A 25-year-old woman with SLE develops diffuse proliferative glomerulonephritis (Class IV). Renal biopsy shows subendothelial immune complex deposits on electron microscopy ('wire loop' lesions). The primary mechanism of glomerular injury in this lesion is:

• A Direct antibody-mediated cytotoxicity against podocytes
• B Anti-GBM antibody linear deposition
• C CD8+ T-cell infiltration of glomeruli
• D Complement activation by deposited immune complexes ✓

Explanation

Lupus nephritis Class IV is an immune complex-mediated (Type III) hypersensitivity reaction. Subendothelial DNA-anti-DNA immune complexes activate complement (C5a), attracting neutrophils and causing glomerular inflammation. Option A describes some podocytopathies. Option C describes T-cell mediated injury. Option B describes Goodpasture syndrome with linear IgG deposition, not the granular IF pattern of lupus.

Reference: Robbins and Cotran Pathologic Basis of Disease, 10th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.