, a defect in the complement system or cellular immunity). The occurrence of the disease is facilitated by congenital renal dysplasia.

PATHOGENESIS

There are immunologically determined and immunologically non-determined variants of the disease. Immunologically caused can be of immunocomplex or, less commonly, autoantibody origin. Most forms of primary chronic glomerulonephritis are classified as immune complex glomerulopathies. Their pathogenesis resembles that of acute glomerulonephritis (see section “Acute glomerulonephritis”). The involvement of immunological processes in minimal change glomerulonephritis is a subject of debate.

Examination of the glomeruli by immunohistochemical method does not reveal specific changes in this variant of the disease. Electron microscopy reveals a reduction in small processes of podocytes, indicating metabolic changes in the cells. Pathology of podocytes leads to disruption of the integrity of the glomerular filter. As a result, excess proteins and lipids penetrate into the primary urine and, being reabsorbed, accumulate in the tubular epithelium. Protein and fatty degeneration of tubular cells develops, clearly visible under light microscopy, which in the past gave rise to calling the pathological process “lipid nephrosis.”

CLINICAL PICTURE

The clinical picture of chronic glomerulonephritis depends on its form.

Nephrotic form

In children from 1 to 5 years of age, the nephrotic form of chronic glomerulonephritis usually corresponds to a morphological variant with minimal changes in the glomeruli. The nephrotic form of chronic glomerulonephritis is characterized by massive proteinuria (more than 40 mg/m2/day or more than 3 g/day), edema, hypo- and dysproteinemia, and hyperlipidemia. In minimal change nephritis, nephrotic syndrome is not accompanied by either hematuria or hypertension, so it is called “pure” or “idiopathic” or “primary nephrotic syndrome.” In this case, proteinuria can reach 20-30 g/day or more, but it is almost always selective and is represented mainly by albumin. A significant loss of protein in the urine leads to hypoproteinemia and dysproteinemia (mainly hypoalbuminemia), and this, in turn, determines a decrease in the oncotic pressure of the plasma, as a result of which water passes into the tissues. BCC decreases, glomerular filtration decreases, edema appears (mostly diffuse, with edema of the cavities). Edema gives patients a characteristic appearance. The skin is white, cold to the touch. Patients feel thirst, dry mouth, and weakness. Due to the accumulation of fluid in the pleural cavity, there may be complaints of cough and shortness of breath. Tachycardia appears; in the absence of ascites, liver enlargement is detected. Along with the development of hypoalbuminemia, the concentration of lipids in the blood serum increases. The number of urinations and urine volume are reduced, but the relative density of urine is increased. The sediment is scanty and mainly contains casts, fat and fat-degenerated epithelium. Red blood cells are detected rarely and for a very short time. ESR increased sharply

chena. During an exacerbation, the amount of IgG and IgA decreases, and the amount of IgM and fibrinogen may be increased. The concentration of complement component C3 is always normal. The prognosis is favorable. Most children recover. The possibility of transition of minimal changes in the glomeruli into focal segmental glomerulosclerosis (a characteristic feature of which is the presence of segmental mesangial sclerosis in some glomeruli) is discussed.

In school-age children with the nephrotic form of chronic glomerulonephritis, membranous and mesangioproliferative morphological variants are usually found. The membranous variant is characterized by the presence of subepithelial deposits and thickening of the glomerular basement membrane in the absence of significant proliferation of endothelial and mesangial cells. The mesangioproliferative variant is observed less frequently. It is characterized by proliferation of mesangial cells and matrix. Proteinuria is low selective, which indicates severe damage to the glomerular capillaries. Hematuria is expressed in varying degrees from micro to macrohematuria. Hypocomplementemia is detected - an indicator of the activity of the pathological process. The course of the disease is undulating, the nitrogen excretory function of the kidneys remains intact for a long time, but in half of the patients, after 5-10 years, nephritis leads to the development of chronic renal failure. Remissions of the nephrotic variant are more often observed in patients with membranous glomerulonephritis.

