Chronic diffuse process in the kidneys. Acute diffuse glomerulonephritis

Many are interested in the answer to the question: what is chronic glomerulonephritis? The disease is classified as a slowly progressive diffuse glomerular lesion of the kidneys with immunoinflammatory reactions. If left untreated, sclerosis (overgrowth of connective tissue) and organ failure develop. Symptoms of the disease depend on the type of chronic process that has developed. The diagnosis of glomerulonephritis is made according to laboratory and instrumental data. The therapeutic regimen includes a complex consisting of diet, medication and antihypertensive therapy.

The chronic form of inflammation of the kidneys can reach the stage of complete organ dysfunction.

General information

Chronic glomerulonephritis is an inflammatory disease characterized by progressive sclerotic, destructive changes in the tissues of the kidneys with their gradual failure.

Chronic diffuse glomerulonephritis can develop at any age, as a result of untreated acute inflammation of nephritis. But more often pathology occurs as an independent process. Diffuse or diffuse glomerulonephritis affects both kidneys. It has a slow flow. As a result, the affected kidney gradually shrinks, and if both structures fail or fail, death occurs.

Etiology and pathogenesis

The causes of chronic glomerulonephritis are well known. More often, the disease develops after acute glomerular inflammation of an infectious-immunological or allergic nature due to ineffective or incorrect therapy. Another provocateur of the disease is the causative agent of such chronic infections as streptococcal, affecting the nasopharynx, oral cavity, gastrointestinal tract, liver, and genitourinary organs.

The appearance of inflammation in the glomerular apparatus of the kidneys can be facilitated by a state of prolonged stress of the immune system against the background of severe and prolonged allergies, chronic poisoning with alcoholism, and the constant use of nephrotoxic drugs. There is a group of people who are at risk due to poor heredity, when, due to a malfunction of the immune system with a pathogen entering the body, protein is deposited in the nephrons, which destroys the glomeruli.

Secondary chronic glomerulonephritis develops against the background of such systemic pathologies as:

• endocarditis;
• rheumatism;
• connective tissue damage;
• allergic purpura.

Species diversity

Forms of chronic glomerulonephritis are determined by the nature of the course and symptoms:

Chronic glomerulonephritis in almost half of the cases can be asymptomatic.

• latent form. Occurs in 45% of cases. It is characterized by weak external signs with moderate edema, a slight increase in blood pressure. More often it is determined only by the results of a general urine test - a high level of protein, blood cells.
• The hematuric form of glomerulonephritis is a rare species (up to 5% of patients). Characteristic symptom: pinkish-red hue of urine. The analyzes reveal an excess of modified erythrocytes, signs of anemia. The pressure is normal, there are no edema.
• hypertonic type. Occurs in 20% of cases. It is distinguished by a bright clinic in the form of high blood pressure, an increased volume of urine excreted per day, and an increase in urges at night. The analysis determines a high protein, modified erythrocytes with a slight deviation in the density of urine from the norm. Problems with urine and its excretion are not expressed, and the pressure jumps from normal to 200 mm Hg. Art. Against the background of high blood pressure, cardiac dysfunction develops, the left ventricle hypertrophies, and asthma attacks are tormented.
• Glomerulonephritis nephrotic form. Occurs in 25% of patients. It is expressed by high blood pressure, high cholesterol, severe edema, weakening of urination up to its complete absence. According to the analyzes, a high density of urine with blood, an excess of protein is determined.
• Mixed type or nephrotic-hypertensive, when the signs and characteristics of these forms of the disease are combined.

Symptoms of pathology

The clinic of chronic glomerulonephritis is characterized by features of the form and course. In most cases, the course is latent - slow, long. The disease can exist for 10-20 years without showing itself. The disease is diagnosed by altered urine tests. As scarring occurs with the replacement of glomerular tissues with connective tissue with exacerbation, the following visual symptoms appear:

• paroxysmal back pain;
• thirst is constant;
• weakening / intensification of urination;
• morning swelling, especially eyelids;
• instability of blood pressure;
• pink, scarlet or dark reddish urine;
• fatigue, apathy;
• migraine.

Features of the disease in children

Symptoms and course of chronic glomerulonephritis in young patients are variable. Renal failure is a common complication. For this reason, 40% of children undergo hemodialysis or kidney transplantation.

Pathogenesis in babies:

• untreated acute glomerulonephritis, malnutrition during therapy (secondary form develops);
• irrational therapy of chronic infections - diseases of the teeth, inflammation in the tonsils;
• severe hypovitaminosis;
• severe hypothermia;
• slow-flowing infections: cytomegalovirus, hepatitis B, parainfluenza;
• congenital anomalies of the kidneys;
• genetic immunodeficiency states;
• reaction to certain vaccinations.

Symptoms of chronic glomerulonephritis

Glomerulonephritis in children is manifested by edema, protein impurities in the urine, back pain.

Children are more likely to develop a mixed, nephrotic, or hematuric variant. Puffiness, protein in the urine with glomerulonephritis appear after a long time or immediately. As the disease develops, children may complain of headaches and lumbar pain, swelling of the limbs and face, fatigue at low energy costs. With a mixed form, small patients will additionally experience dizziness, lethargy, irritability, abdominal pain, convulsions, loss of visual acuity due to high pressure or its surges. Such babies are pale due to the development of anemia. But the disease can develop rapidly, quickly leading to kidney failure.

Treatment and supervision of children

Children with chronic glomerulonephritis are shown dispensary observation with periodic testing, an individual vaccination and rehabilitation plan, exercise therapy, and nutrition. Prevention of chronic glomerulonephritis in such children is based on careful protection of them from infections, hypothermia. With inflammation of the tonsils or adenoids, the decision of doctors is ambiguous due to the risk of exacerbation of the infection.

Illness and pregnancy

Chronic diffuse glomerulonephritis occurs in pregnant women in 0.1-9% of cases. Symptoms are determined by the form of the process. Such women are under the supervision of an obstetrician-gynecologist and a nephrologist with periodic treatment in a hospital. The goal of therapy for this group of patients is symptom relief and rehabilitation. For this, appoint:

Chronic glomerulonephritis is a deadly threat to the fetus.

• BP correctors;
• intravenous protein preparations;
• antihistamines and restorative medicines;
• iron preparations, if anemia is severe.

Risks in chronic glomerulonephritis:

• severe gestosis - edematous symptom complex;
• abortion;
• freezing of the fetus;
• severe bleeding during childbirth.

• Which doctors should you contact if you have Acute diffuse glomerulonephritis

What is acute diffuse glomerulonephritis

Polyetiological infectious-allergic inflammation (glomerulonephritis) with a primary lesion of the glomeruli, as well as the intermediate tissue of the kidneys.

Degeneration of the tubular epithelium is relatively weakly expressed.

The disease occurs as a result of injections, poisoning, colds, injuries, allergic desensitization.

The sensitizing role is played by hypothermia, poor-quality feed, and unsatisfactory conditions for keeping the animal. Jade can be caused by nephrotoxins, toxic substances (turpentine, tar, herbicides, fertilizers).

Pathogenesis (what happens?) during Acute diffuse glomerulonephritis

Currently, the immunoallergic theory of the pathogenesis of acute diffuse glomerulonephritis is generally accepted. The appearance of symptoms of nephritis after an infection is preceded by a 1-3-week latent period, during which the body's reactivity changes, its sensitivity to the infectious agent increases, and antibodies to microbes are formed.

Experimental studies suggest 2 possible mechanisms for the development of nephritis: 1) the formation of circulating antigen-antibody complexes in the blood, which fix in the glomeruli and damage the kidneys, or 2) the production of antirenal autoantibodies in response to damage to the kidneys by complexes of exogenous antibodies with proteins - glomerular antigens. In the first case, antigen-antibody complexes, interacting with complement, are deposited on the outer surface of the basement membrane of glomerular capillaries under epithelial cells in the form of separate clumps, clearly visible with electron and immunofluorescence microscopy. In the second variant of the development of nephritis, complement and globulins are deposited throughout the inner surface of the basement membrane. These complexes, located along the outer surface of the basement membrane of the glomerulus, do little damage to it, but cause a reaction from the complement system, coagulation and kinin systems with the inclusion of platelets, polynuclear cells. The immune complex fixes complement, which favors its settling in the capillaries of the glomeruli, which are affected by the vasomotor substances of complement. The formation of chemotaxis factors contributes to the fixation of polynuclear cells of the subepithelial and basement membranes of the glomerular capillaries. Lysosomal enzymes of polynuclear cells damage the membrane, causing its so-called enzymatic perforation. At the same time, histamine and serotonin secreted by polynuclear cells increase vascular permeability and enhance the synthesis of kinins.

