Ardalan Mohammad Reza, Nasri Hamid, Ghabili Kamyar, Mohajel Shoja Mohammadali
Department of Nephrology, Tabriz University, Tabriz, Iran.
Exp Clin Transplant. 2008 Dec;6(4):312-4.
Renal allograft dysfunction can be caused by renal vessel thrombosis, acute tubular necrosis, hyperacute or acute rejection, nephrotoxicity induced by cyclosporine or tacrolimus, thrombotic microangiopathy, or urinary tract obstruction.
We describe a renal transplant recipient in whom oliguria developed during the first week after transplant, although his early renal allograft function was good.
A Doppler ultrasonographic study revealed a lack of perfusion in the lower pole of the allograft. A perfusion defect was noted in the lower pole that was supplied by a polar artery, which had been damaged during engraftment. Light microscopy disclosed tubular cell necrosis without evidence of vascular or humoral rejection.
We suggest that toxic molecules such as tumor necrosis factor-alpha released from a segmental infarcted area can induce tubular cell damage and necrosis leading to renal allograft dysfunction.
肾移植功能障碍可由肾血管血栓形成、急性肾小管坏死、超急性或急性排斥反应、环孢素或他克莫司引起的肾毒性、血栓性微血管病或尿路梗阻所致。
我们描述了一名肾移植受者，其移植后第一周出现少尿，尽管其早期肾移植功能良好。
多普勒超声检查显示移植肾下极灌注缺乏。在下极由一支在植入时受损的极动脉供血区域发现灌注缺损。光镜检查显示肾小管细胞坏死，无血管或体液排斥反应的证据。
我们认为，从节段性梗死区域释放的诸如肿瘤坏死因子-α等毒性分子可诱导肾小管细胞损伤和坏死，导致肾移植功能障碍。
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