Hematuric form

The main manifestation of this form is persistent hematuria. Slight proteinuria and anemia may occur. The well-being of patients is usually not disturbed. In some cases, pasty eyelids are noted. Morphologically, this is mesangioproliferative glomerulonephritis (a variant with deposition of IgA and complement fraction C3 in the glomeruli).

Hematuria, as a leading symptom, is characteristic of Berger's disease (IgA nephropathy) - focal proliferative glomerulitis with deposition of IgA and C3 in the mesangium. The course of IgA nephropathy is relatively favorable; the outcome in chronic renal failure is rare. The disease is diagnosed in children of any age. Boys get sick 2 times more often than girls. Characteristic is recurrent gross hematuria that occurs during ARVI, “sinpharyngitis hematuria”, less often after other diseases or vaccination. The prognosis for the development of nephrotic syndrome and arterial hypertension is unfavorable.

Mixed form

It develops in older children and has a severe, steadily progressive course that is resistant to therapy. In mixed form

All morphological options are possible (except for minimal changes). More often than others, the mesangiocapillary variant is identified, characterized by proliferation of mesangial cells and thickening or double-circuiting of the capillary wall due to the penetration of mesangial cells into them. The progression of the pathological process leads to the development of sclerosis and the formation of fibroplastic glomerulonephritis - the finale of most forms of chronic glomerulonephritis. Sclerosis of the capillary loops of the glomerulus develops, fibroepithelial and fibrous crescents, thickening and sclerosis of the glomerular capsule are formed. Among the causes are viral and bacterial infections. Mesangiocapillary glomerulonephritis often develops during infection with the hepatitis B, C virus. The same type of glomerulonephritis is detected in SLE, Sjögren's syndrome, Dode's sarcoma, and lymphoma.

The disease often begins with acute nephrotic syndrome with the sudden development of hematuria, severe non-selective proteinuria, edema and persistent arterial hypertension. The disease can manifest itself as rapidly increasing renal failure. A feature of the mixed form is hypocomplementemia with a decrease in the concentration of C3 and/or C4 complement components. The prognosis is unfavorable; children develop chronic renal failure quite quickly.

TREATMENT

The optimal treatment is taking into account the morphological variant of chronic glomerulonephritis, but this is not always possible, especially in children, and one has to focus on the clinical manifestations of the disease. In the active period of the disease, in the presence of edema, gross hematuria and a pronounced increase in blood pressure, bed rest is indicated. It is expanded as the clinical manifestations of the pathological process fade. The diet is prescribed taking into account the state of nitrogen excretion function of the kidneys. If it is intact, the child receives proteins in an amount corresponding to the age norm (2-3 g/kg/day), with azotemia - 1 g/kg/day. In case of severe hyperlipidemia, it is necessary to reduce fat intake. For edema and arterial hypertension, a hypochloride diet is prescribed. The volume of fluid is dosed depending on diuresis. However, in the stage of polyuria, such restrictions are not necessary and are even harmful.

Taking into account the pathogenesis of glomerulonephritis, drugs are used that affect both immune mechanisms (glucocorticoids, cytostatics) and non-immune [anticoagulants (sodium heparin 200-400 IU/kg/day for 2-4 weeks or more), antiplatelet agents (di- pyridamole 3-5 mg/kg), ACE inhibitors (enalapril, lisinopril)], lipid-lowering drugs (statins) are also prescribed for antihypertensive and nephroprotective purposes.

For new-onset nephrotic syndrome with minimal changes in the glomeruli, treatment is recommended to begin with prednisolone at a dose of 1-2 mg/kg/day body weight or 60 mg/m2. The drug at the indicated dose is prescribed for 4-8 weeks. In nephrotic syndrome, sensitive to glucocorticoid therapy (in most children), clinical and laboratory remission occurs. A relapse that develops after discontinuation of glucocorticoids indicates the hormonal dependence of nephrotic syndrome. Treatment of the first relapse is carried out in the same way as therapy at the onset of the disease. For frequent relapses, alkylating cytostatics are added (cyclophosphamide 2 mg/kg/day; chlorambucil 0.1-0.2 mg/kg), while reducing the dose of prednisolone to 40 mg/m2 and transferring the patient to an alternating regimen of taking the drug ( in one day). The lack of effect of glucocorticoid therapy for 8 weeks indicates the resistance of nephrotic syndrome to hormonal therapy. In this case, treatment is carried out with cytostatics or the selective immunosuppressant cyclosporine at a dose of 3-5 mg/kg/day.

