9. Renal Pathology B - Cox

• Minimal Change Disease (MCD)

  • albuminuria
  • diffuse foot processes podocyte effacement
  • no immune deposits
  • lipiduria
• Minimal change disease - podocyte effacement is due to?

  • immune dysregulation
  • epithelial injury --> decreasing glomerular anionic (-) charge
• ** minimal change disease is caused by podocyte effacement
• Focal Segmental Glomerulosclerosis (FSGS)

  • focal sclerosis - only segments of glomerulus affected
  • *** Caused by HIV infection or Heroin abuse
• FSGS - Mechanism for development

  • genetic - GBM disruption causing nephrin mutation
  • structural stress causing decrease glomeruli
• FSGS - there is progressive podocyte loss leading to increase filtration flow
• FSGS - Collapsing variant - characterized by collapse of glomerular tuft and podocyte hyperplasia
• HIV associated FSGS - involve collapse of entire tuft

  • tubules show cystic dilatation filled with protein material
• Membranous nephropathy is an autoimmune glomerular disease
• Membranous Nephropathy (MN) - characterized by diffuse subepithelial immune complex deposition and GBM thickening
• MN pathophysiology

  • circulating autoantibodies bind to autoantigen on podocyte surface
  • in situ immune complex formation will activate lectin complement pathway --> causing podocyte injury leading to nephrotic syndrome
• MN - subepithelial deposits will cause spike and dome appearance
• Membranoproliferative glomerulonephritis (MPGN) characterized by

  • endocapillary or mesangial hypercellularity
  • mesangial and subendothelial deposits
  • GBM duplication
• MPGN is due to immunoglobulin or complement mediated
• MPGN type 1 - discrete *** subendothelial and mesangial dense deposit

  • mostly immune complex - Ig or C1q
• MPGN type 3 - subepithelial and subendothelial deposits

  • GBM disruption
• C3 glomerulopathy is due to uncontrolled activation of alternative complement pathway

  • autoantibodies will increase C3 activation
• ** C3 glomerulopathy will cause hypocomplementemia due to excessive C3 consumption

  • also reduced synthesis by liver