An important role in glomerular damage is played by a violation of the coagulation system, which is due to the activation of complement by immune complexes and an increase in platelet aggregation, activation of coagulation factor XII. The latter, by activating serum kallikreinogen, increases the content of kinin; in addition, factors III and IV are released from platelets. All this leads to the deposition of fibrin in the capillary wall, which causes the proliferation of mesothelial and endothelial cells, which phagocytize them, followed by the deposition of talin substance. The nature of the course of the disease largely depends on the size of the fibrin depot (Scheme 3). Naturally, no less important are the endogenous factors that determine the reactivity of the organism.

Proteinuria develops as a result of increased permeability of the basement membrane of the glomerular capillaries. Edema is caused by several factors, which include a decrease in glomerular filtration, an increase in sodium reabsorption, aldosterone secretion, and vascular wall permeability.

pathological anatomy

The kidneys are often of normal size, less often - slightly enlarged; brown or grey-brown. On the surface and on the section of the kidneys, tubercles of a reddish-gray color are visible, which are enlarged renal glomeruli (“variegated” kidney). Microscopic examination reveals inflammation of the renal capillaries with an increase in glomeruli. In the initial period of the disease, the renal glomeruli are hyperemic; later, their ischemia (due to spasm of capillary loops), fibrinoid swelling of the walls of glomerular capillaries, proliferation of their endothelium, accumulation of protein exudate between the capillary loops and the glomerular capsule, blood stasis, thrombosis of capillary loops, hemorrhages are noted.

Morphological changes affect the tissue of both kidneys. The epithelium of the renal tubules suffers to a lesser extent. In a later period, inflammation in the renal tissue subsides, the proliferation of the endothelium of the glomerular loops decreases, and capillary patency is restored.

Symptoms of acute diffuse glomerulonephritis

Acute diffuse glomerulonephritis characterized by three main symptoms: edematous, hypertensive and urinary.

The disease most often develops acutely. Patients report fever, weakness, swelling of the predominant face, headache, decreased diuresis.

Edema is an early sign of the disease. They occur in 80-90% of patients, are located mainly on the face and create, together with the pallor of the skin, a characteristic "nephritic face". Often, fluid accumulates in cavities (pleural, abdominal, and pericardial cavities). Weight gain due to edema can reach 15-20 kg or more in a short time. The swelling usually disappears after 2-3 weeks.

One of the cardinal symptoms acute diffuse glomerulonephritis is arterial hypertension, which is observed in 70-90% of patients and is associated with impaired blood supply to the kidneys. In most cases, hypertension does not reach high numbers and rarely systolic pressure exceeds 180 mm Hg. Art., and diastolic - 120 mm Hg. Art. The acute development of arterial hypertension complicates the activity of the heart and may manifest as acute heart failure, especially left ventricular, in the form of shortness of breath, cough and attacks of cardiac asthma. In connection with arterial hypertension, hypertrophy of the left ventricle of the heart develops.

An objective study finds an expansion of relative cardiac dullness. Often auscultated systolic murmur at the apex of a functional nature, accent II tone on the pulmonary artery, sometimes the gallop rhythm. Dry and wet rales are found in the lungs. On the electrocardiogram, changes in the R and TV waves in I, II and III standard leads, often a deep Q wave and a slightly reduced voltage of the QRS complex, can be observed.

One of the very first symptoms of acute nephritis is a decrease in urine output (up to 400-700 ml / day), in some cases anuria is observed. The decrease in urine output is mainly due to inflammatory changes in the glomeruli, which leads to a decrease in filtration in them. In this case, there is usually no decrease in the relative density of the weight of urine.

The urinary syndrome in acute glomerulonephritis is characterized by proteinuria, cylindruria, macro- and microhematuria.

Proteinuria in acute nephritis is caused not so much by a violation of vascular permeability as by gross damage to the vascular wall of the glomerular capillaries. Through the damaged walls of the capillaries of the glomeruli, not only finely dispersed albumins are released, but also globulins and fibrinogen.

The amount of protein in the urine usually ranges from 1 to 10%, in some cases reaching 20%. However, the high content of protein in the urine lasts only in the first 7-10 days, therefore, with a late study of urine, albuminuria often turns out to be low, less than 1%. A small proteinuria in some cases may be from the very beginning of the disease, and in some periods it may be completely absent. A small amount of protein in the urine can be observed in acute nephritis for a long time and disappear completely only after 3-4-6 and even 9-12 months.

The number of leukocytes in the urine sediment, as a rule, is insignificant, but in some cases 20-30 leukocytes are found and even much more in the field of view. At the same time, the quantitative predominance of erythrocytes over leukocytes is always noted, which is better detected with a special calculation of the formed elements of the urine sediment according to the methods of Kakovsky - Addis, Nechiporenko. In acute glomerulonephritis, urine leukocytes stain well with safronin (according to Sternheimer-Melbin), in contrast to infectious diseases of the kidneys (pyelonephritis).

Often in acute nephritis, there is a decrease in the amount of hemoglobin and erythrocytes in a late study of urine, albuminuria is often low, less than 1%. A small proteinuria in some cases may be from the very beginning of the disease, and in some periods it may be completely absent. A small amount of protein in the urine can be observed in acute nephritis for a long time and disappear completely only after 3-4-6 and even 9-12 months.

Hematuria is a mandatory and constant sign of acute glomerulonephritis, and in 13-15% of cases there is gross hematuria. In other cases, microhematuria is detected, and the number of erythrocytes in the urine sediment may not exceed 10-15 per field of view.

Cylindruria is not an obligatory symptom of acute glomerulonephritis. In 75% of cases, single hyaline and granular casts are found. Epithelial casts are sometimes seen.

The number of leukocytes in the urine sediment, as a rule, is insignificant, but in some cases 20-30 leukocytes are found and even much more in the field of view. At the same time, the quantitative predominance of erythrocytes over leukocytes is always noted, which is better detected with a special calculation of the formed elements of the urine sediment according to the methods of Kakovsky - Addis, Nechiporenko. When about stroma glomerulonephritis urine leukocytes stain well with safronin (according to Sternheimer - Melbin), in contrast to infectious diseases of the kidneys (pyelonephritis).

Many patients have mild or moderate azotemia. It is associated both with a decrease in the filtration function of the kidneys, and with increased tissue breakdown due to the underlying disease (with secondary nephritis) and is soon replaced by normal values. High progressive azotemia, as a rule, does not occur.

Often in acute nephritis, there is a decrease in the amount of hemoglobin and red blood cells in the peripheral blood. This is due to the edema (hydremia) of the blood characteristic of this disease, but may also be due to the development of true anemia as a result of the influence of the infection underlying the nephritis, for example, with septic endocarditis.

An increase in ESR is observed very often, which is associated with the presence of a focal infection, or is an indicator of the activity of nephritis as an allergic process, reflecting shifts in the protein fractions of the blood. The number of leukocytes in the blood, as well as the temperature reaction, is determined by the initial or concomitant infection: more often the temperature is normal and there is no leukocytosis.

The course of acute glomerulonephritis is varied. There are two of its most characteristic variants.

The first option - a cyclic form - starts violently. Edema, shortness of breath, headache, back pain appear, the amount of urine decreases. The first urine tests revealed large albuminuria and hematuria. The blood pressure rises. Edema lasts 2-3 weeks, and then during the course of the disease a fracture occurs, polyuria develops and blood pressure decreases. The recovery period may be accompanied by hypostenuria. However, often with good health of patients and almost complete recovery of working capacity, proteinuria in small amounts - 0.03-0.1% o and residual hematuria can be observed for a long time, for months.

The second form of acute nephritis is latent. It occurs frequently and is of great importance, as it often becomes chronic. This form is characterized by a gradual onset without any subjective symptoms and is manifested only by slight shortness of breath or swelling in the legs. Such nephritis can only be diagnosed with systematic urine tests. The duration of the relatively active period in such a course of acute glomerulonephritis can be significant - up to 2-6 months or more.

Arterial hypertension in acute nephritis may be accompanied by the development of eclampsia. Eclampsia is caused by the presence of arterial hypertension and edema (hypervolemic cerebral edema) and is manifested by loss of consciousness, visual impairment (central origin) and convulsive seizures with biting the tongue and involuntary discharge of urine and feces. Despite the severe clinical picture, these seizures are rarely fatal and mostly disappear without a trace.

Flow acute glomerulonephritis may be accompanied by the development of nephrotic syndrome with large proteinuria, hypoand dysproteinemia, hypercholesterolemia and edema.

The most common and recognized by many remains the immunological concept of pathogenesis, based, in particular, on the possibility of obtaining nephrotic syndrome in animals using nephrotoxic serum.

The leading pathogenetic factor of nephrotic syndrome is a violation of the structure of the basement membrane. The localization of antibodies on the basement membranes was proven using the method of autoradiography and fluorescent labeling of antibodies.

