Pathogenesis of acute glomerulonephritis

Streptococcus secretes toxins and enzymes (streptolysin, hyaluronidase, streptokinase) that initiate the production of specific antibodies with the subsequent formation of CECs localizing on the capillary wall of the glomerulus and activating the complement system that promotes the production of numerous inflammatory mediators and cytokines that cause cell proliferation.

Streptococcus antigens are precipitated in glomeruli during the acute phase of streptococcal infection. After 10-14 days, the immune response of the child's organism occurs, during which antistreptococcal antibodies bind to the antigen and form circulating immune complexes (CIC) and precipitate them in the glomeruli of the kidneys. Further, the immune complexes interact with the complement system, with the release of its components C3a, C5a, and their participation in damage to the basal membrane of the glomeruli of the kidney. Activation of the membrane-attacking complex (C5v-C9) platelets (secretion of serotonin, thromboxane B); macrophages (secretion of phospholipids and arachidonic acid); activation of mesangial cells (secretion of proteases, phospholipases, free radicals of oxygen, activation of chemotactic factors, leading to a change in the bioenergetic potential of the basal membrane of the glomeruli of the kidneys and damage to endothelial cells with the release of thrombogenic subendothelial layers). Activation of the fibrinolytic system leads to accumulation of fibrin in the glomerulus of the kidneys, and activation of the kinin system to enhance the inflammatory process. Platelets undergo aggregation, and an increase in the level of von Willebrand factor and activation of the kinin system cause microcirculation disorders.

Disorders in the phospholipid composition of erythrocyte membranes lead to the functional destabilization of cell membranes that play a significant role in the origin of hematuria, and the system of endothelin (vasoconstrictive peptides acting on renal and intramedular hemodynamics) leads to the development of intra-cerebral hypertension.

It is not excluded that initially the streptococcal antigens are localized in the mesangium and in the subendothelial space of the glomerulus, and subsequently react with antibodies with the formation of the CEC. Two streptococcal antigens were identified: zymogen and glyceraldehyde phosphate dehydrogenase. They induce the production of antibodies with subsequent activation of inflammatory mediators in glomerular cells.

Morphology of acute glomerulonephritis. The morphological picture is evaluated as endocapillary diffuse proliferative glomerulonephritis, which passes through several stages - exudative, exudative-proliferative, proliferative and a stage of residual phenomena that can persist in children for several months.

Electron microscopy of the biopsy specimen on the epithelial side of the basal membrane of the capillaries of the glomeruli of the kidneys reveals "humps" (IgG and S3 complement fraction). They persist with acute glomerulonephritis until 4-6 weeks. Identification of "humps" is an important and reliable diagnostic sign of acute poststreptococcal glomerulonephritis.

[1], [2], [3], [4], [5], [6], [7], [8], [9], [10],