POSTISCHEMIC INJURY, DELAYED FUNCTION AND NA+/K+-ATPASE DISTRIBUTION IN THE TRANSPLANTED KIDNEY
POSTISCHEMIC INJURY, DELAYED FUNCTION AND NA+/K+-ATPASE DISTRIBUTION IN THE TRANSPLANTED KIDNEY
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DOI：
10.1038/ki.1995.415
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发表时间：
1995-10-01
影响因子：
19.6
通讯作者：
MYERS, BD
中科院分区：
文献类型：
--
作者：
ALEJANDRO, VSJ;NELSON, WJ;MYERS, BD
我们评估了22例肾移植患者的缺血后肾损伤。同种异体移植物再灌注后45 ~ 60分钟获得肾组织，用特异性抗体对Na+/K+- atp酶、fodrin和锚蛋白的部分衍生物亚基进行染色。用激光共聚焦显微镜分析各细胞骨架蛋白的分布。随后在再灌注后1 ~ 3小时和36小时两次评估同种异体移植物功能。受者分为两组：移植后第3天GFR正常者（1组，N = 12）和持续滤过过低者（2组，N = 10）。两组患者术后1 ~ 3小时均表现出钠重吸收受损和等血尿，但这些异常仅在2组患者持续低滤过中持续到第3天。Na+/K+- atp酶、锚定蛋白和fodrin的异常局限于近端小管细胞，仅在组2中被标记。它们包括每个细胞骨架蛋白从基底外侧膜到细胞质的重新分配。我们得出结论，同种异体肾移植术后损伤导致近端小管细胞极性丧失。我们认为，随后的近端钠重吸收损伤可能会激活小管肾小球反馈，从而导致慢性低滤过，这是这种缺血后急性肾功能衰竭的特征。
We evaluated the postischemic renal injury in 22 patients undergoing renal transplantation. Renal tissue obtained 45 to 60 minutes after reperfusion of the allograft was stained with specific antibodies against the partial derivative subunit of Na+/K+-ATPase, fodrin and ankyrin. The distribution of each cytoskeletal protein was analyzed by laser confocal microscopy. Subsequent allograft function was assessed on two occasions, 1 to 3 and 36 hours post-reperfusion, respectively. Recipients were divided into two groups: those who achieved a normal GFR on post-transplant day 3 (group 1, N = 12) and those with persistent hypofiltration (group 2, N = 10). Patients of both groups exhibited impaired sodium reabsorption and isosthenuria one to three hours postoperatively, but these abnormalities persisted on day 3 only in group 2 subjects with persistent hypofiltration. Abnormalities of Na+/K+-ATPase, ankyrin and fodrin were confined to proximal tubule cells and were marked only in the subjects of group 2. They consisted of redistribution of each cytoskeletal protein from the basolateral membrane to the cytoplasm. We conclude that postischemic injury to a renal allograft results in a loss of polarity of proximal tubule cells. We propose that ensuing impairment of proximal sodium reabsorption could activate tubuloglomerular feedback, thereby contributing to the protracted hypo-filtration that characterizes this form of postischemic, acute renal failure.