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Pathogenesis of acute glomerulonephritis
Last reviewed: 06.07.2025
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Streptococcus secretes toxins and enzymes (streptolysin, hyaluronidase, streptokinase) that initiate the production of specific antibodies with subsequent formation of circulating immune complexes (CIC), localized on the capillary wall of the glomeruli and activating the complement system, which promotes the production of numerous inflammatory mediators and cytokines that cause cellular proliferation.
Streptococcal antigens are deposited in the glomeruli during the acute phase of streptococcal infection. After 10-14 days, the child's immune response occurs, during which antistreptococcal antibodies bind to the antigen and form circulating immune complexes (CIC) and are deposited in the glomeruli of the kidneys. Next, the immune complexes interact with the complement system, releasing its components C3a, C5a and participating in the damage of the glomerular basal membrane of the kidney. Activation of platelets by the membrane attack complex (C5b-C9) (secretion of serotonin, thromboxane B); macrophages (secretion of phospholipids and arachidonic acid); activation of mesangial cells (secretion of proteases, phospholipases, free oxygen radicals; activation of chemotactic factors, leading to a change in the bioenergetic potential of the glomerular basement membrane of the kidneys and damage to endothelial cells with the release of thrombogenic subendothelial layers). Activation of the fibrinolytic system leads to the accumulation of fibrin in the glomeruli of the kidneys, and activation of the kinin system to an increase in the inflammatory process. Platelets undergo aggregation, and an increase in the level of von Willebrand factor and activation of the kinin system cause a disruption of microcirculation.
Disturbances in the phospholipid composition of erythrocyte membranes lead to functional destabilization of cell membranes, which play a significant role in the origin of hematuria, and the endothelin system (vasoconstrictor peptides that act on renal and intraglomerular hemodynamics) leads to the development of intraglomerular hypertension.
It is possible that streptococcal antigens are initially localized in the mesangium and in the subendothelial space of the glomeruli, and subsequently react with antibodies to form the CIC. Two streptococcal antigens have been 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 assessed as endocapillary diffuse proliferative glomerulonephritis, which goes through several stages - exudative, exudative-proliferative, proliferative and the stage of residual phenomena that can persist in children for several months.
Electron microscopy of the biopsy specimen reveals "humps" (IgG and complement fraction C3) on the epithelial side of the glomerular capillary basement membrane. They persist in acute glomerulonephritis for up to 4-6 weeks. Detection of "humps" is an important and reliable diagnostic sign of acute poststreptococcal glomerulonephritis.
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