Minutes after reperfusion of a kidney transplant, the graft turns from pink to a mottled, dusky blue, becomes flaccid, and stops producing urine on the table. The anaesthetist confirms good systemic pressure. It emerges that a pre-transplant crossmatch result was misreported. What has happened, and what is the underlying mechanism?
- AAcute tubular necrosis from prolonged cold storage; the graft will recover with supportive care
- BHyperacute rejection: preformed antibodies bind graft endothelium on reperfusion, causing thrombosis and infarction; the graft must be removed
- CAcute cellular rejection, treatable with pulsed steroids
- DChronic allograft nephropathy
- ERenal artery kinking, corrected by repositioning
Show answer and explanation
Correct answer: B
A graft that perfuses pink and then dies on the table — mottling, cyanosis, flaccidity, anuria — with systemic haemodynamics intact is hyperacute rejection: the recipient already possesses circulating antibodies against donor antigens (anti-ABO isohaemagglutinins, or anti-HLA antibodies from prior transplants, transfusions or pregnancies), and the instant blood flows, antibody coats the donor endothelium, fixing complement, recruiting platelets and neutrophils, and thrombosing the entire microvasculature — type II hypersensitivity executed at organ scale. There is no treatment; the infarcted graft is removed. Its importance is almost entirely preventive, and that is the examinable core: ABO compatibility, HLA typing, screening the recipient for anti-HLA antibodies, and the pre-transplant crossmatch — testing recipient serum against donor lymphocytes (now usually virtual, from comprehensive antibody profiling) — exist precisely to make hyperacute rejection a historical rarity; a positive crossmatch vetoes the transplant. The vignette's misreported crossmatch is the classic systems failure behind modern cases.
Why the others are wrong: A — ATN causes delayed function in a viable-looking graft, not intraoperative infarction. C — acute cellular rejection is a T-cell process of days to weeks, treatable with steroids. D — chronic changes evolve over years. E — vascular kinking causes congestion or pallor correctable with repositioning, not diffuse thrombotic mottling with preserved inflow anatomy.
Key point: Hyperacute rejection — preformed anti-donor antibody meeting graft endothelium at reperfusion, complement-driven microvascular thrombosis, graft death within minutes — is untreatable and prevented entirely by ABO matching, antibody screening and the crossmatch; that is why those tests are inviolable.
Guidelines: BSHI/BTS guidance on HLA antibody testing and crossmatching in transplantation: hyperacute rejection from preformed donor-specific antibody is prevented by ABO typing, antibody screening and pre-transplant crossmatching; the graft is removed once it occurs.