Glomerulonephritis Overview

Study Notes

Glomerulonephritis Summary

Postinfectious glomerulonephritis:
- Clinical presentation: Nephritic syndrome
- Pathogenesis: Immune complex mediated, circulating or planted antigen.
- Glomerular pathology: Diffuse endocapillary proliferation, leukocytic infiltration.
- Light microscopy: Granular IgG and C3 in GBM and mesangium, granular IgA in some cases.
- Electron microscopy: Primarily subepithelial humps; subendothelial deposits in early disease stages.
Crescentic (rapidly progressive) glomerulonephritis:
- Clinical presentation: Nephritic syndrome, rapid progression.
- Pathogenesis: Anti-GBM antibody mediated, immune complex mediated, ANCA mediated and unknown.
- Glomerular pathology: Extracapillary proliferation with crescents, necrosis.
  - In anti-GBM antibody mediated GN: Linear IgG and C3 in the GBM.
  - In immune complex mediated: Granular IgG, other Igs, and/or complement in glomerular basement membrane.
  - In ANCA mediated GN: No deposits.
- Electron microscopy: No deposits in anti-GBM and ANCA mediated GN, immune complexes at various locations in immune complex mediated GN.
Membranous nephropathy:
- Clinical presentation: Nephrotic syndrome.
- Pathogenesis: In situ immune complex formation involving PLA2R antigen in most primary cases.
- Glomerular pathology: Diffuse capillary wall thickening.
- Pathology findings: Granular IgG and C3, diffuse, subepithelial deposits.
Minimal change disease:
- Clinical presentation: Nephrotic syndrome.
- Pathogenesis: Unknown; loss of glomerular polyanion, podocyte injury.
- Glomerular pathology: Normal findings; lipid in tubules.
- Pathology findings: effacement of foot processes; no deposits
Focal segmental glomerulosclerosis:
- Clinical presentation: Nephrotic syndrome, non-nephrotic proteinuria.
- Pathogenesis: Unknown; also, ablation nephropathy and podocyte injury are factors implicated.
- Glomerular pathology: Focal and segmental sclerosis and hyalinosis.
- Potential findings: IgM + C3 in many cases.
Membranoproliferative glomerulonephritis (MPGN) type I:
- Clinical Presentation: Nephritic/nephrotic syndrome.
- Pathogenesis: Immune complex mediated.
- Glomerular Pathology: Mesangial proliferative or membranoproliferative patterns of proliferation; GBM thickening; splitting.
- Pathology Findings: IgG ++ C3; C1q ++ C4, subendothelial deposits.
Dense-deposit disease (MPGN type II):
- Clinical presentation: Hematuria, chronic renal failure.
- Pathogenesis: Acquired or genetic dysregulation of the alternative complement pathway.
- Glomerular pathology: Mesangial proliferative or membranoproliferative patterns of proliferation; GBM thickening; splitting.
- Pathology Findings: C3; no C1q or C4; dense deposits.
IgA nephropathy:
- Clinical presentation: Recurrent hematuria or proteinuria.
- Pathogenesis: Unknown.
- Glomerular pathology: Focal mesangial proliferative glomerulonephritis; mesangial widening.
- Pathology Findings: IgA ± IgG, IgM, and C3 in mesangium; mesangial and paramesangial dense deposits.

Abbreviations

ANCA: Antineutrophil cytoplasmic antibodies
GBM: Glomerular basement membrane
IgG: Immunoglobulin G
IgM: Immunoglobulin M
PLA2R: Phospholipase A2 receptor

Description

This quiz explores key aspects of glomerulonephritis, including postinfectious and crescentic types. It covers clinical presentations, pathogenesis, and glomerular pathology observed in various forms. Test your knowledge on the intricate details of nephritic syndromes and their underlying mechanisms.