In renal transplantation, hyperacute rejection occurs within minutes to hours of reperfusion and is mediated by:

• A CD8+ cytotoxic T lymphocytes recognising donor MHC class I antigens on tubular cells
• B Natural killer cells targeting donor endothelial cells without prior sensitisation
• C Preformed recipient antibodies against donor HLA antigens (or ABO blood group antigens) activating complement and causing thrombotic endothelial injury ✓
• D IL-2-mediated T cell proliferation and cytokine release within hours of transplantation

Explanation

Hyperacute rejection is mediated by preformed donor-specific antibodies (DSA) against HLA antigens or ABO blood group antigens in the recipient, which bind donor endothelium immediately upon reperfusion, activating complement (particularly the classical pathway) and causing widespread thrombosis, fibrin deposition, and irreversible ischaemia. It is diagnosed clinically (graft turns purple and fails to produce urine on table) and histologically shows intravascular thrombi and neutrophilic infiltration. It is now rare due to crossmatch testing.

Reference: Bailey & Love's Short Practice of Surgery, 27th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.