A 35-year-old woman with a 2-year history of fatigue, malar rash, photosensitivity, and joint pain has an ANA titer of 1:640 (speckled pattern). Anti-dsDNA and anti-Smith antibodies are positive. Urinalysis shows 2+ protein and RBC casts. Renal biopsy shows glomerular immune complex deposits in the mesangium and subendothelial space with granular (lumpy-bumpy) immunofluorescence for IgG and C3. What is the PRIMARY mechanism of renal injury?

• A T cell-mediated delayed hypersensitivity granuloma formation
• B Direct anti-GBM antibody binding causing linear IgG deposits
• C Pauci-immune vasculitis from ANCA-mediated neutrophil activation
• D Immune complex (Type III) deposition activating the classical complement pathway ✓

Explanation

Lupus nephritis is the classic example of Type III (immune complex) hypersensitivity in the kidney. Circulating anti-dsDNA and other nuclear antigen complexes deposit in glomerular mesangium and subendothelial spaces, fix complement via the classical pathway (C1q binding), and trigger neutrophil recruitment and cytokine release, causing glomerulonephritis. The granular (lumpy-bumpy) immunofluorescence pattern reflects focal immune complex deposits, in contrast to the linear IgG staining of anti-GBM (Goodpasture) disease.

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

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.