Internal illnesses. Diffuse glomerulonephritis (etiology, pathogenesis, clinical picture of acute glomerulonephritis) (most important)

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Internal illnesses. Diffuse glomerulonephritis (etiology, pathogenesis, clinical picture of acute glomerulonephritis) (most important)

Lecture notes, cheat sheets

Directory / Lecture notes, cheat sheets

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43. DIFFUSE GLOMERULONEFRITIS (ETIOLOGY, PATORENESIS, CLINIC OF ACUTE GLOMERULONEFRITIS)

Immune-mediated inflammation with a predominant initial lesion of the glomeruli and involvement of all renal structures in the pathological process.

It is divided into acute and chronic glomerulonephritis. True acute glomerulonephritis is only one that is proven by intravital morphological examination. In other cases, chronic glomerulonephritis develops, which has an acute onset.

Etiology. Exogenous factors: bacteria (b-hemolytic streptococcus of group A (strains 12, 43, 49), white staphylococcus, bovine corynebacterium, enterococci, typhoid salmonella, treponema pallidum, diplococci), viruses (cytomegalovirus, herpes simplex viruses, hepatitis B, Epstein- Barra), fungi (Candida albicans), parasites (malarial plasmodium, schistosome, toxoplasma), drugs, poisons, foreign serum.

Endogenous factors: nuclear, brush border antigen, thyroglobulin, immunoglobulins, tumor and embryonic antigens, carcinomatous antigen.

Pathogenesis. There is a passive transfer of the immune complex into the glomerulus and its deposition. Antibodies that react with a structural antigen or with a trigger non-glomerular autologous or exogenous antigen circulate in the bloodstream. There is hyperfiltration, an increase in the transcapillary gradient - acceleration of sclerosis in the remaining glomeruli.

Clinic. The main syndromes of acute glomerulonephritis are the following: urinary, edematous, hypertensive, nephrotic.

Diseases can occur in the form: deployed (cyclic) and monosymptomatic (latent).

The cyclic form never begins at the height of infection, no earlier than 14-25 days after the onset of infection. It is characterized by an obligatory cyclical course, it develops acutely, weakness, swelling (mainly of the face), headache, decreased diuresis, urine the color of meat slop, and lower back pain appear. Arterial hypertension develops (systolic blood pressure does not exceed 180 mm Hg, diastolic blood pressure - 120 mm Hg), tachycardia, and there may be signs of acute cardiac (left ventricular) failure (shortness of breath, cough, attacks of cardiac asthma). There is an expansion of the boundaries of relative cardiac dullness, systolic murmur at the apex, emphasis of the second tone on the aorta, sometimes a gallop rhythm, dry and moist rales in the lungs. Urinary syndrome is characterized by proteinuria, cylindruria, macro- and microhematuria. Proteinuria is associated with gross damage to the vascular wall of the glomerular capillaries, through which albumins, globulins, and fibrinogen are released. Hematuria is a constant symptom. There is a small number of leukocytes. Edema persists for 10-15 days, disappears by the end of the 3rd week, blood pressure decreases, polyuria develops, urinary syndrome persists for more than 2 months, hyposthenuria appears, slight proteinuria may persist for a long time (0,03-0,1 g/day), residual hematuria, leukocyturia disappears at the end of the first month.

The latent form is characterized by a gradual onset, without subjective manifestations, headaches, slight shortness of breath or swelling in the legs are possible, the duration of the condition is up to 2-6 months or more, the presence of an isolated urinary syndrome. Acute nephritis that has not resolved within a year is considered chronic glomerulonephritis.

Author: Myshkina A.K.

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