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人类膜性肾小球病中肾小球损伤的程度及病程

Extent and course of glomerular injury in human membranous glomerulopathy.

作者信息

Guasch A, Sibley R K, Huie P, Myers B D

机构信息

Department of Medicine, Stanford University Medical Center, California 94305.

出版信息

Am J Physiol. 1992 Dec;263(6 Pt 2):F1034-43. doi: 10.1152/ajprenal.1992.263.6.F1034.

DOI:10.1152/ajprenal.1992.263.6.F1034
PMID:1282782
Abstract

Glomerular permselectivity and dynamics were evaluated serially in 14 nephrotic patients with membranous glomerulopathy (MG). Analysis of transglomerular dextran sieving, before and again after proteinuria remitted, revealed persistent depression by 60-80% of glomerular pore density and the two-kidney ultrafiltration coefficient, Kf. The glomerular filtration rate was lowered by half on each occasion. Morphometric examination of glomeruli in a second group of 16 nephrotic patients with MG revealed a low prevalence of glomerulosclerosis (5 +/- 3%) and a twofold increase in filtration surface due to marked glomerular hypertrophy. Presumably, widening by threefold of the basement membrane and/or epithelial podocytes accounted for the computed reduction in ultrafiltration capacity. There was no correlation between glomerular structure and the subsequent course of MG over the ensuing 24-96 mo. Rather, a twofold expansion of the interstitial compartment predicted those who went on to exhibit progressive renal insufficiency. We conclude that increasing resistance to water flow by walls of patent and perfused glomerular capillaries is the proximate cause of progressive renal insufficiency in MG.

摘要

对14例膜性肾小球病(MG)肾病患者的肾小球滤过选择性和动力学进行了系列评估。在蛋白尿缓解前后对跨肾小球葡聚糖筛分进行分析,结果显示肾小球孔密度和双肾超滤系数Kf持续降低60%-80%。每次肾小球滤过率均降低一半。对另一组16例MG肾病患者的肾小球进行形态计量学检查,结果显示肾小球硬化的发生率较低(5±3%),且由于明显的肾小球肥大,滤过面积增加了两倍。据推测,基底膜和/或上皮足细胞增宽三倍导致了超滤能力的计算值降低。在随后的24-96个月里,肾小球结构与MG的后续病程之间没有相关性。相反,间质腔室扩大两倍可预测哪些患者会出现进行性肾功能不全。我们得出结论,开放且灌注的肾小球毛细血管壁对水流的阻力增加是MG患者进行性肾功能不全的直接原因。

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引用本文的文献

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Structural basis for reduced glomerular filtration capacity in nephrotic humans.肾病患者肾小球滤过能力降低的结构基础。
J Clin Invest. 1994 Sep;94(3):1187-95. doi: 10.1172/JCI117435.
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Mechanisms of filtration failure during postischemic injury of the human kidney. A study of the reperfused renal allograft.
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J Clin Invest. 1995 Feb;95(2):820-31. doi: 10.1172/JCI117732.
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