Patients with focal segmental glomerular sclerosis are currently prescribed glucocorticoids and cytostatics for a long course (up to 6 months), which makes it possible to achieve remission in patients previously considered unpromising.

For mesangiocapillary glomerulonephritis, different treatment options are used: monotherapy with glucocorticoids, a 4-component treatment regimen (glucocorticoids + cytostatics + antiplatelet agents + anticoagulants), a combination of glucocorticoids and cytostatics (can be in the form of pulses) - methylprednisolone at a dose of 10-20 mg/kg and/or or cyclophosphamide 5-15 mg/kg/day; cyclosporine in combination with low doses of glucocorticoids.

In the hematuric form of chronic glomerulonephritis (mesangioproliferative glomerulonephritis) and IgA nephropathy with preserved renal function, slight proteinuria (less than 1 g/day), with episodes of “sinpharyngitis macrohematuria,” ACE inhibitors (for nephroprotective purposes) and dipyridamole can be prescribed. In case of development of nephrotic syndrome, it is advisable to use glucocorticoids and cytostatics.

In the fibroplastic variant of glomerulonephritis (pronounced sclerotic changes in the glomeruli), glucocorticoids are not indicated.

PREVENTION

Prevention of chronic glomerulonephritis is aimed at preventing relapses of the disease (limiting physical activity, eliminating stressful conditions, cooling, preventing

intercurrent diseases, sanitation of foci of chronic infection, vaccine prophylaxis according to an individual plan). Patients are advised to undergo clinical observation with monitoring of renal function.

FORECAST

The prognosis depends on the clinical and morphological features of nephritis. The most unfavorable course of the mixed form of chronic glomerulonephritis. CRF can develop within a period of several months to 15-20 years after the onset of the disease. For end-stage chronic renal failure, hemodialysis and kidney transplantation are indicated.

HEREDITARY NEPHROPATHIES

Hereditary nephritis [Allport syndrome (Alport)] is a hereditary non-immune glomerulopathy caused by pathology of the collagen of the basement membranes of the glomeruli, manifested by hematuria and/or proteinuria, often in combination with hearing loss or pathology of the visual organs.

Epidemiology.The prevalence of the disease is 17 cases per 100,000 children (9ΐ and ρ). The dominant type of inheritance (K) is characteristic of hereditary nephritis with hearing loss and early development of chronic renal failure, i.e. for classic Allport syndrome.

Pathogenesis.The pathogenetic basis of the disease is genetically determined metabolic disorders of type IV collagen, which serves as the main component of the basement membrane of capillaries and the capsule of the glomeruli of the kidneys, lens and spiral (organ of Corti).

Clinical picture. The first signs of the disease can be detected at any age, most often at 5-10 years. Micro or macrohematuria is usually detected, proteinuria is possible; Leukocyturia is less commonly noted in the absence of bacteria in the urine (manifestation of interstitial changes). When examining a patient, stigmas of dysembryogenesis are often detected. Hearing loss characteristic of Allport syndrome is more often diagnosed in boys. Anomalies of the visual organs in the form of cataracts, astigmatism, spherophakia (spherical shape of the lens) and others are found in approximately 25% of patients with Allport syndrome.

In hereditary nephritis, the content of T- and B-lymphocytes is reduced. A decrease in the concentration of IgA, an increase in IgM and IgG, and a decrease in phagocytic activity are often noted.

