Post-streptococcal glomerulonephritis pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Manpreet Kaur, MD [2]

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
  • Nephritis-associated plasmin receptor

The mechanism which leads to immunologic injury to the glomerulus are:

• There is deposition of immune complexes with streptococcal antigenic components
• Immune complexes are deposited in glomerular basement membrane and antibodies bind to the GBM
• Further antigen reacts with antibodies bind to GBM and cross glomerular membranes

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:

• Glomeruli are enlarged and hypercellular due to the deposition of neutrophils and macrophages
  • There is a proliferation of mesangial and endothelial cells
  • There is a swelling of endothelial cells and presence of inflammatory cells obstructs capillary lumina
  • There is an accumulation of mononuclear leucocytic infiltrate and edema in the interstitium