There is a constant decrease in complement titer at the height of manifestations of nephrotic syndrome, a high titer of antirenal antibodies in the blood of patients with nephrotic-type glomerulonephritis, fixation of complement and immune globulins in the glomeruli of the kidneys of persons with nephrotic-type nephritis, and finally, the effect of immunosuppressant therapy (corticosteroids, cytostatics). This speaks in favor of the immunological theory of pathogenesis.

According to the metabolic concept of the pathogenesis of nephrotic syndrome, proteinuria is mainly due to increased permeability of the glomerular filter.

Currently, the presence of increased proteolytic activity in the kidneys and urine in nephrotic syndrome, an increase in the content of histamine in the blood, a high concentration of lysosomal enzymes in the kidneys, and their participation in the formation of inflammatory reactions have been shown. The resulting serum dysproteinemia is associated with the predominant leakage of finely dispersed protein fractions, as well as with immune shifts in the body.

There is evidence of a violation of protein synthesis in nephrotic syndrome due to changes in the activity of the reticuloendothelial system. Hyperlipidemia, which occurs with nephrotic syndrome, is apparently compensatory in nature and is inversely proportional to hypoproteinemia.

The pathogenesis of edema cannot be reduced to a single hypoproteinemia and a decrease in plasma colloid osmotic pressure. The sodium retention in the body found in nephrotic syndrome due to its increased reabsorption is associated with secondary hyperaldosteronism, which in turn is caused by a decrease in the amount of circulating blood. It is also impossible to exclude the factor of increased capillary permeability not only of the kidneys, but also of other tissues, which occurs as a result of immunological damage to the entire capillary network.

From a clinical point of view, the pathogenesis of proteinuria is very important, since nephrotic syndrome is primarily a large loss of protein in the urine (up to 20 g / day or more). Proteinuria can only be associated with damage and increased permeability of the basement membrane of the glomeruli and, as a result, free penetration of even large protein molecules through the glomerular filter. The dysfunction of podocytes, which normally retain a small amount of protein that penetrates through the basement membrane, is also important.

Any acute nephritis that has not passed without a trace within a year should be considered to have passed into chronic nephritis, and the apparent clinical recovery should be regarded as a long asymptomatic latent period of essentially chronic nephritis.

It should be pointed out that in some cases acute onset diffuse glomerulonephritis can take on the character of subacute malignant extracapillary nephritis with a rapidly progressive course and end in the coming months with death from chronic renal failure.

Diagnosis of acute diffuse glomerulonephritis

The diagnosis of acute diffuse glomerulonephritis does not present great difficulties with severe clinical manifestations of the disease, especially at a young age.

Difficult differential diagnosis between acute nephritis and chronic exacerbation. It is important here to reduce the time from the onset of an infectious disease to acute manifestations of nephritis. At acute glomerulonephritis this period is 1-3 weeks, and in case of exacerbation of the chronic process - only a few days (1-2). The urinary syndrome may be the same, but a persistent drop in urine density below 1015 and the filtration function of the kidneys are more characteristic of an exacerbation of a chronic process.

It is important to emphasize that often leading in the clinic of acute nephritis is a picture of heart failure (shortness of breath, edema, cardiac asthma, etc.). For the recognition of acute nephritis in these cases, the acute development of the disease without signs of a previous heart disease, the presence of a pronounced urinary syndrome, especially hematuria (albuminuria is also characteristic of a congestive kidney), as well as a tendency to bradycardia, are essential.

It is difficult to diagnose the latent form of acute nephritis. The predominance of erythrocytes over leukocytes in the urine sediment, the absence of pale leukocytes (when stained according to Sternheimer-Malbin) and the absence of anamnestic indications of dysuric phenomena help to differentiate from chronic latent pyelonephritis. Data from X-ray urological studies may be important for differentiation from pyelonephritis, nephrolithiasis, kidney tuberculosis and other renal diseases that occur with a small urinary syndrome.

Treatment of acute diffuse glomerulonephritis

Treatment of acute diffuse glomerulonephritis

When treating patients acute glomerulonephritis in the case of a pronounced clinical picture (edema, hypertension), bed rest and a diet with a sharp restriction of salt in food (no more than 1.5-2 g / day) are recommended.

Long-term protein restriction in acute nephritis is not sufficiently substantiated, since retention of nitrogenous wastes, as a rule, is not observed, and an increase in blood pressure under the influence of protein nutrition has not been proven.

Antibacterial therapy (antibiotics, antimicrobials) is indicated with a clear connection between nephritis and the underlying infection, for example, with prolonged septic endocarditis, chronic tonsillitis, etc. In chronic infection of the tonsils, tonsillectomy is also indicated - 2-3 months after the subsidence of acute symptoms. jade jade.

Great importance is attached to desensitizing therapy, large doses of vitamin C.

Very effective in the treatment of acute nephritis is the use of steroid hormones - prednisolone (prednisone), triamcinolone, dexamethasone. Treatment with prednisolone is more indicated after 3-4 weeks from the onset of the disease, when there is a decrease in general symptoms (in particular, hypertension). The use of corticosteroids is especially indicated in the nephrotic form or the prolonged course of acute nephritis, as well as in the presence of the so-called residual urinary syndrome, including hematuria.

Prednisolone is used at an average of 20 mg / day, if necessary, bringing this dose to 60 mg / day.

Corticosteroid therapy has a good effect on both edematous and urinary syndrome. It can promote recovery and prevent the transition of acute nephritis to chronic.

If there is a tendency to increase blood pressure and increase in edema, treatment with corticosteroid hormones should be combined with antihypertensive and diuretic agents.

With complication acute glomerulonephritis eclampsia, bloodletting is used, magnesium sulfate (10 ml of a 25% solution) is administered intravenously, hypnotics and narcotic drugs (chloral hydrate, etc.) are given. Ganglioblockers are shown, for example, hexonium, 10-20 mg 0.5-1 ml of a 2% solution intramuscularly. In the pre-eclamptic period, it is advisable to prescribe reserpine, as well as uregit, hypothiazide or lasix; the latter is especially valuable in the form of injections as a dehydrating agent for cerebral edema.

Forecast, work capacity. In acute nephritis, the prognosis is different. There may be a complete recovery. A lethal outcome in the acute period of the disease is rare, it is more often associated with cerebral hemorrhages against the background of eclampsia, less often with heart failure, pneumonia or acute uremia.

The prognosis of acute nephritis largely depends on early recognition and proper treatment of the disease. In connection with the use of corticosteroid therapy in recent years, it has improved significantly.

In the acute period, patients are disabled and; must be in the hospital. In a typical course, a complete recovery can occur in 2-3 months: patients can return to work even if there is a moderate urinary syndrome or residual albuminuria.

Dispensary observation of persons who have had acute nephritis is very important, since clinical recovery can often be apparent. This is especially important in the presence of even moderate urinary syndrome. In order to avoid relapses, special attention should be paid to the fight against infectious foci in the body. It is necessary to avoid work connected with cooling during the year, especially with the action of damp cold.

• Prevention of chronic diffuse glomerulonephritis
• Which doctors should you contact if you have Chronic diffuse glomerulonephritis

What is chronic diffuse glomerulonephritis

Chronic glomerulonephritis- a long-term immunoinflammatory bilateral kidney disease with clinical manifestations of classic Bright's disease, leading to progressive death of the glomeruli, a decrease in kidney activity, the development of arterial hypertension, followed by the development of renal failure.

What causes chronic diffuse glomerulonephritis

Chronic nephritis can be the outcome of both acute nephritis and primary chronic, without a previous acute attack. Often there are chronic glomerulonephritis of a predominantly immune nature: serum, vaccine, associated with the intake of food antigens, poisons, after an injury, cooling. A number of drugs, in addition to the usual damage to the kidneys such as "acute" toxic kidney, also cause diffuse nephritis, often simultaneously with fever, damage to the skin, joints, liver and spleen.

Chronic glomerulonephritis is a common complication of subacute septic endocarditis. Cases of the development of diffuse kidney damage in patients suffering from tuberculosis, syphilis are described.

Diffuse severe lesions of the renal parenchyma are observed in systemic autoimmune diseases - such as hemorrhagic vasculitis, periarteritis nodosa, systemic lupus erythematosus.

Pathogenesis (what happens?) during Chronic diffuse glomerulonephritis

With the transition of nephritis to a chronic form in the progression, its main role belongs to the reactivity of the macroorganism, the degree of autoimmune disorders.

pathological anatomy

Chronic glomerulonephritis is characterized by damage to the glomeruli, which has an intracapillary character (in contrast to subacute extracapillary nephritis). However, anatomical changes in the kidneys in various forms chronic glomerulonephritis differ significantly both in terms of the nature and degree of damage to the glomeruli and their number, and in relation to the degree of damage to the tubules.

