In C3 glomerulopathy (C3G), the pathogenic mechanism that differentiates it from immune-complex MPGN is:

• A Classical pathway activation by circulating immune complexes leading to C3 and Ig deposition
• B Dysregulation of the complement alternative pathway causing isolated C3 accumulation without Ig ✓
• C Antibody-dependent cellular cytotoxicity targeting glomerular endothelium
• D Deficiency of terminal complement components (C5-C9) causing MAC formation in GBM

Explanation

C3 glomerulopathy results from alternative pathway complement dysregulation, most commonly due to gain-of-function mutations in C3/factor B/factor H genes or presence of C3 nephritic factor (C3NeF, an autoantibody stabilizing C3 convertase). This leads to dominant C3 deposits with minimal or absent Ig — a key IF criterion. Immune-complex MPGN has both IgG and C3 by IF because classical pathway activation accompanies complement activation.

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

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.