Hyperacute onset of haemolytic–uraemic syndrome associated with hyperacute rejection in the recipient of an ABO‐incompatible kidney

Haemolytic–uraemic syndrome (HUS), characterizedby microangiopathic haemolysis, thrombocytopeniaand renal dysfunction, is uncommon but can result inserious complications in transplantations of kidneys,and even other organs [1]. Any factors that damagevascular endothelial cells can trigger HUS [2,3].Humoral vascular rejection and calcineurin inhibitorssuch as cyclosporin A (CSA) and tacrolimus are recog-nized as factors that instigate HUS in organ trans-plantation [4,5]. Meanwhile, an extreme shortage of organdonors necessitates widening the sources of donatedorgans, e.g. to ABO-incompatible donors [6]; well-refined pre- and post-operative treatments, includingpowerful immunosuppresion and diminution of anti-A and -B antibodies using plasmapheresis, make thispossible [7,8]. The major cause of early graft loss ishyperacute and acute humoral rejection brought onby abundant antibodies against surface A or B anti-gens ubiquitously expressed on cell surfaces [6–8].Whereas HUS associated with hyperacute rejection(HAR) in ABO-incompatible transplantations hasnever been reported, this kind of devastating rejectionwould result in immediate graft necrosis because ofthe complete occlusion of the vessels. We report aunique case of acute-onset HUS caused by HAR in arecipient of an ABO-incompatible renal graft whowas rescued by plasma exchange [9] and nafamostatmesilate [10].