Two minutes after reperfusion of a cadaveric renal allograft, the surgeon notes the graft turning flaccid, dusky, and mottled, and urine output is nil. Biopsy shows neutrophilic vasculitis, fibrinoid necrosis of arterioles, thrombosis, and infarction. The underlying mechanism is:

• A Preformed recipient antibodies against donor ABO or HLA antigens activating complement on graft endothelium ✓
• B Recipient CD4+ and CD8+ T cells recognizing donor MHC molecules and destroying parenchymal cells
• C De novo antidonor antibodies developing weeks to months later, causing intimal thickening
• D Ischemia-reperfusion injury with oxygen free radical damage to tubules

Explanation

Hyperacute rejection occurs within minutes to hours of reperfusion when preformed circulating antibodies (anti-ABO, anti-HLA, or natural anti-Gal) bind graft endothelial antigens, fix complement, and trigger endothelial injury, platelet adhesion, thrombosis, and immediate graft infarction. Option B describes acute cellular rejection, which takes days and shows interstitial lymphocytic infiltrates. Option C describes chronic rejection, and option D causes delayed graft function with acute tubular injury, not instantaneous vascular thrombosis.

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.