Minutes after reperfusion of a renal allograft in the operating room, the kidney becomes flaccid and cyanotic. Biopsy shows neutrophilic arteritis, fibrinoid necrosis, and extensive interstitial hemorrhage with immunoglobulin and complement deposition in vessel walls. The pathogenesis involves:

• A Donor T cells recognizing recipient alloantigens
• B De novo recipient T cell priming over the first post-transplant week
• C Preformed recipient antibodies against donor HLA or blood group antigens activating complement ✓
• D Ischemia-reperfusion injury mediated by donor macrophages

Explanation

Hyperacute rejection is a Type II hypersensitivity reaction occurring within minutes, driven by preformed circulating antibodies in the recipient that bind donor vascular endothelium (ABO antigens or HLA from prior sensitization by pregnancy, transfusion, or transplantation). Complement activation causes endothelial injury, thrombosis, and immediate graft ischemia. Donor T cell responses underlie acute cellular rejection, which takes days to weeks, not minutes.

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

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.