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微小病变性肾病:肾小球膜的一种电化学紊乱。

Minimal change nephropathy: an electrochemical disorder of the glomerular membrane.

作者信息

Carrie B J, Salyer W R, Myers B D

出版信息

Am J Med. 1981 Feb;70(2):262-8. doi: 10.1016/0002-9343(81)90760-9.

Abstract

To investigate the mechanism of proteinuria in minimal change nephropathy, the renal handling of dextrans was studied in seven nephrotic patients with this disorder. Although the urinary excretion of albumin was greatly increased, the urinary excretion and fractional clearance of dextrans (Einstein-Stokes radius (ESR), range 20 to 48 A) were depressed relative to those in nonproteinuric healthy volunteers. This suggests that mean glomerular pore size or pore density was reduced. Uptake of colloidal iron by glomeruli obtained from these patients by needle biopsy was diminished, suggesting loss of glomerular polyanion. Since the fractional clearance of dextrans similar in size to albumin was depressed, not increased, it is proposed that the lack of electrostatic interaction between the glomerular capillaries and polyanionic plasma albumin (ESR = 36 A) accounts for the selective albuminuria which characterizes minimal change nephropathy.

摘要

为研究微小病变肾病蛋白尿的机制,对7例患有该疾病的肾病患者的右旋糖酐肾脏处理情况进行了研究。尽管白蛋白的尿排泄量大幅增加,但相对于无蛋白尿的健康志愿者,右旋糖酐(爱因斯坦-斯托克斯半径(ESR),范围为20至48埃)的尿排泄量和分数清除率降低。这表明平均肾小球孔径或孔密度降低。通过针吸活检从这些患者获取的肾小球对胶体铁的摄取减少,提示肾小球多阴离子丢失。由于与白蛋白大小相似的右旋糖酐的分数清除率降低而非增加,因此提出肾小球毛细血管与多阴离子血浆白蛋白(ESR = 36埃)之间缺乏静电相互作用是微小病变肾病特征性选择性蛋白尿的原因。

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