What is the pathophysiology of acute poststreptococcal glomerulonephritis (APSGN)?

Updated: Dec 05, 2018
  • Author: Rajendra Bhimma, MBChB, MD, PhD, DCH (SA), FCP(Paeds)(SA), MMed(Natal); Chief Editor: Craig B Langman, MD  more...
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Most forms of acute poststreptococcal glomerulonephritis (APSGN) are mediated by an immunologic process. Cellular and humoral immunity is important in the pathogenesis of this disease, and humoral immunity particularly in APSGN. Nonetheless, the exact mechanism by which APSGN occurs remains to be determined. The 2 most widely proposed theories include (1) glomerular trapping of circulating immune complexes and (2) in situ immune antigen-antibody complex formation resulting from antibodies reacting with either streptococcal components deposited in the glomerulus or with components of the glomerulus itself, which has been termed “molecular mimicry.”

Additional evidence has also been presented to support the anti-immunoglobulin activity or glomerular plasmin-binding activity of streptococcal antigens. The cross-reactivity of streptococci and mammalian tissue implicating molecular mimicry in acute rheumatic fever led to evidence of a similar mechanism involved in APSGN. However, the similar cross-reactivity patterns of rheumatogenic and nephritogenic strains of streptococci argue against molecular mimicry involving M proteins

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