Glomerulonephritis - inflammation of the renal glomeruli, to a lesser extent tubules, accompanied by secondary circulatory disturbances in the kidneys with a delay in the body of water and salt, often the development of severe fluid overload and hypertension. In most cases, glomerulonephritis develops as a result of an excessive immune response to infectious antigens. The most common cause of the disease is streptococcal infection (tonsillitis, tonsillitis , pneumonia, infectious skin lesions), less often tuberculosis, malaria , syphilis . The disease can be triggered by vaccination, the poison of bees or other insects, pollen allergies to plants, drugs. The emergence of glomerulonephritis and its transition to a chronic form is promoted by cooling, excessive intake of salt, chronic infection (tonsillitis, dental caries , adnexitis, hepatitis, tuberculosis), alcohol intoxication.

With glomerulonephritis, the antigen-antibody complexes are deposited in the glomerular capillaries, renal circulation is impaired, antihypertensive factors are developed, and the water and salt retention in the body is stimulated, which is the basis for the formation of arterial hypertension. With a marked decrease in renal glomerular blood flow, the rate of filtration decreases and the process of renal purification of blood from metabolic products is violated, which is the basis of renal failure. With excessively active or prolonged inflammation, the capillaries of the renal glomeruli are emptied and the glomeruli are subjected to sclerosis. With the death of more than half of the renal glomeruli, chronic renal failure develops .

Acute glomerulonephritis often develops in young people 10-12 days after an infectious disease, characterized by edema, arterial hypertension and pathological changes in urine. Patients with headache , dyspnea , sometimes passing into attacks of suffocation (cardiac asthma), a sharp decrease in urination, sometimes to complete anuria, and rapid development of edema (mainly on the face). Edema combined with pallor of the skin create a characteristic appearance of the patient ("face of a nephritic"). Then the swelling spreads throughout the body, and sometimes the fluid accumulates in the pleural, abdominal cavity and pericardium.

Arterial hypertension often precedes other symptoms of the disease. Usually it is moderate, but a significant increase in blood pressure (up to 200/120 mm Hg) is possible. Hypertension causes the development of severe circulatory insufficiency (shortness of breath, hemoptysis, attacks of cardiac asthma). In the examination of the patient, the expansion of the heart boundaries is determined, the second tone accent on the aorta, systolic murmur at the apex, bradycardia , wet wheezing is heard in the lungs. With high blood pressure, brain edema can develop nephritic eclampsia , which manifests itself with severe headaches, vomiting, epileptiform convulsive attacks; Uremia while not. Hypertension and retinal edema cause visual impairment with the appearance of "fog" before the eyes, fuzzy vision of objects. Sometimes due to detachment of the retina, a complete loss of vision occurs. Hematuria and proteinuria are observed. Microhematuria is noted from the first day of the disease, sometimes turns into a macrohematuria (urine is the color of meat slops). In the urine sediment, leached erythrocytes are found - 100-200 in the visual field and more, as well as leukocytes, cylinders and renal epithelium.

The diagnosis is based on an anamnesis (characterized by rapid development of the disease after cooling or a recent infection) and clinical data. In the absence of typical signs of the disease, the diagnosis can be made on the basis of the results of a systematic measurement of blood pressure and urinalysis.

Treatment is carried out in a hospital. With severe swelling and arterial hypertension, strict bed rest, a diet with restricted fluid, sodium chloride, and in the case of renal failure, a protein are prescribed. Consumption of salt is limited when recovering or during the period of chronic process subsidence. With increased blood pressure and edematous syndrome, furosemide (lasix) is used at 40-60 mg per day in the mornings or hypothiazide at 100-150 mg per day. In addition, veroshpiron 100-150 mg per day or aldactone, euphylline 2,4 % Solution of 5-10 ml intravenously slowly 1-2 times a day. Of the antihypertensive agents, calcium antagonists (corinfar), angiotensin-converting enzyme (kapoten) inhibitors are recommended. With a good state of circulation for the treatment of hypertension, anaprilin is administered 40 to 80 mg 2 to 3 times a day under the control of the pulse rate. When the pulse is reduced to 60 -56 in 1 min, the dose of anaprilin is reduced or the drug is temporarily canceled. In the presence of focal infection, the hearth is sanitized (for example, tonsillectomies) and administered for 6 to 7 days by antibiotic therapy. For the treatment of immune inflammation, glucocorticoid hormones (prednisolone, methylprednisone, dexazone) are used. And cases complicated by acute heart failure with asthma attacks, strophantin 0,05% solution 0.5-1 ml intravenously, nitroglycerin intravenously drip, fentanyl 0.005% solution of 1-2 ml. In patients with oliguria, ultrafiltration or continuous arteriovenous hemofiltration is performed in order to remove excess fluid and restore the proper volume of circulating blood. At attacks of eclampsia apply 2% solution of papaverine for 2-4 ml, 2.4% solution of euphyllin for 5-10 ml in 10-20 ml of 20-40% glucose solution, 2.5% solution of aminazine for 1 - 2 ml, 25 % Solution of magnesium sulfate 10-20 ml intravenously slowly, Relanium 5-10 mg (or 1-2 ml) intravenously.