Diagnostics.To substantiate the diagnosis, a genealogical study should be carried out, anamnestic data on the initial manifestations of nephritis should be carefully studied, the patient should be examined in detail (including audiometry to detect hearing loss), and pathology should be excluded

vision, identify possible stigmas of disembryogenesis. Biochemical examination of urine, reflecting increased excretion of certain collagen components, can serve as one of the confirmations of the diagnosis of hereditary nephritis. If necessary, they resort to a kidney biopsy, which makes it possible to identify partial underdevelopment and defective formation of the structural elements of the nephron, as well as the accumulation of “foam cells” and fibrinous changes in the interstitium.

Treatment.There is no specific treatment for hereditary nephritis. Every effort should be made to preserve kidney function. The child is limited in physical activity. Nutrition should be balanced and take into account the functional state of the kidneys. Sanitation of foci of chronic infection is necessary. With the development of chronic renal failure, kidney transplantation is indicated. In recent years, there have been reports of the effectiveness of cyclosporine in Allport syndrome.

Forecast.The prognosis is unfavorable, especially for boys and men, since they often develop chronic renal failure by the age of 15-30.

HEREDITARY TUBULOPATHIES

Tubulopathy (tubular dysfunction) is a group of nephropathies caused by disruption of transport processes in the tubules. There are primary (hereditary) tubulopathies and secondary ones, which develop with inflammatory kidney diseases, metabolic diseases and drug-induced kidney damage.

Primary tubulopathies can be caused by a defect in enzymes that ensure the transport of substances in tubular cells, dysfunction of specific membrane carrier proteins, changes in the sensitivity of tubular epithelial receptors to the action of hormones, and tubular dysplasia. The variety of causes and the possibility of selective localization of anomalies in the tubules explain the polymorphism of the clinical manifestations of this pathology. In accordance with the main syndromes, hereditary tubulopathies are divided into 3 groups. One of them includes tubulopathies accompanied by rickets-like changes in the skeleton [phosphate-diabetes, glucoaminophosphate-diabetes, or de Toni-Debreu-Fanconi disease, renal tubular acidosis (see chapter “Rickets and rickets-like diseases”)], the second - tubulopathies with polyuria ( renal glycosuria, renal diabetes insipidus, renal salt diabetes), the third group is accompanied by nephrolithiasis (cystinuria, glycinuria).

RENAL GLUCOSURIA

Impaired glucose transport in the proximal nephron due to a defect in the enzyme systems that provide reabsorption

tion of glucose. The main signs of the disease: glycosuria with normal fasting blood sugar levels; polyuria, thirst.

Treatment.A proper diet with a sufficient amount of carbohydrates, since their excess administration increases glucosuria, and a deficiency can cause hypoglycemia.

RENAL DIABETES INDIPELLUS

Renal diabetes insipidus - a hereditary disease (K, dominant) - is characterized by the insensitivity of the distal tubules to ADH, which is manifested by the inability of the kidneys to concentrate urine. As a result, a large amount of osmotically free water is lost. This leads to hyperosmia of the extracellular fluid and, consequently, to cell dehydration.

Clinical picture. The first signs of the disease appear immediately after birth and intensify with the transition to artificial feeding, which is associated with an increase in osmotic load. The child develops fever, vomiting, constipation and convulsions from the first week of life, as well as dehydration and hypernatremia. Symptoms of older children: polyuria, nocturia, polydipsia, growth retardation. Differential diagnosis is carried out with pylorospasm, many diseases accompanied by fever, and other tubulopathies occurring with polyuria, as well as pituitary diabetes insipidus (with preserved sensitivity to ADH).

Treatment.Symptomatic.

CYSTINURIA

The disease is genetically determined (ρ), the main clinical manifestations are associated with the formation of cystine kidney stones (nephrocalcinosis). Possible delay in physical development; leukocyturia, proteinuria.

Treatment.Limiting foods rich in sulfur-containing amino acids in the diet; purpose of membrane stabilizers.

