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依库珠单抗治疗肾移植受者吉西他滨诱导的血栓性微血管病

Eculizumab therapy in gemcitabine-induced thrombotic microangiopathy in a renal transplant recipient.

作者信息

Martin Kylie, Roberts Veena, Chong Geoff, Goodman David, Hill Prue, Ierino Francesco

机构信息

Department of Nephrology, St Vincent's Hospital Melbourne, Fitzroy 3065 Victoria, Australia.

Olivia-Newton John Cancer, Wellness and Research Centre, Austin Hospital, Heidelberg, Australia.

出版信息

Oxf Med Case Reports. 2019 Jun 14;2019(6):omz048. doi: 10.1093/omcr/omz048. eCollection 2019 Jun.

Abstract

A renal transplant recipient 7 years post-transplantation, diagnosed with locally advanced pancreatic adenocarcinoma developed thrombotic microangiopathy (TMA) after treatment with gemcitabine and nab-paclitaxel. Gemcitabine was the most likely cause for TMA and was ceased. He received methylprednisolone and plasma exchange with fresh frozen plasma and albumin. Despite plasma exchange, his renal allograft function worsened, and he had persistent haematological evidence of haemolysis. Eculizumab was commenced with resolution-significant improvement in his renal and haematological markers. This case highlights an unusual occurrence of progressive gemcitabine-induced TMA in a renal allograft that had an excellent response to eculizumab. The clinical response also demonstrates involvement of complement dysregulation in gemcitabine-induced TNA.

摘要

一名肾移植受者在移植后7年,被诊断为局部晚期胰腺腺癌,在接受吉西他滨和纳米白蛋白紫杉醇治疗后发生血栓性微血管病(TMA)。吉西他滨最有可能是导致TMA的原因,随后停用。他接受了甲泼尼龙治疗,并进行了新鲜冰冻血浆和白蛋白的血浆置换。尽管进行了血浆置换,他的肾移植功能仍恶化,并且持续存在溶血的血液学证据。开始使用依库珠单抗治疗后,他的肾脏和血液学指标显著改善。该病例突出了吉西他滨诱导的TMA在肾移植中罕见的进展情况,而依库珠单抗对此有良好反应。临床反应也表明补体调节异常参与了吉西他滨诱导的TNA。

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