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肾移植受者血栓性微血管病/溶血尿毒症综合征的无钙调神经磷酸酶抑制剂免疫抑制治疗

Calcineurin inhibitor-free immunosuppression in renal allograft recipients with thrombotic microangiopathy/hemolytic uremic syndrome.

作者信息

Oyen O, Strøm E H, Midtvedt K, Bentdal O, Hartmann A, Bergan S, Pfeffer P, Brekke I B

机构信息

Surgical Department, Transplant Section, The Rikhospitalet University Hospital, 0027 Oslo, Norway.

出版信息

Am J Transplant. 2006 Feb;6(2):412-8. doi: 10.1111/j.1600-6143.2005.01184.x.

Abstract

Thrombotic microangiopathy (TMA) and hemolytic uremic syndrome (HUS) represent serious threats to kidney allograft recipients. During a 4-year period, among 850 kidney transplantations, seven recipients with primary HUS and seven recipients (eight transplants) with previous or de novo TMA/HUS were identified and given calcineurin inhibitor (CNI)-free immunosuppression by sirolimus (SRL), mycophenolate mofetil and steroids. Thirteen out of 15 transplantations were successful in the long term; resulting in a mean creatinine of 101 mumol/L (16.4 months follow-up). In patients maintained on CNI-free regimen, no TMA/HUS recurrences were observed. A high rate of acute rejections (53%) may indicate insufficient immunosuppressive power and/or a causative relationship between TMA/HUS and rejection. Wound-related complications were abundant (60%), and call for surgical/immunosuppressive countermeasures. Our experience supports the idea that CNI's are major offenders in TMA/HUS induction. Total CNI elimination seems essential, as the nephrotoxic combination CNI + SRL may promote TMA. Features of TMA/HUS should be carefully explored in recurrent 'high responders'.

摘要

血栓性微血管病(TMA)和溶血尿毒综合征(HUS)对肾移植受者构成严重威胁。在4年期间,在850例肾移植中,确定了7例原发性HUS受者以及7例既往有或新发TMA/HUS的受者(8例移植),并通过西罗莫司(SRL)、霉酚酸酯和类固醇给予无钙调神经磷酸酶抑制剂(CNI)的免疫抑制治疗。15例移植中有13例长期成功;随访16.4个月时平均肌酐为101μmol/L。在接受无CNI方案维持治疗的患者中,未观察到TMA/HUS复发。高比例的急性排斥反应(53%)可能表明免疫抑制力度不足和/或TMA/HUS与排斥反应之间存在因果关系。伤口相关并发症很常见(60%),需要采取手术/免疫抑制对策。我们的经验支持以下观点,即CNI是TMA/HUS诱发的主要因素。似乎必须完全消除CNI,因为具有肾毒性的CNI+SRL组合可能会促进TMA。对于反复出现的“高反应者”,应仔细探究TMA/HUS的特征。

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