10. Renal Pathology C - Cox

• Glomerulonephritis - lesion that cause nephritic syndrome - proliferation of glomerular cells
• Glomerulonephritis - accompanied by

  • inflammatory leukocytic infiltration causing injuries to capillary walls
  • leading to blood in urine
  • Decrease GFR
  • hypertension
• Postinfectious glomerulonephritis (PIGN) - acute poststreptococcal glomerulonephritis

  • occur commonly in children 1 to 2 week after sore throat
  • or 6 weeks after skin infection
• APSGN characterized by diffuse exudative, hypercellular glomerulonephritis

  • organism antigen deposition in subepithelial GBM
  • neutrophil attraction and endocapillary hypercellularity
• APSGN - scattered granular deposits of IgG and C3 within capillary walls and mesangial areas
• Infection-Related Glomerulonephritis (IRGN) is ongoing and distant infection
• IRGN - IgA dominant infection
• IRGN - most common cause is S aureus
• IRGN pathophysiology

  • bacterial antigen trapped in glomeruli causing circulating or in situ complex
  • bacterial antibodies cross reacting with self - molecular mimicry
  • complement activation
• IRGN - Crescentic glomerulonephritis

  • endocapillary hypercellularity + neutrophil
  • exudative GN
• IRGN - Clinical

  • acute kidney injury - creatinine level > 3 mg/dL
• IgA Nephropathy (IgAN): Berger's disease - occur in children and young adults
• Berger's disease - onset

  • hematuria
  • proteinuria
• Berger's disease - occur 1 to 2 days post nonspecific upper respiratory tract infection
• Berger's disease - IgA nephropathy
• IgAN (Berger's disease) - Pathology - 4 Hit hypothesis

  1. abnormal galactosylated IgA1
  2. autoantibody against GD-IgA1
  3. immune complex (IgG-GD-IgA1) formation
  4. immune complex deposition
  5. cause podocyte injury --> scarring and fibrosis
• IgA vasculitis - characterized by

  • cutaneous
  • arthritis
  • GI tract and kidney involvement
• IgAV and IgAN - IgA deposition is mostly in mesangium