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Microbiology · Immunology
Sample itemWithin minutes of reperfusion of a transplanted kidney, the graft becomes cyanosed and mottled with fibrinoid necrosis of vessels. The recipient was sensitised by multiple prior transfusions. What is the mechanism?
Original practice item, not a recalled exam question. Nothing here is recorded.
The answer and the reasoning
B. Preformed anti-donor HLA antibodies causing complement-mediated endothelial injury
Hyperacute rejection occurs within minutes to hours in a recipient with preformed antibodies, usually from transfusion, previous transplant or pregnancy. Antibodies bind donor endothelium, activate complement and cause thrombosis and necrosis. A negative cross-match prevents it.
Option by option
A. Chronic graft arteriopathy from repeated low-grade injury
Chronic rejection develops over months to years with vascular intimal thickening.
B. Preformed anti-donor HLA antibodies causing complement-mediated endothelial injury (correct)
Correct. Preformed antibodies and complement cause immediate endothelial injury.
C. Donor T cells attacking recipient tissues
Donor T cells attacking the recipient describe graft-versus-host disease, not graft rejection.
D. Donor-specific cytotoxic T cells attacking graft parenchyma over weeks
T-cell mediated attack is the mechanism of acute cellular rejection, over days to weeks.
Source note: Original NextPrep sample item — pending expert review. This item is original practice material awaiting independent expert review, so confirm important facts in a standard textbook.
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