Abstract

Transplantation-associated thrombotic microangiopathy (TMA) is one of the most disastrous complications of renal transplantation. It may be either de novo (more common with a poor prognosis) or recurrent (with genetic background due to underlying mutations). Varied presentation mandates a high index of clinical suspicion, and the diagnosis usually requires allograft biopsy demonstrating TMA with or without underlying etiology. It has never been reported to mimic hyperacute rejection. In this context, we describe an end-stage renal disease patient with underlying IgA nephropathy, who underwent blood group incompatible renal transplant following successful desensitization and after that had systemic TMA in the 1st-h posttransplant itself, with allograft biopsy revealing florid TMA with no evidence of rejection, tacrolimus toxicity, or infection. Etiology remained elusive despite exhaustive workup and all possible attempts to salvage the allograft went in vain, with subsequent graft nephrectomy at 3 months. The patient after that has undergone a blood group compatible deceased-donor renal transplant and fortunately has normal graft function at 2 years follow-up, enthralling us to hypothesize possible interaction between the endothelial cells of renal allograft and anti-donor hemagglutinin antibodies; a mechanism already avowed for graft loss in blood group incompatible liver transplantation. We, therefore, suggest that patients willing for blood group incompatible renal transplantation need to be counseled beforehand about this, although a rare but devastating entity.

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