Renal Path I

Question 1

Answer 1

Minimal Chase Disease

• Effacement of podocyte food proceeses
• Podocyte w/ an defect in the charge barrier
• Children
• Nephrotic => massive proteinuria
• Responsive to steroid treatment

Question 2

Answer 2

FSGS = Focal segmental glomerulosclerosis

• Segmental solidification of glomerular tuft
• Presence of hyalinosis and foam cells
• Nephrotic => non-selective proteinuria
• Usually steroid resistant
• Genetic defect in nephrin

Question 3

Answer 3

MGN = Membraneous Glomerulonephropathy

• Immune complex mediated
  
  • Usually primary: anti-PLA2R antibodies
• See electron dense immune complex deposits in the sub-epithelial space
• Spikes on LM b/c the BM sticks up btwn ICs

Question 4

Answer 4

Crescentic GN on PAS

• Crescents: outside the tuft is a cellular infiltrate
• Messy, disorganized, and proliferative urinary space
• Severe form of injury, not specific
• Clinical correlate = RPGN (rapidly progressive GN)

Question 5

Answer 5

Goodpasture’s GF

• Picture also showing crescents (means disease is severe)
• Green highlighting of the GBM = antibodies lining what is left of the GBM

Question 6

Answer 6

Post Infectious EM

• Usually nephrotoxic strep, usually self-resolves
• ICs and planted bacterial antigens cause activation of alternative complement pathway
• Diffuse glomerular hypercellularity
  
  • Prolif of endothelial and mesangial cells
  • Infiltration of neutrophils and monocytes
  • => Occlusion of capillaries
• EM: Subepithelial humps due to non-uniformly placed immune deposits into the sub-epithelial space

Question 7

Answer 7

Diabetic GN H&E

• Thickened GBM
• Nodular pattern of mesangial scloerosis and thickened BM
• Glomerular hypertrophy => podocyte loss

Question 8

Answer 8

Diabetic GN on PAS

• Thickened GBM w/ nodular glomerulosclerosis