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typical hemolytic–uremic syndrome (aHUS) is an extremely are, genetic, chronic, and progressive inflammatory disease1 aused by defects in complement system. These defects result n systemic thrombotic microangiopathy involving damage o multiple organ systems including renal dysfunction.1–7 enetic mutations have been detected in around 50% of the eported cases. Regarding renal transplant patients, expanded riteria donors, infection by cytomegalovirus or BK, use of NI or m-TOR inhibitors and antibody-mediated rejection AMR) have been related to de novo post-transplant aHUS.8 raft failure is reported in 60–90% of patients within 1 year.10 culizumab is a monoclonal antibody that binds to C5 comlement protein avoiding the formation of the cell membrane ttack complex.6,7 We report herein a case of late onset of de ovo post-transplant aHUS on a simultaneous pancreas and idney recipient with severe systemic manifestations, withut presenting acute graft rejection, successfully treated with imited doses of eculizumab remaining stable after one year f follow-up. A 46-year-old woman with end stage renal disease econdary to type 1 Diabetes Mellitus underwent simulaneous pancreas and kidney transplant on October 2012 rom deceased donor. Received induction with Basiliximab nd maintenance treatment with mycophenolate mofetil, acrolimus, and prednisone. Pancreatic and renal function ere stable, creatinine (SCr) of 110 mol/L. Tacrolimus through evels remained between 6 and 8 ng/ml. Seven months fter transplant presented fever, abdominal pain, diarrhea nd vomiting, acute graft dysfunction (SCr 438 mol/L) and

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Late onset of de novo atypical hemolytic–uremic syndrome presented on a simultaneous pancreas and kidney transplant recipient successfully treated with eculizumab