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GLOMERULONEPHRITIS

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GLOMERULONEPHRITIS - inflammation of the renal glomeruli, to a lesser extent tubules, accompanied by secondary circulatory disorders 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 due to an excessive immune response to infectious antigens. The most common cause of the disease is streptococcal infection (tonsillitis, tonsillitis, pneumonia , infectious skin lesions), less commonly tuberculosis, malaria , syphilis . The disease can be triggered by vaccination, poison of bees or other insects, allergies to pollen of plants, drugs. The emergence of glomerulonephritis and its transition to a chronic form is facilitated by cooling, excessive salt intake, chronic infection (tonsillitis, dental caries , adnexitis , hepatitis , tuberculosis), alcohol intoxication.

With glomerulonephritis, the antigen-antibody complexes are deposited in the glomerular capillaries, renal blood circulation, the production of antihypertensive factors are disturbed, the delay in the body of water and salt is stimulated, which serves as the basis for the formation of arterial hypertension. With a marked decrease in renal glomerular blood flow, the filtration rate decreases and the process of renal cleansing of the blood from metabolic products is disrupted, which underlies renal failure. In case of excessively active or prolonged inflammation, the capillaries of the renal glomeruli start and the glomeruli undergo 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, is characterized by edema, arterial hypertension and pathological changes in urine. Patients have a headache , shortness of breath , sometimes turning into asthma attacks (cardiac asthma), a sharp decrease in urination, sometimes to complete anuria, and the rapid development of edema (mainly on the face). Edema in combination with pallor of the skin creates a characteristic appearance of the patient (“jade face”). Then, edema spreads throughout the body, and sometimes fluid accumulates in the pleural, abdominal cavities and pericardium.

Arterial hypertension more often precedes other symptoms of the disease. Usually it is moderate, but a significant increase in blood pressure is possible (up to 200/120 mm Hg. Art.). Hypertension is the cause of the development of severe circulatory failure (shortness of breath, hemoptysis, attacks of cardiac asthma). When examining a patient, the expansion of the borders of the heart, the emphasis of the second tone on the aorta, systolic murmur at the apex, bradycardia are determined, moist rales are heard in the lungs. With high blood pressure, cerebral edema, nephritic eclampsia can develop, which is manifested by severe headaches, vomiting, epileptiform convulsive attacks; there is no uremia. Hypertension and edema of the retina cause visual impairment with the appearance of “fog” in front of the eyes, blurred vision of objects. Sometimes due to retinal detachment, complete loss of vision occurs. Hematuria and proteinuria are observed. Microhematuria is observed from the 1st day of the disease, sometimes it goes into macrohematuria (urine is the color of meat slops). In urine sediment, leached red blood cells are found - 100-200 in the field of view or more, as well as leukocytes, cylinders and renal epithelium.

The diagnosis is made on the basis of an anamnesis (a rapid development of the disease is characteristic 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 edema and arterial hypertension, strict bed rest is prescribed, a diet with a restriction of fluid, sodium chloride, and in the case of renal failure, a protein. Salt consumption is also limited during recovery or during the period of subsiding of the chronic process. With increased blood pressure and edematous syndrome, furosemide (lasix) is used at 40-60 mg per day in the morning or hypothiazide at 100-150 mg per day, to stimulate diuresis, veroshpiron 100-150 mg per day or aldactone, aminophylline 2.4 are additionally used % solution of 5-10 ml intravenously slowly 1-2 times a day. Of antihypertensive drugs, calcium antagonists (Corinfar), angiotensin-converting enzyme inhibitors (capoten) are recommended. With a good state of blood circulation for the treatment of hypertension, anaprilin is used at 40 - 80 mg 2-3 times a day under the control of the pulse rate. When the pulse decreases to 60-56 in 1 min, the dose of anaprilin is reduced or the drug is temporarily canceled. If there is a focal infection, the foci are sanitized (for example, tonsillectomy) and antibacterial therapy is given in courses of 6-7 days. Glucocorticoid hormones (prednisone, methylprednisone, dexazone) are used to treat immune inflammation. And cases complicated by acute heart failure with asthma attacks, use strophanthin 0.05% solution of 0.5-1 ml intravenously, nitroglycerin intravenously, fentanyl 0.005% solution of 1-2 ml. In patients with oliguria, ultrafiltration or permanent arteriovenous hemofiltration is performed in order to remove excess fluid and restore the proper volume of circulating blood. For attacks of eclampsia, use a 2% solution of papaverine in 2–4 ml, 2.4% solution of aminophylline in 5–10 ml in 10–20 ml of a 20–40% glucose solution, 2.5% solution of chlorpromazine in 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 with treatment after 1 - 2 months, and recovery gradually comes. In exceptional cases, death is possible due to cerebral hemorrhage or acute heart failure. In cases where the symptoms of the disease do not disappear within a year, the transition of acute glomerulonephritis to chronic is likely.

Prevention of acute glomerulonephritis is the prevention and treatment of acute infectious diseases and the rehabilitation of foci of infection in the oral cavity and nasopharynx. Recovering is prohibited work related to physical stress and cooling. Pregnancy and childbirth are undesirable for the next three years. Patients who have undergone acute glomerulonephritis should be under clinical supervision (periodic measurements of blood pressure and urinalysis are necessary).

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

Chronic glomerulonephritis develops after acute or without a previous acute onset as a result of a latent low-symptom process. A significant role in the development of chronic glomerulonephritis belongs to the reactivity of the body and autoimmune disorders. Chronic glomerulonephritis is characterized by a predominant lesion of the renal glomeruli. Like acute, it is clinically 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, a moderate increase in blood pressure is sometimes noted, usually there are no significant edema.

Hematuric glomerulonephritis is manifested by constant hematuria, sometimes with episodes of macrohematuria without significant proteinuria and general symptoms (elevations in blood pressure, edema).

Chronic glomerulonephritis with nephrotic syndrome is manifested by severe edema, significant proteinuria and cylindruria. In the blood, there is a decrease in the amount of total protein (up to 40 - 50 g / l), an increase in blood cholesterol 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 nosebleeds, visual impairment, and cardiac asthma may develop. Changes in urine are minor - moderate microhematuria and proteinuria.

Mixed chronic glomerulonephritis is characterized by persistent edema, high blood pressure. All forms of chronic glomerulonephritis are characterized by the development of chronic renal failure.

The diagnosis is established on the basis of an anamnesis (information about a previous acute glomerulonephritis) and characteristic clinical symptoms. In cases where only individual symptoms are expressed or there is no connection with acute glomerulonephritis, it is necessary to carry out a differential diagnosis with other kidney lesions. Unlike hypertension, in the hypertonic type of chronic glomerulonephritis, changes in the urine are preceded by arterial 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 from nephrotic syndrome of a different 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. In pregnant women, it is necessary 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 chronic glomerulonephritis in pregnant women, premature birth , premature detachment of the placenta , intrauterine fetal death are possible. The severe course of glomerulonephritis in pregnant women with an increase in blood pressure, severe renal failure is an indication for termination of pregnancy.

Treatment of chronic glomerulonephritis includes the appointment of a diet, in particular, with the restriction of salt intake for nephrotic and hypertensive forms; elimination of foci of infection (removal of the tonsils, sanitation of the oral cavity); pathogenetic therapy with glucocorticosteroids, non-steroidal anti-inflammatory drugs (indomethacin, etc.). Symptomatic therapy is carried out with diuretics and antihypertensive drugs.

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

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