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依库珠单抗在多囊肾病患者肾移植术后即刻发生的移植相关血栓性微血管病中的应用:一例报告

Use of Eculizumab in Transplant-Associated Thrombotic Microangiopathy in a Patient With Polycystic Kidney Disease Immediately Post-Kidney Transplant: A Case Report.

作者信息

Godara Amandeep, Migliozzi Daniel R, Pilichowska Monika, Goyal Nitender, Varga Cindy, Gordon Craig E

机构信息

Department of Hematology-Oncology, Tufts Medical Center, Boston, MA.

Kidney Transplant Team, Division of Nephrology, Tufts Medical Center, Boston, MA.

出版信息

Kidney Med. 2020 Aug 5;2(5):652-656. doi: 10.1016/j.xkme.2020.06.007. eCollection 2020 Sep-Oct.

Abstract

Transplant-associated thrombotic microangiopathy (TMA) in the post-organ transplantation setting occurs from a number of potential inciting factors, such as the use of calcineurin inhibitors, ischemic injury, infections, or antibody-mediated rejection leading to unchecked complement activation and end-organ damage. Delayed recognition of this condition can result in allograft loss. In this case description, we describe the first case of de novo TMA in a patient with polycystic kidney disease that occurred immediately after kidney transplantation. The diagnosis was made promptly on the basis of clinical and laboratory characteristics by a multidisciplinary team and confirmed through kidney biopsy, which showed acute TMA. The patient was successfully managed by replacing tacrolimus with belatacept, which targets cytotoxic T lymphocyte antigen 4, and use of eculizumab, a C5 inhibitor. Eculizumab treatment was discontinued after 3 months of complement inhibition on the patient's request, and relapse of TMA has not been encountered after more than 1 year of follow-up.

摘要

器官移植后发生的移植相关血栓性微血管病(TMA)由多种潜在诱发因素引起,如使用钙调神经磷酸酶抑制剂、缺血性损伤、感染或抗体介导的排斥反应,导致补体激活失控和终末器官损伤。对这种情况的延迟识别可能导致移植肾丢失。在本病例描述中,我们描述了一例多囊肾病患者肾移植后立即发生的新发TMA的首例病例。多学科团队根据临床和实验室特征迅速做出诊断,并通过肾活检得以证实,肾活检显示为急性TMA。通过将他克莫司替换为靶向细胞毒性T淋巴细胞抗原4的贝拉西普,并使用C5抑制剂依库珠单抗,成功治疗了该患者。应患者要求,在补体抑制3个月后停用依库珠单抗治疗,随访1年多后未出现TMA复发。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/291c/7568057/ab687cf3e49b/gr1.jpg

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