General characteristics, functions of the urinary system.
As a result of metabolism in cells and tissues, energy is generated, but at the same time
end products of metabolism are also formed that are harmful to the body and must be removed. These
waste products from cells enter the blood. The gaseous part of the final products of metabolism,
for example, CO2 is removed through the lungs, and protein metabolism products through the kidneys. So, the main one
kidney function - removal of metabolic end products from the body (excretory or
excretory function). But the kidneys also perform other functions:
1. Participation in water-salt metabolism.
2. Participation in maintaining normal acid-base balance in the body.
3. Participation in the regulation of blood pressure (hormones and renin).
4. Participation in the regulation of erythrocytopoiesis (by the hormone erythropoietin).

2. Sources, the principle of the structure of 3 consecutive buds in
embryonic period. Age-related changes in the histological structure of the kidneys.
Sources of development, the principle of the structure of 3 consecutive buds.
In the embryonic period, 3 excretory organs are sequentially laid down:
the pronephros, the first kidney (mesonephros) and the terminal kidney (metanephros).
The preference is formed from the anterior 10 segmental legs. Segmental legs come off
from somites and turn into tubules - protonephridia; at the end of the attachment to
in splanchnotomes, the protonephridia open freely into the coelomic cavity (the cavity between
parietal and visceral leaves of splanchnotomes), and the other ends connecting to form
The mesonephric (Wolffian) duct flows into the expanded portion of the hindgut - the cloaca.
The human kidney does not function (an example of repetition of phylogeny in ontogenesis), soon
protonephridia undergo reverse development, but the mesonephric duct is preserved and
participates in the formation of the first and final kidneys and reproductive system.
The first kidney (mesonephros) is formed from the next 25 segmental legs located in
areas of the body. Segmental legs are detached from both somites and splanchnotomes,
turn into tubules of the first kidney (metanephridia). One end of the tubules ends blindly
bubble-like expansion. Branches from the aorta and depressions approach the blind end of the tubules.
pour into it, turning the blind end of the metanephridia into a 2-walled glass - a
renal corpuscle. The other end of the tubules flows into the mesonephric (Wolffian) duct,
left over from the preference. The first kidney functions and is the main excretory organ in
embryonic period. In the renal corpuscles, waste products are filtered from the blood into the tubules and
enter the cloaca through the Wolffian duct.
Subsequently, part of the tubules of the first kidney undergo reverse development, part - accepts
participation in the formation of the reproductive system (in men). The mesonephric duct is preserved and
takes part in the formation of the reproductive system.
87
The final kidney is formed in the 2nd month of embryonic development from the nephrogenic
tissue (unsegmented part of the mesoderm connecting somites with splanchnatoms),
mesonephric duct and Renal tubules are formed from nephrogenic tissue.
which with their blind end interacting with blood vessels form renal corpuscles
(see kidney I above); the tubules of the final kidney, in contrast to the tubules of the first kidney, are strongly
elongate and successively form the proximal convoluted tubules, loop of Henle and
distal convoluted tubules, i.e. The nephron epithelium is formed from nephrogenic tissue as a whole.
A protrusion of the wall grows towards the distal convoluted tubules of the final kidney
Wolffian duct, from its lower section the epithelium of the ureter, pelvis, renal
calyces, papillary tubules and collecting ducts.
In addition to nephrogenic tissue and the Wolffian duct during the formation of the urinary system
participate:
1. The transitional epithelium of the bladder is formed from the endoderm of the allantois (urinary
pouch - protrusion of the endoderm of the posterior end of the first intestine) and ectoderm.
2. The epithelium of the urethra is from the ectoderm.
3. From - connective tissue and smooth muscle elements of the entire
urinary system.
4. From the visceral layer of splanchnotomes - mesothelium of the peritoneal cover of the kidneys and
Bladder.
Age-related features of the kidney structure:
- in newborns: in the preparation there are a lot of renal cells located close to each other
corpuscles, renal tubules are short, the cortex is relatively thin;
- in a 5-year-old child: the number of renal corpuscles in the field of view decreases (diverges
from each other due to an increase in the length of the kidney tubules; but the tubules are smaller and their diameter
less than in adults;
- by the time of puberty: the histological picture does not differ from adults.

