Successful retransplantation of a kidney allograft affected by thrombotic microangiopathy into a second transplant recipient.
Successful retransplantation of a kidney allograft affected by thrombotic microangiopathy into a second transplant recipient.
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将受血栓性微血管病影响的同种异体肾成功重新移植到第二个移植受者体内。
DOI：
10.1053/j.ajkd.2008.03.037
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发表时间：
2008
期刊：
影响因子：
--
通讯作者：
L. Rostaing
中科院分区：
文献类型：
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作者：
N. Kamar;P. Rischmann;C. Guilbeau;F. Sallusto;M. Khedis;M. Delisle;D. Noury;M. Fort;L. Rostaing
捐赠器官短缺迫使移植中心使用非传统来源的器官。一个例子是重复使用以前移植的器官，如从脑死亡的同种异体移植受体中取出的肾脏或肝脏。我们第一次重复使用了以前移植的肾，该肾经历了来自活体同种异体移植物受体的顽固性复发性血栓性微血管病（TMA）。在移植后几周内，一名死亡的肾移植受者在移植物中发生了顽固性严重复发性特发性TMA，尽管进行了密集的血浆置换和类固醇及利妥昔单抗治疗。这需要肾切除术来治愈TMA。尽管存在TMA（血清肌酐，1.36 mg/dL [120 μ mol/L]）和微量白蛋白尿（白蛋白为1.2 g/dL [12 g/L]），但认为索引受体的同种异体移植物功能良好，活检检查显示轻度受损。在获得供体和受体知情同意并获得法国生物医学机构批准后，TMA同种异体移植物被重复使用并移植到原始肾脏疾病为多囊肾疾病的受体中。再次移植是顺利的，在移植后6个月，最终受体的血清肌酐水平为1.06 mg/L（97 μ mol/L），白蛋白尿为0.5 g/dL（5 g/L）。常规肾活检显示轻度肾小球病变。移植肾切除术后，供者的血液TMA症状在10天内消失。我们的结论是，肾移植与TMA复发可以成功地再移植到另一个受体与良好的肾功能，同时仍然治愈第一个受体的复发TMA。这可能会增加来自扩展标准供体的肾移植数量。
The donor organ shortage has compelled transplant centers to use organs from nontraditional sources. One example is the reuse of a previously transplanted organ, such as a kidney or liver retrieved from a brain-dead allograft recipient. For the first time, we reused a previously transplanted kidney that experienced intractable recurrent thrombotic microangiopathy (TMA) from a living allograft recipient. Within a few weeks posttransplantation, a deceased kidney allograft recipient developed intractable severe recurrent idiopathic TMA in the allograft despite intensive plasma exchanges and steroid and rituximab therapy. This required nephrectomy to cure TMA. The index recipient was believed to have a well-functioning allograft despite TMA (serum creatinine, 1.36 mg/dL [120 micromol/L]) and microalbuminuria with albumin of 1.2 g/dL [12 g/L]), and it appeared mildly damaged on biopsy examination. After donor and recipient informed consents were obtained and after approval of the French Agency of Biomedicine, the TMA allograft was reused and transplanted into a recipient whose original kidney disease was polycystic kidney disease. The retransplantation was uneventful, and at 6 months posttransplantation, the ultimate recipient's serum creatinine level was 1.06 mg/L (97 micromol/L) and albuminuria was 0.5 g/dL (5 g/L). A routine kidney biopsy showed mild glomerular lesions. After allograft nephrectomy, the donor's hematologic TMA symptoms dissipated within 10 days. We conclude that a kidney allograft with TMA recurrence can be successfully retransplanted into another recipient with excellent kidney function while still curing the first recipient of recurrent TMA. This might increase the number of kidney allografts from extended criteria donors.