A 45-year-old woman with SLE develops diffuse proliferative lupus nephritis (Class IV). The key immunological mechanism driving glomerular injury is:
- A Deposition of anti-dsDNA IgG immune complexes in the mesangium and subendothelial space activating complement via classical pathway ✓
- B Type IV hypersensitivity with CD4+ Th1 cells directly attacking glomerular endothelium
- C ANCA-mediated neutrophil activation causing pauci-immune glomerulonephritis
- D IgA1-dominant immune complex deposition in mesangium (analogous to IgA nephropathy)
Explanation
Lupus nephritis class IV is caused by type III hypersensitivity (immune complex disease). Anti-dsDNA and anti-Smith antibodies form immune complexes that deposit in the mesangium, subendothelium ('wire-loop' lesions by LM), and occasionally subepithelium. These complexes activate complement C1q → C3 → C5-C9 MAC causing endothelial and mesangial injury with infiltrating neutrophils and monocytes. Full-house immunofluorescence (IgG, IgM, IgA, C3, C1q) is diagnostic. Pauci-immune GN has ANCA but minimal immune deposits.
Reference: Robbins & Cotran Pathologic Basis of Disease, 10th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
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