3. Histological structure of the kidneys.
The kidney is covered with a connective tissue capsule. In the kidney parenchyma there are:
1. Cortex - located under the capsule, macroscopically dark red in color.
Consists mainly of renal corpuscles, proximal and distal convoluted tubules
nephron, i.e. from renal corpuscles, nephron tubules and connective tissue layers between
them.
2. The medulla - lies in the central part of the organ, macroscopically lighter,
consists of: part of the nephron loops, collecting ducts, papillary tubules and
connective tissue layers between them.
The structural and functional unit of the kidney is the nephron. The nephron consists of the renal
corpuscles (glomerular capsule and choroidal glomerulus) and renal tubules (proximal convoluted
and straight tubules, nephron loop, distal straight and convoluted tubules).
The glomerular capsule is shaped like a 2-walled glass, consists of
parietal (outer) and visceral (inner) layers, between them there is a cavity
capsules continuing into the proximal convoluted tubules. Outer leaf of the capsule
the glomerulus has a simpler structure, consisting of a 1-layer squamous epithelium on the basal
membrane. The inner leaf of the glomerular capsule has a very complex configuration; the outside
covers all glomerular capillaries located inside the capsule (each separately),
consists of podocyte cells (“cells with legs”). Podocytes have several long legs -
processes (cytotrabeculae) with which they encircle the capillaries. They arise from the cytotrabeculae

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numerous small processes - cytopodia. Inner leaf of own basal
It has no membrane and is located on the outside of the basement membrane of the capillaries.
Urine with a volume of about 100 l/day is filtered into the capsule cavity from the capillaries and
then enters the proximal convoluted tubules.
The choroid glomerulus is located inside the glomerular capsule (2-walled glass) and consists of
afferent arteriole, capillary glomerulus and efferent arteriole. Afferent arteriole
has a larger diameter than the outflow one - therefore pressure is created in the capillaries between them,
necessary for filtering.
The glomerular capillaries belong to the fenestrated (visceral) type capillaries,
the inside is lined with endothelium with fenestrae (thinned areas in the cytoplasm) and slits,
the basement membrane of the capillaries is thickened (3-layer) - the inner and outer layers are less
dense and light, and the middle layer is denser and darker (consists of thin fibrils,
forming a network with a cell diameter of about 7 nm); due to the fact that the diameter of the afferent arteriole
more than the outflow, the pressure in the capillaries is high (50 or more mm Hg) - provides
filtration of the first urine from the blood); on the outside, the capillaries are enclosed by the cytotrabeculae of podocytes
visceral layer of the glomerular capsule. Between podocytes there are small numbers of
mesangial cells (processed, similar in structure to pericytes; function:
phagocytose, participate in the production of the hormone renin and the main substance, are capable of
contraction and regulate blood flow in the capillaries of the glomerulus).
Between the blood in the capillaries of the glomerulus and the cavity of the glomerular capsule there is a renal
filter or filtration barrier consisting of the following components:
1. Endothelium of the glomerular capillaries.
2. 3-layer basement membrane, common to endothelium and podocytes.
3. Podocytes of the inner layer of the glomerular capsule.
The kidney filter has selective permeability and allows all components to pass through
blood except for blood cells, large molecular plasma proteins (A-bodies,
fibrinogen, etc.).
The renal tubules begin with the proximal convoluted tubules, which receive urine.
from the cavity of the glomerular capsule, then continues: proximal straight tubules - loop
nephron (Henle) - distal straight tubules - distal convoluted tubules.
Morphofunctional differences between the proximal and distal convoluted tubules:
Signs Proximal convoluted tubules Distal convoluted tubules
Diameter approx. 60 µm 20-50 µm
Epithelium Single layer cubic bordered: Single layer cubic
has microvilli, basal (low prismatic): no
striations, the cytoplasm is cloudy due to microvilli, there is basal
pinocyte. vesicle striations, cytoplasm
transparent
Function Reabsorption of proteins, carbohydrates, salts, Reabsorption of salts, water
water

In the basal part of the epithelial cells of the proximal and distal convoluted tubules there is
striations formed by deep folds of the cytolemma and lying in them
mitochondria. A large number of mitochondria in the basal striation zone of the tubules
necessary to provide energy for the processes of active reabsorption of proteins from urine into the blood,
carbohydrates and salts in the proximal convoluted tubules, salts in the distal convoluted tubules.