If the nephrotic syndrome prevailed during the life of the patient, then the kidney is enlarged, the capsule is removed easily, its surface is smooth, pale gray (the so-called large white kidney). The cortical layer is expanded, pale gray and sharply demarcated from the reddish medulla. Light microscopy in the proximal parts of the convoluted tubules reveals an expansion of their lumen, edema, atrophy or necrosis of the epithelium, phenomena of granular, hyaline droplet or vacuolar dystrophy, fatty infiltration and the presence of various types of cylinders (hyaline, granular, waxy, fatty). Immunomorphological study in many diseases that occur with nephrotic syndrome reveals the fixation of L-globulin and complement in areas of thickening of the basement membranes (deposit zones), and in lupus nephrotic syndrome, in the area of ​​fibrinoid necrosis of glomerular loops. Electron microscopy reveals early changes in the epithelial cells that cover the outer layer of the main membrane. These cells or podocytes lose their characteristic process formations, numerous vacuoles appear in them.

The change in the basement membranes of the capillary loops of the glomerulus is reduced to edema, thickening, homogenization, loosening and lamellarity.

In recent years, due to the widespread use in the clinic of the method of puncture biopsy, the histological picture of the kidneys in various clinical forms and stages of chronic glomerulonephritis has been well studied. Allocate:

1. membranous glomerulonephritis, characterized by thickening and thickening of the basement membranes of the capillaries of the renal glomeruli,
2. proliferative glomerulonephritis, in which proliferation of cellular elements of the glomeruli is observed, and 3) proliferative fibroplastic or sclerosing type of chronic glomerulonephritis, in which significant sclerosing or fibroplastic changes are already observed. With all these histological types of glomerular lesions, certain changes in the tubular epithelium (dystrophy, degeneration, atrophy), interstitial tissue can be observed.

At the final stage of chronic glomerulonephritis, the kidneys are significantly reduced in size, have a granular surface, a thinned cortical layer - secondary wrinkled kidneys. Histological examination reveals empty glomeruli, growth of connective tissue in their place, and atrophy of the corresponding tubules. In the remaining glomeruli, hyalinosis of capillary loops is noted.

Symptoms of chronic diffuse glomerulonephritis

The clinical picture of chronic glomerulonephritis is polymorphic. It includes the development of edema, hypertension, urinary syndrome (proteinuria, hematuria, cylindruria), hypoproteinemia, hypercholesterolemia. The most common complaints of patients are associated with renal hypertension - visual impairment, development of heart failure, attacks of cardiac asthma; with symptoms of renal failure - weakness, dry skin, sleep disturbance, itching, poor appetite; with kidney damage - pain in the lumbar region, dysuric phenomena, nocturia, etc. Depending on the prevalence of certain syndromes, E. M. Tareev distinguishes the following forms of chronic glomerulonephritis: malignant (extracapillary), latent, hypertonic, nephrotic and mixed . Common to the course of these forms of glomerulonephritis is the progressive nature of the course with the possibility of maintaining normal kidney function for a long time, followed by the development of chronic renal failure.

Subacute, malignant nephritis leads to progressive death of nephrons, deformity of the architectonic junction.

In the biopsy material, proliferative glomerulonephritis with fibrinous-epithelial crescents is determined, which can develop a week after the onset of the disease. At the same time, tubular and interstitial lesions are noted, and fibrinoid necrosis of the glomeruli and arterioles is often found.

A clinically malignant course of nephritis can be suspected if, after 4-6 weeks of an acute onset of the disease, a decrease in the relative density of urine is observed, an increase in the content of creatinine and indican in the blood serum, and blood pressure remains stable at high numbers. The development of edematous syndrome is rare in subacute nephritis. The main clinical manifestation is a rapid and persistent decrease in kidney function, increasing changes in the fundus. The prognosis of the malignant course of glomerulonephritis remains extremely difficult.

Latent chronic diffuse glomerulonephritis. This is a fairly common form, usually manifested only by a mild urinary syndrome without arterial hypertension and edema. The latent form of chronic glomerulonephritis takes on a dramatic form in cases where chronic renal failure is detected, it would seem, among complete health. For years, these patients remain fully functional, not considering themselves sick. Most often, the disease is detected during medical examination, when the doctor pays attention to urinary syndrome (hematuria, proteinuria), a decrease in relative density, nocturia, a slight increase in blood pressure. Sometimes elevated ESR, hypoproteinemia, hypercholesterolemia are detected. This form of chronic glomerulonephritis has a long course (30-40 years), especially in cases where patients manage to exclude factors provoking exacerbation.

Nephrotic form (formerly called nephrosonephritis, or parenchymal nephritis). The nephrotic form is characterized by large proteinuria (more than 3.5 g / day), hypoproteinemia and dysproteinemia with a decrease in plasma albumin content, a significant decrease in the albumin-globulin coefficient, high hypercholesterolemia 104-260 mmol / l (400-1000 mg%), excretion with urine doubly refracting substances. For the most part, patients with this form have massive edema, mainly due to a decrease in the colloid osmotic pressure of plasma proteins associated with hyloproteinemia and dysproteinemia, due to loss of protein in the urine. Edema syndrome develops gradually. Usually in the morning there is swelling under the eyes, swelling of the eyes. In the future, the edema becomes permanent, spreads to the trunk, hydrothorax, ascites, and hydropericardium join. At this stage, dry skin, a decrease in its elasticity, and muscle hypertrophy are observed. The degree of proteinuria correlates with an increase in the content of triglycerides and free cholesterol in the blood plasma, with the formation of large lipoproteins—latexence (EM Tareev).

The nephrotic form of chronic glomerulonephritis, in contrast to pure lipoid nephrosis, is characterized by a combination of nephrotic syndrome with symptoms. inflammatory lesions of the kidneys: moderate hematuria and a decrease in filtration function. An increase in blood pressure, as a rule, is not observed. The clinical picture of the disease can be determined by the nephrotic syndrome for a long time, and only later does the progression of nephritis occur with a violation of the nitrogen excretion function of the kidneys and arterial hypertension.

Hypertensive form of chronic nephritis

For a long time, the leading and often the only symptom is hypertension.

Occasionally, chronic glomerulonephritis develops according to the hypertensive type after the first violent attack of nephritis. It is more often the result of a latent course of acute nephritis, which may go unnoticed. An increase in blood pressure for a long time can be intermittent in nature, in the future it becomes permanent with an increase in systolic and diastolic pressure in the evening up to 200/120 mm Hg. Art. Under the influence of various factors: cold, emotional influences - blood pressure can be subject to large fluctuations. On examination, attention is drawn to the rising apex beat, expansion from. relative dullness of the heart to the left, accent II tone over the aorta, in some patients a gallop rhythm is heard. With the progression of heart failure, a clinic of stagnation develops in a small circle, hemoptysis, attacks of cardiac asthma are possible, and in rare cases, pulmonary edema.

As a rule, hypertension in chronic glomerulonephritis, in contrast to subacute, does not acquire a malignant character. It is not prone to rapid progression; blood pressure, especially diastolic, does not reach extremely high numbers. Changes in the fundus in the form of neuroretinitis are expressed relatively little. For a long time only narrowing of the arteries is observed, retinal hemorrhages are rare;

retinal exudation and edema, as well as changes in the papillae of the optic nerve, appear only at the end of the disease. As for the pathogenesis of arterial hypertension in this form of nephritis, there are more or less certain data indicating the importance of the renal ischemic, renin-hypertensive mechanism of its development. With the progression of the disease, chronic renal failure develops and the disease can acquire the features of malignant hypertension.

Mixed form of diffuse glomerulonephritis. The mixed form of chronic glomerulonephritis is characterized by the presence of most of the main syndromes and symptoms of classic parenchymal nephritis: edema, hematuria, proteinuria, hypertension, but the degree of their manifestation in most cases is not as pronounced as it is noted in other forms. Biopsy reveals a proliferative component. The mixed form of chronic glomerulonephritis is characterized by a progressive course. Renal failure develops rather quickly (2-5 years), steroids and immunosuppressants rarely have a positive effect. In most cases, the clinic of exacerbations of chronic glomerulonephritis is characterized by the predominance of one or another syndrome. Quite often, only urinary symptoms can be observed for a long time and the well-being of patients is not disturbed. At this time, only with special studies, some violations of kidney function are detected, first of all, a decrease in filtration, and then a concentration ability. Signs of chronic renal failure appear much later - chronic azotemic uremia.

During chronic nephritis allocate:

a) the stage of renal compensation, i.e. sufficient nitrogen excretion function of the kidneys. This stage may be accompanied only by urinary symptoms and is latent for a long time;

b) the stage of renal decompensation, which is characterized by insufficient nitrogen excretion of the kidneys. At this stage, urinary symptoms may be less severe; as a rule, there is high arterial hypertension, edema is often moderate.

