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What causes acute glomerulonephritis?
Last reviewed: 04.07.2025
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Acute glomerulonephritis is caused by nephritogenic strains of group A beta-hemolytic streptococcus, most often serotypes 4 and 12, 18, 29, 49. The disease develops 10-14 days after a nasopharyngeal infection (tonsillitis) or 3 weeks after skin infections (impetigo, pyoderma). Nephritogenic M-strains of beta-hemolytic streptococcus include: strains 1, 4, 12, causing acute glomerulonephritis after pharyngitis, and strains 2, 49, 55, 57, 60, causing acute glomerulonephritis after skin infections.
Provoking factors for the development of acute post-streptococcal glomerulonephritis can be hypothermia and acute respiratory viral infections.
A high frequency of occurrence of HLA antigens B12, B17, B35, DR5, DR7 in patients with glomerulonephritis has been established. Moreover, carriage of the B12 gene is especially characteristic of patients with nephrotic syndrome.
The possibility of developing glomerulonephritis in a number of hereditary immune abnormalities has been demonstrated: homozygosity of the C6 and C7 complement fraction deficiency, T-cell dysfunction; hereditary antitardimbin deficiency. Inadequacy of T-cell immunity leads to disruption of the reparation of individual parts of the nephron with subsequent changes in their antigen structure and formation of immune complexes that are localized in the affected areas of the glomerular basal membrane of the kidneys.
Predisposing factors:
- a burdened heredity with respect to infectious and allergic diseases;
- increased susceptibility in the family to streptococcal infections;
- the presence of chronic foci of infection in the child's tonsils, teeth, previous erysipelas; streptoderma;
- carriage of hemolytic streptococcus in the pharynx, on the skin.