Forecast. Most of the symptoms disappear in the treatment after 1 to 2 months, and recovery gradually begins. In exceptional cases, a fatal outcome is possible due to cerebral hemorrhage or acute heart failure. In those cases when the symptoms of the disease do not disappear within a year, the transition of acute glomerulonephritis into a chronic one is possible.

Prevention of acute glomerulonephritis consists in the prevention and treatment of acute infectious diseases and the rehabilitation of foci of infection in the oral cavity and nasopharynx. Recoverers are prohibited from working with physical stress and cooling. Pregnancy and childbirth are undesirable during the next three years. Patients who have undergone acute glomerulonephritis should be under clinical supervision (periodic BP measurements and urinalysis are necessary).

Subacute malignant glomerulonephritis is characterized by persistent severe arterial hypertension, persistent edema, increased cholesterol level in the blood, a decrease in the relative density of urine and a rapidly progressive violation of the nitrogen excretory function of the kidneys.

Chronic glomerulonephritis develops after acute or without a previous acute onset as a result of a latent flowing malosymptomatic process. An essential role in the development of chronic glomerulonephritis belongs to the reactivity of the organism and autoimmune disorders. For chronic glomerulonephritis, a predominant lesion of the renal glomeruli is characteristic. Like acute, clinically it is manifested by edema, arterial hypertension and changes in the urine.

There are 5 main clinical forms of chronic glomerulonephritis - latent, hematuric, nephrotic, hypertonic and mixed type. Latent glomerulonephritis is manifested only by changes in urine - moderate proteinuria, hematuria, leukocyturia, sometimes there is a moderate increase in blood pressure, there is usually no significant edema.

Hematuric glomerulonephritis manifests a permanent hematuria sometimes with episodes of macrogematuria without significant proteinuria and general symptoms (BP rises, edema).

Chronic glomerulonephritis with nephrotic syndrome is manifested by pronounced edema, significant proteinuria and cylindruria. In the blood there is a decrease in the amount of the total protein (up to 40-50 g / l), an increase in the blood cholesterol level to 15.5 mmol / l (600 mg / 100 ml and above).

Chronic glomerulonephritis with secondary hypertension is manifested by changes in the cardiovascular system: a significant increase in blood pressure, repeated nasal bleeding, impaired vision, possibly the development of cardiac asthma. Changes in the urine are insignificant - moderate microhematuria and proteinuria.

Chronic glomerulonephritis of mixed type is characterized by persistent edema, high blood pressure. For all forms of chronic glomerulonephritis is characterized by the development of chronic renal failure.

The diagnosis is made on the basis of anamnesis (information on the previously transferred acute glomerulonephritis) and the characteristic clinical symptoms. In cases where only individual symptoms are expressed or there is no connection with acute glomerulonephritis, a differential diagnosis with other kidney lesions is necessary. In contrast to hypertensive disease in the hypertonic type of chronic glomerulonephritis, changes in urine are preceded by hypertension, myocardial hypertrophy is less pronounced, hypertensive crises occur less often, and atherosclerosis develops less intensively . For chronic pyelonephritis, bacteriuria is characteristic (over 100,000 microbial bodies in 1 ml of urine). Chronic glomerulonephritis with nephrotic syndrome should be differentiated with nephrotic syndrome of another genesis. In chronic glomerulonephritis, along with nephrotic syndrome, there are always signs of inflammatory kidney damage in the form of moderate hematuria and a tendency to increase blood pressure. Pregnant women need to differentiate chronic glomerulonephritis with nephropathy. It should be borne in mind that nephropathy of pregnant women is observed in the second half of pregnancy. In severe course of chronic glomerulonephritis, pregnant women may have premature births , premature placental abruption , intrauterine fetal death. The severe course of glomerulonephritis in pregnant women with increased blood pressure, expressed by renal failure is an indication for the termination of pregnancy.

Treatment of chronic glomerulonephritis includes the appointment of a diet, in particular, with the restriction of the intake of table salt in nephrotic and hypertonic forms; Elimination of foci of infection (removal of tonsils, sanation of the mouth); Pathogenetic therapy with glucocorticosteroids, non-steroidal anti-inflammatory drugs (indomethacin, etc.). Symptomatic therapy is carried out by diuretics and hypotensive drugs.

Forecast. In the outcome of chronic glomerulonephritis, the kidneys shrivel and uremia develops.

The basis for the prevention of chronic glomerulonephritis is the timely elimination of foci of infection in the body.