Immediately after reperfusion of a renal allograft from a deceased donor, the surgeon notes the kidney becomes flaccid, mottled, and cyanotic with absent perfusion. Biopsy shows fibrinoid necrosis of arterioles, glomerular thrombi, and neutrophilic infiltration. Pretransplant testing most likely would have revealed:

• A Recipient Th1-mediated delayed hypersensitivity to donor minor histocompatibility antigens
• B Donor-specific expansion of recipient CD8 cytotoxic T lymphocytes against graft parenchyma
• C De novo recipient antibodies to donor vascular smooth muscle developed days after surgery
• D Recipient sensitization to donor HLA antigens with preformed circulating anti-donor antibodies ✓

Explanation

Hyperacute rejection occurs within minutes of revascularization when preformed recipient antibodies, usually from prior transfusions, pregnancies, or transplants, bind donor HLA or ABO antigens on graft endothelium, fix complement, and trigger endothelial injury, thrombosis, and immediate infarction. CD8 T cell cytotoxicity defines acute cellular rejection occurring days later, and chronic rejection manifests months to years later as graft arteriosclerosis, both incompatible with the intraoperative timing.

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.