Kidney Center, Japanese Red Cross Nagoya Daini Hospital, Nagoya, Japan.
Clin Transplant. 2011 Jul;25 Suppl 23:15-8. doi: 10.1111/j.1399-0012.2011.01453.x.
De novo thrombotic microangiopathy(TMA) is most commonly triggered by calcineurin inhibitors (CNI) and the prognosis is less severe than with recurrent TMA. However, it is difficult to distinguish de novo TMA from CNI toxicity and acute antibody-mediated rejection(AMR) soon after renal transplantation. We present a case of tacrolimus-associated TMA soon after ABO blood type incompatible renal transplantation that was difficult to differentiate from acute AMR. On day 9 his urine output decreased dramatically and the Scr level increased. His anti-blood type A antibody titer increased to ×16 postopratively and the tacrolimus trough level was higher than in our immunosuppressive regimen. Although we gave priority to anti-AMR treatment, adequate dose adjustment of tacrolimus after tacrolimus nephrotoxicity was diagnosed from graft biopsy could correct allograft dysfunction.
新发性血栓性微血管病（TMA）最常由钙调磷酸酶抑制剂（CNI）触发，其预后比复发性 TMA 轻。然而，在肾移植后不久，区分新发性 TMA 与 CNI 毒性和急性抗体介导的排斥反应（AMR）很困难。我们报告了一例 ABO 血型不合肾移植后不久发生的与他克莫司相关的 TMA，该病例很难与急性 AMR 区分。术后第 9 天，他的尿量明显减少，Scr 水平升高。他的抗 A 血型抗体滴度术后增加到×16，他克莫司谷浓度高于我们的免疫抑制方案。尽管我们优先考虑抗 AMR 治疗，但从移植物活检诊断出他克莫司肾毒性后，他克莫司的充分剂量调整可以纠正同种异体功能障碍。