The onset of the second period varies widely - from 1 year to 40 years; this period is the shortest in the malignant nature of the disease and the longest in its latent course.

A sudden exacerbation of the disease, characterized by a deterioration in general well-being, with a pronounced manifestation of the main syndromes, a decrease in the specific gravity of urine, an increase in protein excretion - all this may indicate an unfavorable evolution of the disease. The progression of the disease is further manifested by an increase in the level of urea, creatinine, indican in blood plasma, a decrease in glomerular filtration and an increase in the filtration fraction.

Forecast

The outcome of chronic glomerulonephritis is the wrinkling of the kidneys with the development of chronic renal failure - chronic uremia. Until recently, this outcome was observed in all cases of chronic glomerulonephritis, however, at different times from the onset of the disease. Over the past 10-15 years, the prognosis of chronic glomerulonephritis in connection with the introduction of immunosuppressive therapy into clinical practice has become much better. With the use of immunosuppressive therapy, in particular corticosteroid, in 70-80% of cases a positive effect is observed, and in 14-18% of cases, a complete remission of the disease with the disappearance of all general and urinary symptoms.

Diagnosis of chronic diffuse glomerulonephritis

In the presence of acute nephritis in history and a pronounced clinical picture, the diagnosis of chronic nephritis does not present great difficulties. However, with a latent course, with a hypertonic form, its recognition can be very difficult (Table 35).

If there are no definite indications of acute nephritis in the anamnesis, then with a moderately severe urinary syndrome one has to reckon with the possibility of having one of the many unilateral or bilateral kidney diseases: chronic pyelonephritis, anomalies in the development of the kidneys, stenosing lesions of the renal arteries, etc. One should also remember the possibility of orthostatic albuminuria.

When differentiating with hypertension, the time of onset of the urinary syndrome is important in relation to arterial hypertension. In chronic glomerulonephritis, urinary syndrome may long precede arterial hypertension or occur simultaneously with it. Chronic glomerulonephritis is also characterized by a lesser severity of cardiac hypertrophy, a lesser tendency to hypertensive crises (with the exception of exacerbations that occur with eclampsia) and less intense development of atherosclerosis, including coronary arteries.

The hypertensive and latent form of chronic glomerulonephritis should be uremia with chronic pyelonephritis, as well as renovascular hypertension. In favor of aphonic glomerulonephritis is the predominance of erythrocytes over leukocytes in the urine sediment and the absence of active leukocytes (when stained according to Sternheimer-Malbin), as well as the same size and shape of the two kidneys and the normal structure of the pelvis and calyces (which can be detected by X-ray urological studies).

Nephrotic form of chronic nephritis must be differentiated from lipoid nephrosis, amyloidosis, diabetic glomerulosclerosis, heart failure, liver cirrhosis. In favor of chronic nephritis, along with the nephrotic syndrome, there are also signs of inflammatory damage to the kidneys in the form of microhematuria, a decrease in kidney function, and a tendency to arterial hypertension. Of decisive importance in many cases belongs to the morphological study of the biopsy of the affected organ.

In relation to differentiation with amyloidosis of the kidneys, the following matters: 1) the presence in the body of foci of chronic infection in the form of suppurative processes in the lungs, osteomyelitis, tuberculosis, rheumatoid arthritis and other diseases; 2) the presence of amyloid degeneration of another localization. In some cases, there is a need for differential diagnosis with a congestive kidney with circulatory failure. However, this syndrome is accompanied by edema, sometimes moderate arterial hypertension. A congestive kidney is indicated by the presence of an independent primary heart disease, an enlarged liver, the location of edema mainly in the lower extremities, a lesser severity of hypercholesterolemia, and an improvement or disappearance of the urinary syndrome with a decrease in cardiac decompensation.

Special mention requires the so-called idiopathic edema, sometimes reaching a significant size. However, they do not show any proteinuria or biochemical disorders characteristic of nephrotic syndrome. Differentiation from cachectic edema, which occurs, for example, in malignant neoplasms, usually does not present difficulties.

Treatment of chronic diffuse glomerulonephritis

Patients with chronic nephritis should avoid cooling, especially exposure to damp cold. They prefer a dry and warm climate. With a satisfactory general condition and the absence of complications, sanatorium treatment is indicated in the resorts of Central Asia (Bayram-Ali) or on the southern coast of Crimea (Llta). Bed rest is necessary only during periods of significant edema or heart failure, as well as in the terminal stage with symptoms of uremia. The regimen for chronic nephritis in the remission phase should be gentle. Hard physical labor, work on the night shift, outdoors during the cold season, in hot shops, stuffy, poorly ventilated rooms are contraindicated. Patients should avoid nervous and physical overwork. In cases of acute intercurrent disease, appropriate treatment with antimicrobial drugs against the background of bed rest is recommended.

In the treatment of patients with chronic glomerulonephritis, the diet is essential, which should vary depending on the form and stage of the disease. In nephrotic and mixed forms (in the presence of edema), the content of sodium chloride in the diet should be limited to 1.5–2.5 g. provided that the excretory function of the kidneys is sufficient, the diet should contain a sufficient amount of proteins - up to 2-2.5 g per 1 kg of the patient's body weight, which contributes to a positive nitrogen balance and compensation for protein losses. In the hypertensive form, it is recommended to moderately limit the intake of sodium chloride - up to 5 g / day with a normal content of proteins and carbohydrates in the diet. The latent form does not require significant restrictions in the diet of patients; nutrition should be complete, varied and rich in vitamins. Vitamins (C, complex B, A) should be included in the diet for other forms of chronic glomerulonephritis. It should be pointed out that a long-term protein-free diet without salt does not prevent the progression of nephritis and has a bad effect on the general condition of patients.

In recent years, anticoagulants have been used to treat chronic diffuse glomerulonephritis. The pathogenetic rationale for anticoagulant therapy is the deposition of fibrin observed in glomerulonephritis in the glomeruli and arterioles, the participation of fibrin in the formation of capsular crescents, and a frequent increase in plasma fibrinogen.

With nephrotic and mixed forms (in the presence of edema), the content of sodium chloride in the diet should be limited to 1.5-2.5 g. Provided that the excretory function of the kidneys is sufficient, the diet should contain a sufficient amount of proteins - up to 2-2.5 g per 1 kg of the patient's body weight, which contributes to a positive nitrogen balance and compensation for protein losses. In the hypertensive form, it is recommended to moderately limit the intake of sodium chloride - up to 5 g / day with a normal content of proteins and carbohydrates in the diet. The latent form does not require significant restrictions in the diet of patients; nutrition should be complete, varied and rich in vitamins. Vitamins (C, complex B, A) should be included in the diet for other forms of chronic glomerulonephritis. It should be pointed out that a long-term protein-free diet without salt does not prevent the progression of nephritis and has a bad effect on the general condition of patients.

Most clinicians recommend 35–50 g of protein per day plus the amount of protein lost in the urine per day. The amount of dietary protein is reduced only with a decrease in renal function. The diet should be rich in fruit and vegetable juices containing vitamins A, B, C and E.

Of particular importance is corticosteroid therapy, which is the basis of pathogenetic therapy in this disease. Treatment usually begins with 15-20 mg of prednisolone, if necessary, increasing the dose to 60-80 mg / day, 4 then gradually reduce it. With an exacerbation of the disease, courses of treatment with glucocorticoids are repeated.

Sometimes intermittent glucocorticoid therapy is used - 3 days (in a row) per week, which reduces the possibility of developing "steroid cushingoid", steroid ulcers, while maintaining the therapeutic effect of hormones.

The use of corticosteroids leads to a decrease in the inflammatory process in the glomeruli of the kidneys, which improves filtration and is expressed in a decrease in urinary syndrome, hematuria and proteinuria, which secondarily leads to an improvement in the protein composition of the blood. In the treatment of corticosteroids, Cushing's syndrome, steroid ulcers, osteoporosis can often develop.

A contraindication to the use of corticosteroids in patients with chronic nephritis is progressive azotemia. In case of contraindications to the use of corticosteroids or treatment failure, non-hormonal immunosuppressants are recommended: azathioprine (imurana), 6-mercaptopurine. These drugs are more effective, but they cause severe leukopenia. Treatment with them is better tolerated with the simultaneous use of prednisolone in a moderate dose of 10-30 mg / day, which prevents the toxic effects of non-hormonal immunosuppressants on leukopoiesis.

In the later stages - with glomerular sclerosis and atrophy with high hypertension - immunosuppressants and steroid hormones are contraindicated. since immunological activity in

Other glucocorticoid drugs are prescribed in a dose converted to prednisolone.

the glomeruli are no longer there and the continuation of such treatment only exacerbates hypertension.

