In chronic rejection of a transplanted kidney, the predominant mechanism of graft damage (distinct from acute rejection) is:

• A Hyperacute rejection mediated by preformed antibodies and complement
• B Donor-specific antibodies causing chronic antibody-mediated rejection with transplant glomerulopathy and intimal arterial fibrosis ✓
• C CD8+ cytotoxic T cells directly killing tubular epithelial cells
• D IL-2-driven proliferation of CD4+ Th1 cells causing acute tubular injury

Explanation

Chronic antibody-mediated rejection (CAR) is now recognized as the dominant cause of late graft failure. Donor-specific antibodies (DSA) against HLA antigens activate complement (C4d deposition in peritubular capillaries is a marker) and trigger endothelial injury, leading to transplant glomerulopathy (glomerular capillary wall duplication), peritubular capillaritis, and progressive intimal arterial fibrosis. Hyperacute rejection occurs within minutes. Acute T-cell-mediated rejection causes tubulointerstitial nephritis.

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

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.