Tuesday, April 17, 2012

Renal Pathology

IgA Nephropathy

  • common in NM
  • often triggered by upper respiratory infection (sometimes GI)
    • 1-3 days after infection; e.g., tonsillitis
  • presents as nephritic syndrome
  • most common in young adults, less so in children
  • clinical course highly variable
    • heal with return to normal function
    • progess to renal failure
    • can be treated with immune suppressants
    • can be associated with systemic vasculitis =  Henoch Schonlein Purpura
      • skin rash (purpura)
  • pathogenesis
    • IgA = antibodies of mucosal immune response
    • IgA forms complexes with antigens in circulation
    • IgA antibodies deposit in mesangium=incite inflammation
    • IgA antibodies deposit in walls of small arteries (in Henoch Schonlein Purpura)
  • histopathology - "antler guy"


Rapidly Progressive Glomerulonephritis 

  • includes 3 different diseases
    • post strep (post infectious) GN
      • 1-4 weeks after strep/other infections
      • common in children 6-10 years
      • most recover completely
      • pathogenesis
        • formation of immune complexes
        • circulate and deposit in glomerular basement membrane
        • incite inflammation
        • elevated antistreptolysin-O (ASO) titer in serum
        • swelling of endothelial cells obstructs capillaries
        • red cells pass through damaged basement membrane
    • pauci immune GN = ANCA 
    • anti-glomerular basement membrane GN (anti-GBM GN)

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