A mild immunosuppressive effect is possessed by drugs of the 4-aminoquinoline series - chingamine (delagil, rezoquin, chloroquine), hydroxychloroquine (plaquenil). Rezoquin (chloroquine) is used at 0.25 g 1-2-3 times a day for 2-3-8 months. For the treatment of inflammatory changes in the renal parenchyma, non-steroidal anti-inflammatory drugs are also used, in particular indomethacin, which, in addition to analgesic and antipyretic effects, acts on mediators of immunological damage. Under the influence of indomethacin, proteinuria decreases. Assign it inside at 25 mg 2-3 times a day, then, depending on tolerance, increase the dose to 100-150 mg / day. Treatment is carried out for a long time, for several months. The simultaneous use of steroid hormones and indomethacin allows you to significantly reduce the dose of corticosteroids with a gradual complete withdrawal.

In recent years, anticoagulants have been used to treat chronic diffuse glomerulonephritis. The pathogenetic rationale for anticoagulant therapy is the deposition of fibrin observed in glomerulonephritis in the glomeruli and arterioles, the participation of fibrin in the formation of capsular crescents, and a frequent increase in plasma fibrinogen. By enhancing fibrinolysis, neutralizing complement (a component of immune reactions), heparin affects many allergic and inflammatory manifestations, reduces proteinuria, reduces dysproteinemia, and improves the filtration function of the kidneys. Assigned intramuscularly (20,000 IU per day) or intravenous drip (1000 U / h), heparin can be used in combination with steroids and cytostatics. In the presence of severe hematuria due to an increase in plasma fibrinolytic activity, aminocaproic acid, which is a plasminogen inhibitor, is successfully used at a dose of 3 g intravenously every 6 hours. A good effect in hematuria is provided by taking nettle extract for 4-5 weeks.

is a progressive diffuse immunoinflammatory lesion of the glomerular apparatus of the kidneys with an outcome in sclerosis and renal failure. It can be asymptomatic, include an increase in blood pressure, edema, and violations of the general condition. In the diagnosis, clinical and biochemical examination of urine, ultrasound of the kidneys, morphological examination of the renal tissue (biopsy), excretory urography, and renography are used. Treatment includes nutritional regulation, corticosteroid, immunosuppressive, anticoagulant, diuretic, antihypertensive therapy.

General information

Chronic glomerulonephritis in urology and nephrology is understood as primary glomerulopathies of different etiology and pathomorphology, accompanied by inflammatory and destructive changes and leading to nephrosclerosis and chronic renal failure. Among all therapeutic pathology, the disease is about 1-2%, which allows us to talk about its relatively high prevalence. Pathology can be diagnosed at any age, but more often the first signs of nephritis develop in 20-40 years. Signs of a chronic process are a long (more than a year) progressive course of glomerulonephritis and bilateral diffuse kidney damage.

Causes

Chronicization and progression of the disease may be the result of untreated acute glomerulonephritis. However, there are often cases of development of primary chronic glomerulonephritis without a previous episode of an acute attack. It is not always possible to find out the cause of the disease. Leading importance is attached to nephritogenic strains of streptococcus and the presence in the body of foci of chronic infection (pharyngitis, tonsillitis, sinusitis, cholecystitis, caries, periodontitis, adnexitis, etc.), persistent viruses (influenza, hepatitis B, herpes, chicken pox, infectious mononucleosis, rubella, cytomegalovirus infection).

In some patients, chronic glomerulonephritis is due to hereditary predisposition (defects in the cellular immunity or complement system) or congenital renal dysplasia. Also, non-infectious factors include allergic reactions to vaccination, alcohol and drug intoxication. Other immunoinflammatory diseases can cause diffuse damage to nephrons - hemorrhagic vasculitis, rheumatism, systemic lupus erythematosus, septic endocarditis, etc. Cooling and weakening of the overall resistance of the body contribute to the emergence of pathology.

Pathogenesis

In the pathogenesis of chronic glomerulonephritis, the leading role belongs to immune disorders. Exogenous and endogenous factors cause the formation of specific CECs, consisting of antigens, antibodies, complement and its fractions (C3, C4), which are deposited on the glomerular basement membrane and cause its damage. In chronic glomerulonephritis, glomerular damage is intracapillary in nature, disrupting microcirculation processes with the subsequent development of reactive inflammation and dystrophic changes.

The disease is accompanied by a progressive decrease in the weight and size of the kidneys, thickening of the kidney tissue. Microscopically, the fine-grained surface of the kidneys, hemorrhages in the tubules and glomeruli, loss of clarity of the medulla and cortical layer are determined.

Classification

In etiopathogenetic terms, infectious-immune and non-infectious-immune variants of chronic glomerulonephritis are distinguished. According to the pathomorphological picture of the detected changes, minimal, proliferative, membranous, proliferative-membranous, mesangial-proliferative, sclerosing types of the disease and focal glomerulosclerosis are distinguished. During the pathology, a phase of remission and exacerbation is distinguished. According to the rate of development, the disease can be rapidly progressive (within 2-5 years) and slowly progressive (more than 10 years).

In accordance with the leading syndrome, several forms of chronic glomerulonephritis are distinguished: latent (with urinary syndrome), hypertension (with hypertensive syndrome), hematuric (with a predominance of gross hematuria), nephrotic (with nephrotic syndrome), mixed (with nephrotic-hypertensive syndrome). Each of the forms proceeds with periods of compensation and decompensation of the nitrogen-excreting function of the kidneys.

Symptoms of chronic glomerulonephritis

Symptoms are due to the clinical form of the disease. The latent form occurs in 45% of patients, occurs with an isolated urinary syndrome, without edema and arterial hypertension. It is characterized by moderate hematuria, proteinuria, leiocyturia. The course is slowly progressive (up to 10-20 years), the development of uremia comes late. In the hematuric variant (5%), persistent hematuria, episodes of gross hematuria, and anemia are noted. The course of this form is relatively favorable, uremia occurs rarely.

The hypertensive form of chronic glomerulonephritis develops in 20% of cases and proceeds with arterial hypertension with mild urinary syndrome. BP rises to 180-200/100-120 mm Hg. Art., often subject to significant daily fluctuations. There are changes in the fundus of the eye (neuroretinitis), left ventricular hypertrophy, cardiac asthma, as a manifestation of left ventricular heart failure. The course of this form is long and steadily progressing with an outcome in renal failure.

The nephrotic variant, occurring in 25% of cases, occurs with massive proteinuria (over 3 g / day), persistent diffuse edema, hypo- and dysproteinemia, hyperlipidemia, dropsy of serous cavities (ascites, hydropericardium, pleurisy) and associated shortness of breath, tachycardia , thirsty. Nephrotic and hypertensive syndromes are the essence of the most severe, mixed form of chronic glomerulonephritis (7% of cases), which occurs with hematuria, severe proteinuria, edema, arterial hypertension. An unfavorable outcome is determined by the rapid development of renal failure.

Diagnostics

The leading diagnostic criteria are clinical and laboratory data. When collecting anamnesis, the fact of the presence of chronic infections, acute glomerulonephritis, and systemic diseases is taken into account. Typical changes in the general analysis of urine are the appearance of erythrocytes, leukocytes, cylinders, protein, a change in the specific gravity of urine. To assess kidney function, Zimnitsky and Reberg tests are performed. Hypoproteinemia and dysproteinemia, hypercholesterolemia are detected in the blood, the titer of antibodies to streptococcus (ASL-O, antihyaluronidase, antistreptokinase) increases, the content of complement components (C3 and C4) decreases, the level of IgM, IgG, IgA increases.

Ultrasound of the kidneys in the progressive course of chronic glomerulonephritis reveals a decrease in the size of organs due to sclerosis of the renal tissue. Excretory urography, pyelography, nephroscintigraphy help to assess the state of the parenchyma, the degree of impaired renal function. To detect changes from other systems, an ECG and EchoCG, ultrasound of the pleural cavities, and an examination of the fundus are performed.

Depending on the clinical variant of the disease, differential diagnosis is required with chronic pyelonephritis, nephrotic syndrome, polycystic kidney disease, nephrolithiasis, kidney tuberculosis, kidney amyloidosis, arterial hypertension. To establish the histological form of chronic glomerulonephritis and its activity, as well as to exclude pathology with similar manifestations, a kidney biopsy is performed with a morphological study of the obtained sample of renal tissue.

Treatment of chronic glomerulonephritis

Features of therapy are dictated by the clinical form of the disease, the rate of progression of disorders and the presence of complications. It is recommended to observe a sparing regime with the exception of overwork, hypothermia, occupational hazards. During periods of remission, treatment of chronic infections is required to support the course of the process. The diet prescribed for chronic glomerulonephritis requires limiting salt, alcohol, spices, accounting for fluid intake, and increasing the daily protein intake.

