03324nas a2200301   4500008004100000020001400041024001700055245012700072210006900199260027500268300001200543490000700555520213300562653002702695653002102722653001402743653003102757100002302788700001802811700002102829700001802850700002302868700002102891700002202912700001802934700002102952856004902973       2008                        eng d  a0902-0063  abb5, 871024000aSuccessful treatment of de novo thrombotic microangiopathy after minor ABO-mismatched living donor kidney transplantation.0 aSuccessful treatment of de novo thrombotic microangiopathy after  aCopyright (C) 2008 Blackwell Publishing Ltd.b(a)Department of Transplantation and Regenerative Surgery, (b)Department of Organ Interaction Research Medicine, (c)Department of Pathology, Kyoto Prefectural University Graduate School of Medical Science, Kyoto, Japanc2008  a25 - 300 v223 aWe report a case of thrombotic microangiopathy developing after minor ABO-mismatched living donor kidney transplantation. The patient was a 57-yr-old woman whose blood group was B-positive. She received a kidney transplant from her husband whose blood group was O-positive. The recipient human leukocyte antigen haplotype was entirely different from that of the donor and the direct lymphocyte cross-match test was negative. The patient's hemoglobin and platelet (Plt) count fell rapidly from 11.0 g/dL and 34 x 104/[mu]L to 6.0 g/dL and 0.4 x 104/[mu]L between days 10 and 15 after kidney transplantation, with no evidence of bleeding. On day 8, anti-group B IgG and IgM antibodies were found in her serum. This anti-B antibody was thought to be produced from passenger B lymphocytes in the donor's kidney. Although in the case of hemolytic anemia after minor mismatched transplantation, the kidney function usually remains stable, the serum creatinine (s-Cr) rose from 0.8 to 5.2 mg/dL. On day 16, the helmet cells appeared in the serum and a total of 20 units of group O packed red blood cells and 30 units of group O Plts were transfused. Biopsy of the transplanted kidney was performed, which revealed thrombotic microangio-pathy, and appropriate therapy for DIC was administered, including anticoagulants, and cyclosporine A and mizoribine were replaced with tacrolimus and mycophenolate mofetil. Frequent plasma exchanges (PEX) with fresh frozen plasma were carried out. Furthermore, the anti-CD20 antibody rituximab was administered, because PEX had no effect. Following the adoption of these measures, the anti-donor antibodies disappeared to reduce the reaction on flow cytometric cross-match test; an anti-groupB antibody did not completely disappear but decreased in titer, and all the symptoms resolved immediately. The graft function recovered to a s-Cr level of 1.6 mg/dL by 34 d after the transplantation and she was discharged by 36 d after the transplantation. At present, she is entirely healthy and the graft function remains good with a s-Cr level of 1.1 mg/dL., Copyright (C) 2008 Blackwell Publishing Ltd.10aKidney Transplantation10aplasma exchanges10arituximab10athrombotic microangiopathy1 aUshigome, Hidetaka1 aSakai, Kazuki1 aSuzuki, Tomoyuki1 aNobori, Syuji1 aYoshizawa, Atsushi1 aKaihara, Satoshi1 aOkamoto, Masahiko1 aUrasaki, Koji1 aYoshimura, Norio  uhttps://www.notifylibrary.org/reference/4127