Post-streptococcal glomerulonephritis pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Pathophysiology

Pathogenesis

• It is thought that post-streptococcal glomerulonephritis (PSGN) is caused by nephritogenic strains of group A beta-hemolytic streptococcus (GAS).
• Other strains of Group A streptococci which cause PSGN include:
  • Group A streptococci M protein types 47, 49, 55, 2, 60.
  • Group A streptococci M types 1, 2, 4, 3, 25, 49, and 12.
• Two antigens isolated from nephritogenic streptococci are commonly implicated in APSGN: streptococcal pyrogenic exotoxin B (SPEB) and nephritis-associated plasmin receptor (NAPlr).
• Following infection with nephritogenic strains of group A beta-hemolytic streptococcus,

Genetics

• [Disease name] is transmitted in [mode of genetic transmission] pattern.
• Genes involved in the pathogenesis of [disease name] include [gene1], [gene2], and [gene3].
• The development of [disease name] is the result of multiple genetic mutations.

Gross Pathology

• On gross pathology, following features are seen:
  • Kidney are enlarged and pale in color.
  • Glomeruli is having red dots

Microscopic Pathology

• On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].

Pathophysiology

The exact pathology remains unclear, but it is believed to be Type III hypersensitivity reaction. Immune complexes (antigen-antibody complexes formed during an infection) become lodged in the glomerular basement membrane. Complement activation leads to the destruction of the basement membrane. It has also been proposed that specific antigens from certain nephrotoxic streptococcal infections have a high affinity for basement membrane proteins, giving rise to particularly severe, long-lasting antibody response.