In IgA nephropathy (Berger disease), the pathogenic mechanism involves deposition of galactose-deficient IgA1. In which part of the nephron do these deposits characteristically localise?
- A Subepithelial space beneath the GBM (analogous to PSGN humps)
- B Subendothelial space causing a tram-track GBM appearance
- C Mesangium with or without extension to the capillary walls ✓
- D Tubular basement membrane causing cast nephropathy
Explanation
IgA nephropathy deposits galactose-deficient IgA1 immune complexes (IgA1 + anti-glycan IgG antibodies) primarily in the mesangium, with IgA as the dominant immunoglobulin on immunofluorescence; deposits may extend into the paramesangial capillary walls in more severe cases. Subepithelial humps are the hallmark of PSGN. Subendothelial deposits with tram-track appearance characterise membranoproliferative GN Type I. Tubular cast formation occurs in myeloma cast nephropathy, not IgA nephropathy.
Reference: Robbins & Cotran Pathologic Basis of Disease, 10th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
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