A patient with systemic lupus erythematosus has antibodies to double-stranded DNA and Smith antigen. The primary mechanism of glomerular injury in lupus nephritis is:
- A Type II hypersensitivity — anti-GBM antibodies
- B Type IV hypersensitivity — T-cell mediated granuloma formation
- C Type III hypersensitivity — immune complex deposition activating complement ✓
- D Type I hypersensitivity — IgE-mediated mast cell degranulation
Explanation
Lupus nephritis is the prototypical Type III (immune complex) hypersensitivity. DNA-anti-DNA immune complexes deposit in the mesangium, subendothelial, and subepithelial glomerular spaces, activating complement (C3a, C5a) and recruiting neutrophils that release proteases and ROS. The IF pattern shows 'full house' staining (IgG, IgM, IgA, C3, C1q). Anti-GBM disease is Type II; granulomatous nephritis is Type IV.
Reference: Robbins & Cotran Pathologic Basis of Disease, 10th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
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