A 30-year-old woman develops systemic lupus erythematosus. Renal biopsy reveals proliferative lupus nephritis (class III/IV). The dominant immunopathological mechanism of glomerular injury in proliferative lupus nephritis is:

• A Type I hypersensitivity: IgE-mediated complement activation in the mesangium
• B Type II hypersensitivity: anti-GBM antibodies causing linear IgG deposition
• C Type IV hypersensitivity: CD8+ T-cell cytotoxicity of podocytes
• D Type III hypersensitivity: IC deposition of dsDNA-anti-dsDNA complexes in subendothelial/mesangial locations activating complement ✓

Explanation

Proliferative lupus nephritis (class III/IV) is the classic example of type III (immune complex) hypersensitivity in the kidney. Circulating immune complexes of nuclear antigens (dsDNA, histones, nucleosomes) with complementary autoantibodies deposit in glomerular subendothelial and mesangial locations. These complexes fix complement via classical pathway, generating C3a and C5a — attracting neutrophils and monocytes that mediate glomerular destruction. The 'full-house' immunofluorescence pattern (IgG, IgM, IgA, C3, C1q) is characteristic.

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

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.