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The proximal and distal convoluted tubules are intertwined with a peritubular network of capillaries
(branches of the efferent arterioles of the glomerulus of the renal corpuscles).
The nephron loop is located between the proximal and distal straight tubules,
consists of a descending (lined by 1-layer squamous epithelium) and ascending knee
(lined by 1-layer cubic epithelium).
Based on location and structural features, cortical (superficial and
intermediate) and pericerebral (juxtamedullary) nephrons, which differ in
following signs:
Signs Cortical nephrons Peri-cerebral nephrons
Location Cortical substance, loop On the border with the medulla
Henle descends into the substance, the loop of Henle leaves
medulla deep into medulla
The ratio of d afferent and d afferent arterioles in d are equal
efferent arteriole 2p >
The pressure in the capillaries of the glomerulus is 70-90 mm Hg. Art. 40 mmHg Art. And<
Severity of peritubular +++ +
capillary network

General hydrodynamic High Low
nephron vascular resistance

Amount in kidneys 80% 20%
Function Urinary formation Vascular shunt

4. Endocrine kidney function.
The kidneys have a juxtaglomerular apparatus (periglomerular apparatus),
producing the hormone renin (regulates blood pressure) and is involved in
production of erythropoietin (regulates erythrocytopoiesis). YUGA consists of the following
components:
1. Juxtaglomerular cells - lie under the endothelium of the afferent arterioles, in the efferent arterioles
there are few of them in arterioles. The cytoplasm contains PAS-positive renin granules.
2. Cells of the macula densa - thickened epithelium of the section of the wall of the distal convoluted
tubules lying between the afferent and efferent arterioles. Have receptors for
trapping Na+ concentration in urine.
3. Juxtavascular cells (Gurmagtig cells) – polygonal cells lying in
triangular space between the macula densa and the afferent and efferent arterioles.
4. Mesangial cells (located on the outer surface of the glomerular capillaries
among podocytes, see above the structure of renal corpuscles).
JGA produces the hormone renin; under the influence of renin blood plasma globulin
angiotensinogen is converted first to angiotensin I, then to angiotensin II. Angiotensin II c
on the one hand has a direct vasoconstrictor effect and increases arterial
pressure, on the other hand, increases the synthesis of aldosterone in the zona glomerulosa of the adrenal glands =>
reabsorption of Na+ and water in the kidneys increases => the volume of tissue fluid in the kidneys increases
body => increased circulating blood volume => increased arterial
pressure.
Prostaglandins are produced in the epithelial cells of the loops of Henle and collecting ducts.
having a vasodilating effect and increasing glomerular blood flow, as a result
which increases the volume of urine excreted.

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Kallekrein is synthesized in the epithelial cells of the distal tubules of the nephron, under the influence of
which converts the plasma protein kininogen into the active form of kinin. Kinins have
strong vasodilatory effect, reduce the reabsorption of Na+ and water? increases
urination.

5. Regulation of kidney functions.
1. Kidney function depends on blood pressure, i.e. from vascular tone, regulated
sympathetic and parasympathetic nerve fibers.
2. Endocrine regulation:
a) aldosterone of the zona glomerulosa of the adrenal glands enhances the active reabsorption of salts in
to a greater extent in the distal, to a lesser extent in the proximal convoluted tubules of the kidneys;
b) antidiuretic hormone (vasopressin) of supraoptic and paraventricular nuclei
anterior part of the hypothalamus, increasing the permeability of the walls of the distal convoluted tubules and
collecting ducts, enhances passive reabsorption of water.