Glomerulonephritis types

Question 1

Non-inflammatory/non-proliferative glomerulopathies

Answer 1

Minimal change disease
FSGS
Membranous nephropathy
Diabetic nephropathy
Amyloid nephropathy
Alport syndrome

Minimal change disease - podocyte effacement only seen on EM, selective albuminuria.

Focal Segmental Glomerulosclerosis - usually idiopathic, may be part of continuum with minimal change disease. podocyte effacement, increased mesangial matrix, and segments of some glomeruli having thickened hyaline wall deposition, and obliterated lumens.

Membranous nephropathy - Antibodies generated against podocyte foot process antigens, with sub-epithelial deposition. -subepithelial, doesn’t irritate/stimulate mesangial prolif. Spike and dome on EM, diffuse capillary wall thickening

Diabetic nephropathy - non-enzymatic glycosylation of efferent arteriole–> hyaline arteriolosclerosis, increased glomerular pressure and initial GFR increase, hyperfiltration –> GBM thickening and microalbuminuria –> nephrosis syndrome. In later stages, mesangial proliferation occurs, and glomerular sclerosis.

Question 2

Inflammatory glomerulopathies

Answer 2

IgA nephropathy –>Mesangial proliferation

Post-strep GN –> Endocapillary proliferation

Membranoproliferative GN, aka Mesangiocapillary GN –> SLE, HBV, HCV, and Cryoglobulin associated. Circulating immune complex driven. Get trapped in the subEndothelial layer.
Mesangial and endothelial proliferation, thickened, tram-track splitting of the GBM.

Wegener’s granulomatosis and Crescentic PRGN. Crescents are formed by parietal epithelial cells of Bowman’s capsule proliferating, and by invasion of leukocytes into Bowman’s space.

Anti-GBM crescentic GN