Medical expert of the article
New publications
What causes acute glomerulonephritis?
Last reviewed: 19.10.2021
All iLive content is medically reviewed or fact checked to ensure as much factual accuracy as possible.
We have strict sourcing guidelines and only link to reputable media sites, academic research institutions and, whenever possible, medically peer reviewed studies. Note that the numbers in parentheses ([1], [2], etc.) are clickable links to these studies.
If you feel that any of our content is inaccurate, out-of-date, or otherwise questionable, please select it and press Ctrl + Enter.
The cause of development of acute glomerulonephritis is nephritogenic strains of beta-hemolytic streptococcus group A, more often serotypes 4 and 12,18,29,49. The disease develops 10-14 days after nasopharyngeal infection (sore throat) or 3 weeks after skin infections (impetigo, pyoderma). To nephritogenic M-strains of beta-hemolytic streptococcus are: strains 1, 4, 12, causing acute glomerulonephritis after pharyngitis, and strains 2, 49, 55, 57, 60, causing acute glomerulonephritis after skin infections.
Provoking factors of acute poststreptococcal glomerulonephritis may be hypothermia and acute respiratory viral infection.
The high incidence of antigens HLA B12, B17, B35, DR5, DR7 was detected in patients with glomerulonephritis. Moreover, carriage of the B12 gene is especially characteristic for patients with nephrotic syndrome.
The possibility of developing glomerulonephritis in a number of genetically determined anomalies of immunity is shown: the homozygosity of the C6 and C7 deficiency of complement fractions, T cell dysfunction; hereditary deficit of antidrbin. Incompleteness of T-cell immunity leads to a disruption in the repair of individual parts of the nephron with a further change in their antigenic structure and the formation of immune complexes that are localized on the affected parts of the basal membrane of the glomeruli of the kidneys.
Predisposing factors:
- burdened heredity with respect to infectious-allergic diseases;
- increased susceptibility in the family to streptococcal infections;
- the presence of chronic foci of infection in the tonsils, teeth, and transferred erysipelas; streptoderma;
- carriage of hemolytic streptococcus in throat, on the skin.