Urology

Acute interstitial nephritis

• Presentation:
  
  • fever, rash, White blood cell casts
• Caused by:
  • NSAIDs
  • furosemide
  • penicillin
  • sulfa drugs 

Chronic Tubulointerstitial nephritis

• Caused by:
  • Chronic NSAID use and Lead exposure
  • Lithium and Autoimmune diseases 

Minimal change disease

• Dx:
  • EM – Podocyte effacement and fusion
• Treatment:
  • Steroids

Focal Segmental Glomerulosclerosis

• Causes:
  • Heroin abuse or systemic disease or viral infection like HIV/HCV
• Prognosis: 
  • Poor
  • 50% have end stage renal disease in 10 years

Diabetic nephropathy

• Dx:
  • EM – Thickening of the basement membrane from non enzymatic glycosylation
  • Diabetes! Kimmelstiel Wilson bodies – Nodular glomerulosclerosis

Membranous nephropathy

• EM – spike and dome subepithelial deposits (helmet with spikes on archer) spike is due to basement membrane engulfing domes of sub epithelial immune deposits
• antibodies to phospholipase A2 receptors on podocytes

IgA nephropathy (Berger disease)

• Most common nephritic syndrome
• EM – Deposition of IgA and complexes in the mesangium
• Treatment:
  • steroids

Post strep glomerulonephritis

• Occur – After Strep Pharyngitis or impetigo
• Low ASO in impetigo. (because skin oils degrade ASO).
• But would still have anti-DNAse B

Diffuse proliferative glomerulonephritis

• Lupus

Membranoproliferative glomerulonephritis

• Light microscopy shows hypercellularity and enlarged, lobular glomeruli
• “Tram tracking” – splitting of GBM to two layers
• immune complexes deposited in the sub endothelial space