Drug treatment consists of immunosuppressive therapy with glucocorticosteroids, cytostatics, NSAIDs; prescribing anticoagulants (heparin, phenindione) and antiplatelet agents (dipyridamole). Symptomatic therapy may include taking diuretics for edema, antihypertensive drugs for hypertension. In addition to full inpatient courses of therapy during periods of exacerbation, supportive outpatient therapy during remission, treatment at climatic resorts is indicated.

Forecast and prevention

Effective treatment of chronic glomerulonephritis eliminates the leading symptoms (hypertension, edema), delays the development of renal failure and prolongs the life of the patient. All patients are under dispensary registration with a nephrologist. The most favorable prognosis has a latent form; more serious - hypertensive and hematuric; unfavorable - nephrotic and mixed forms. Complications that worsen the prognosis include pleuropneumonia, pyelonephritis, thromboembolism, and renal eclampsia.

Since the development or progression of irreversible changes in the kidneys is most often initiated by streptococcal and viral infections, wet hypothermia, their prevention is of paramount importance. With the pathology associated with chronic glomerulonephritis, it is necessary to observe related specialists - an otolaryngologist, dentist, gastroenterologist, cardiologist, gynecologist, rheumatologist, etc.

The content of the article:

Glomerulonephritis is a diffuse multifactorial disease of the glomerular apparatus of the kidneys of immune or allergic origin.

A chronic inflammatory process in the glomeruli leads to the loss of the functional ability of the kidneys to rid the blood of toxins.

A long-term pathology is always complicated by the development of chronic renal failure.

Chronization of the process is discussed when immune inflammation in the kidneys exists for a year.

Code according to the international classification of diseases ICD-10:

N03 Chronic nephritic syndrome

Pathogenesis

1. The following changes occur in the walls of the vessels of the renal glomeruli:

The permeability of the vascular wall of the renal glomerulus for cellular elements increases.

The formation of microthrombi occurs, followed by blockage of the lumen of the vessels of the glomerular apparatus.

Blood circulation in the modified vessels is disturbed, up to complete ischemia.

Erythrocytes settle on important renal structures of the nephron: Bowman's capsule, renal tubules.

The process of filtering the blood and the production of primary urine is disrupted.

Violation of blood circulation in the renal glomerulus entails the desolation of the lumen and the gluing of the walls, followed by the transformation of the nephron into connective tissue. The gradual loss of structural units leads to a decrease in the volume of filtered blood (one of the causes of CRF). There are fewer and fewer nephrons capable of performing their work normally, which leads to poisoning of the body with metabolic products, while the necessary substances are returned to the blood in an incomplete volume.

Etiology and provoking factors

The etiology of CGN is as follows:

Infectious agents - bacterial (Str, Staf, Tbs, etc.), viral (hepatitis B, C, cytomegalovirus, HIV)

Toxic agents - alcohol, drugs, organic solvents, mercury

The cause in most cases is group A beta-hemolytic streptococcus.

Diseases that contribute to the development of pathology:

Angina and chronic tonsillitis,
Scarlet fever,
infectious diseases of the heart,
Sepsis,
Pneumonia,
mumps,
rheumatic diseases,
Autoimmune pathology.

Classification of chronic glomerulonephritis

Form of glomerulonephritis	The activity of the renal process	Status of kidney function
1. Acute glomerulonephritis With nephritic (hematuric) syndrome - with nephrotic syndrome - with isolated urinary syndrome - with nephrotic syndrome, hematuria and hypertension	1. The period of initial manifestations (peak) 2. Period of reverse development 3. Transition to chronic glomerulonephritis	3. Acute renal failure
2. Chronic glomerulonephritis Hematuric form - nephrotic form - mixed form	1. Period of exacerbation 2. Period of partial remission 3. The period of complete clinical and laboratory remission	1. No kidney dysfunction 2. With impaired renal function 3. Chronic renal failure
3. Subacute (malignant) glomerulonephritis		1. With impaired renal function 2. Chronic renal failure

Morphological classification of CGN

diffuse proliferative

With half moons

Mesangioproliferative

Membrane-proliferative (mesangiocapillary)

membranous

With minimal changes

Focal segmental glomerulosclerosis

Fibrillar-immunotactoid

fibroplastic

The classification is based on an assessment of clinical and laboratory syndromes, pathogenesis (primary, secondary), functional ability of the kidneys (with loss, without loss, CRF) and morphology.

The course of CG is:

Recurrent (remission is replaced by an exacerbation).
Persistent, (constant activity of immune inflammation in the glomeruli with the preservation of the functional abilities of nephrons for a long time).
Progressive (constant activity of the process with a tendency to renal failure, and a gradual decrease in glomerular filtration).
Rapidly progressive (the process is so active that after a short period of time CRF is formed).

Clinical manifestations

In most cases, the pathology is characterized by slow development. Many patients cannot remember when the onset was and after which they fell ill.

The most typical signs:

Diuresis depends on the severity of chronic renal failure: a decrease in daily diuresis (oliguria) at the initial stage, with progression - polyuria (a lot of urine) with an outcome in anuria in the terminal stage of CRF, in the clinical analysis of urine, the pathological content of protein and erythrocytes.
Urination predominates, mainly at night: nocturia.
Edema: from minor to severe, localization is different.
Weakness, fatigue.
Increasing the temperature response.
development of persistent hypertension.
Thirst, the smell of acetone in the exhaled air, skin itching indicate the neglect of the disease and the progress of CRF.

There are several forms of chronic glomerulonephritis

Glomerulonephritis with isolated urinary syndrome

Isolated urinary syndrome is characterized by the following features:

Asymptomatic hematuria

Asymptomatic proteinuria

No complaints

No edema, AH

The most common variant is characterized by a benign course (aggressive treatment is not prescribed). The patient has no complaints with this form.

When examined in the urine, a small amount of protein and erythrocytes are found.

Since the disease proceeds secretly, and the progression of renal failure is slow but constant, sometimes all laboratory and clinical signs of chronic renal failure are found in first-time patients.

The latent form of chronic glomerulonephritis, despite the benign course with timely diagnosis, can be the cause of renal failure.

Nephrotic form of glomerulonephritis

Occupies a little over 20% of cases. It differs by pronounced clinical manifestations, the leading symptom is the appearance of significant edema.

In the clinical analysis of urine, the loss of protein (mainly albumin) is more than 3 g / day, due to which, on the contrary, there is not enough protein substances in the plasma.

Increased blood cholesterol, triglycerides and low-density lipoproteins.
The nephrotic form of glomerulonephritis is an indication for emergency hospitalization of the patient, since his condition is regarded as severe due to the development of ascites, pleurisy, etc. against the background of massive edema. In addition, the patient has a risk of developing a secondary infection against the background of reduced immunity, osteoporosis, thrombosis, hypothyroidism, atherosclerosis, heart attack, stroke.

All of the above pathology is a consequence of a violation of water and electrolyte balance (loss of zinc, copper, vitamin D, calcium, thyroid-stimulating hormones, etc. in the urine).

The most formidable complications of the nephrotic form of glomerulonephritis are cerebral edema and hypovolemic shock.

Mixed variant or hypertensive form of glomerulonephritis

It is characterized by a combination of nephrotic syndrome and persistent hypertension (increased blood pressure). Typically, rapid progression with an outcome in chronic renal failure, due to the detrimental effect of hypertension on the renal vessels.

Hematuric form of glomerulonephritis

Chronic glomerulnephritis in men is more often in the hematuric form.

Edema does not appear, there is no increase in blood pressure.

There is no pronounced proteinuria (no more than 1g/day), but there is hematuria (erythrocytes in the urine).

Factors provoking hematuric chronic glomerulonephritis include:

alcohol intoxication,
poisoning with any substance
colds in Berger's disease.

Nephrologists note the following pattern: the brighter the clinical manifestations, the greater the chances of a complete restoration of the functional ability of the kidneys.

It must be remembered that any form of CG, under certain circumstances, can go into an acute stage with a clinic typical of acute glomerulonephritis.

Chronic glomerulonephritis in the acute stage will be treated according to the scheme used in the treatment of acute immune inflammation of the kidneys.

How to diagnose chronic glomerulonephritis

An important role in the diagnosis of CG is assigned to clinical and laboratory studies. During the conversation between the doctor and the patient, attention is paid to the presence of infectious diseases in the anamnesis, comorbidities, in particular, systemic diseases, and the urological history is clarified.

General clinical analysis of urine

Urine in chronic glomerulonephritis is variable, it depends on the morphology of the pathological process. Typically, a decrease in specific gravity; the greater the amount of protein in the urine (up to 10 g / day), the more data for the nephrotic form.

Erythrocytes are present: gross hematuria or microhematuria. In the urine sediment, hyaline and granular casts (nephrotic and mixed form), fibrin are found.

For the hypertensive form, a decrease in glomerular filtration is typical.

Biochemistry of blood

1. increase in the level of cretinin, urea,
2. hypoproteinemia and dysproteinemia,
3. hypercholesterolemia.
4. increase in the titer of antibodies to streptococcus (ASL-O, antihyaluronidase, antistreptokinase),
5. decrease in the level of C3 and C4,
6. increase in all immunoglobulins M, G, A
7. electrolyte imbalance.

Urine culture for flora and sensitivity to drugs.
Zimnitsky test.
Nechiporenko test.
Rehberg's test.

Instrumental diagnostics

Doppler ultrasound of the kidneys
At the initial stages, ultrasound diagnostics does not reveal pronounced changes.
If there is a progression of chronic glomerulonephritis, sclerotic processes in the kidneys with a decrease in their size are possible.

Survey and excretory urography, radioisotope scintigraphy allow to evaluate the function of each kidney separately and the general condition of the parenchyma.

ECG
If the patient has persistent hypertension, electrocardiography will confirm hypertrophy (enlargement) of the left ventricle.

Fundus examination

The symptoms are similar to those of hypertension:

1. narrowing of the arteries,
2. varicose veins,
3. pinpoint hemorrhages,
4. microthrombosis,
5. puffiness.

To determine the morphological component of the form of chronic hepatitis, it is possible to conduct a diagnostic biopsy. According to the results of the morphological conclusion, the treatment tactics are chosen.

The procedure is considered invasive and has a number of contraindications:

Solitary kidney or no collateral kidney function.
Coagulopathy.
Right ventricular failure.
infectious processes.
Hydronephrosis.
Polycystic.
Thrombosis of the renal arteries.
Kidney cancer.
Heart attacks, acute stroke.
Confusion of consciousness.

Differential diagnosis is carried out with the following diseases:

chronic pyelonephritis,
hemorrhagic fever with renal syndrome,
nephrolithiasis,
hypertension,
tuberculous lesions of the genitourinary organs, etc.

Treatment for chronic glomerulonephritis

The treatment regimen will depend on the form of the disease, clinical manifestations, comorbidities, and the presence of complications.

The main aspects of treatment for chronic glomerulonephritis are to normalize blood pressure, eliminate edema and maximize the lengthening of the pre-dialysis time period.
It is recommended to normalize the regime of work and rest, to avoid hypothermia, work with toxic substances.

Pay attention to the timely sanitation of foci of possible infection: caries, tonsils, throat, etc.

Diet for chronic glomerulonephritis

Great importance is attached to the correct diet.

Chronic renal failure leads to a violation of the electrolyte balance of the blood, self-poisoning of the body as a result of the accumulation of toxic substances.

Properly selected nutrition is able to correct the adverse effects of toxins on the body at the initial stage of CRF. Yes, and at all other stages of chronic renal failure without a diet, nowhere.

What can you eat with glomerulonephritis - unites diet (table number 7).

Her main theses:

Rejection of salt.
Reducing the amount of fluid consumed.
Introduction to the diet of foods with a high content of potassium and calcium.
Limiting the intake of animal proteins.
Introduction to the diet of vegetable fats and carbohydrates.

Proper nutrition with chronic hepatitis will allow you to do without hemodialysis or kidney transplantation for longer

Medicines for chronic glomerulonephritis

Immunosuppressive drugs

First line drugs are immunosuppressive agents. Due to the overwhelming effect on the activity of the immune system, the pathological processes in the glomerular apparatus of the kidney are slowed down.

Steroids

The dosage of prednisolone is calculated individually, 1 mc / kg per day, for 2 months, with a gradual decrease in order to avoid withdrawal syndrome. Periodically prescribed pulse therapy (the introduction of corticosteroid drugs in a high dose for a short time). With irregular intake, incorrect dosage, untimely therapy, and with a severe degree of immune disorders, the effectiveness is reduced.

Contraindications for treatment with nonsteroidal hormones are the following conditions:

Tuberculosis and syphilis in active form,
viral ophthalmic diseases,
infectious processes,
lactation,
pyoderma.

Steroids are used with caution in diabetes mellitus, thromboembolism, herpes,
systemic candidiasis, hypertension, Itsenko-Cushing's disease, severe chronic renal failure.

Cytostatics

Applied with progressive forms of chronic pyelonephritis in men and women, and in all cases where there are contraindications to the appointment of steroid drugs, or the appearance of complications, or in the absence of the effect of therapy.

Sometimes hormonal drugs and cytostatics are included in the treatment regimen at the same time.

Contraindications: pregnancy and the active phase of infectious processes.

With caution: severe violations of the liver and kidneys, blood pathology.

List of cytostatics for chronic glomerulonephritis in men and women:

Cyclophosphamide,
Chlorambucil,
Cyclosporine
Azathioprine

Complications: hemorrhagic cystitis, pneumonia, agranulocytosis (pathological changes in the blood, oppression of hematopoiesis).

With developed side effects, cytostatic therapy for chronic glomerulonephritis in men and women is canceled.

Non-steroidal anti-inflammatory drugs

It was believed that Indomethacin, Ibuklin, Ibuprofen are able to suppress the autoimmune response. Not all nephrologists prescribe NSAIDs, since drugs from the NSAID group have a toxic effect on the kidneys and often provoke the development of drug-induced nephropathy even without glomerulonephritis.

Anticoagulants and antiplatelet agents

Contribute to the improvement of the rheological properties of blood. They prevent the processes of thrombosis in the renal glomeruli and the adhesion of blood vessels. Heparin is most often used in a course of 3 to 10 weeks in individual dosages, which depend on many factors, including coagulation parameters.

Symptomatic therapy

Symptomatic therapy depends on the clinical manifestations of chronic glomerulonephritis and includes:

Antihypertensive drugs.
Diuretics.
Antibiotics.

Antihypertensive drugs

Some forms of GM are characterized by a persistent increase in blood pressure, therefore, the appointment of antihypertensive drugs from the group of ACE inhibitors is justified:

captopril,
enalapril,
ramipril.

Diuretics

To activate the flow of fluid in the nephron, diuretics are used:

Antibacterial drugs

Sometimes chronic hepatitis occurs against the background of any infections, in which case antibacterial drugs are prescribed to prevent secondary infection. Protected penicillins are more often prescribed, since the drugs are less toxic and effective against group A beta-hemolytic streptococcus.

In case of intolerance to penicillins, cephalosporin antibiotics can be used. The use of antibiotics is justified when there is a proven connection between the development of glomerulonephritis and an infectious process, for example, in a man or woman, glomerulonephritis after streptococcal tonsillitis appeared 14 days later.

The outcome of chronic diffuse glomerulonephritis is always secondary wrinkling of the kidneys and the onset of chronic renal failure.

If chronic renal failure has led to significant disturbances in the functioning of the body, when the creatinine level reaches 440 µmol/l, program hemodialysis is indicated. In this case, the direction of the patient for examination for disability is justified. By itself, the diagnosis of CG, without impaired renal function, does not give the right to disability.

Hypercholesterolemia is treated with statins to lower cholesterol levels.
There are good reviews from the use of plasmapheresis for glomerulonephritis.

Chronic glomerulonephritis in children

In pediatrics, glomerulonephritis in children ranks second after urinary tract infections. Most often, children aged 3 to 9 years are affected.

Boys experience immune inflammation in the kidneys 2 times more often than girls. In some cases, the pathology develops 10-14 days after the childhood infection. As well as in adult men and women, chronic glomerulonephritis is the outcome of an acute immunological process in the kidneys.

Clinical manifestations, forms, signs are identical.

Treatment is less aggressive due to age.

Chronic glomerulonephritis in children is treated by a nephrologist.

Prevention of exacerbations in chronic glomerulonephritis comes down to timely sanitation of foci of inflammation, regular monitoring of clinical and laboratory parameters, diet, avoidance of hypothermia, timely treatment.

Prognosis for chronic glomerulonephritis depending on the morphological variant

GN minimal changes - the safety of kidney function after 5 years - 95%;

Membranous GN - preservation of kidney function after 5 years - 50-70%

FSGS - preservation of kidney function after 5 years - 45 -50%

Mesangioproliferative - preservation of kidney function after 5 years - 80%

Membrano-proliferative - preservation of kidney function after 5 years - 45 - 60%

Life expectancy depends on the clinical variant of the disease and the characteristics of the functional state of the kidneys.

Favorable prognosis for the latent variant (subject to timely treatment), doubtful for hematuric and hypertonic variants.

The prognosis is unfavorable for nephrotic and mixed forms of glomerulonephritis.