糖尿病肾脏的结构改变。

R Osterby
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引用次数: 0

摘要

糖尿病肾小球病变的特点是基底膜(BM)积累发展非常缓慢,表现为外周基底膜增厚,系膜样物(BMLM)体积增加,并伴有系膜扩张。该过程的开始可能是在糖尿病发病时,因为BM增厚是在几年后检测到的。肾小球丛中两个部位(PBM和BMLM)的BM积累被认为是基础BM异常的两种不同表达。这两个位置呈现不同的定量条件,可能具有不同的生化组成,并且异常的直接功能含义也可能不同。然而,从长远来看,两者共同导致肾小球簇最终凝固,毛细血管表面损失。终末期肾小球关闭,肾小球功能丧失。肾小球毛细血管的总残余表面积与GFR水平之间存在非常密切的相关性。随着糖尿病肾小球病变的经典变化,肾小球大小的变化是可检测的。在早期糖尿病肾小球功能亢进阶段,糖尿病发病时急剧肥大,导致毛细血管表面增加,相应的滤过率增加。在肾小球闭合的晚期,一部分肾单位代偿性肥厚形成,因此可能有助于在一段时间内保持毛细血管表面。可能影响这些发展的确切机制尚不清楚,但它们背后都是糖尿病的代谢异常。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Structural changes in the diabetic kidney.

Diabetic glomerulopathy is characterized by a very slow development of basement membrane (BM) accumulation, manifested as thickening of the peripheral BM and increased volume of the mesangial BM-like material (BMLM) with mesangial expansion. The initiation of the process is probably at the onset of diabetes since the BM thickening is detectable after a few years. The BM accumulations at the two sites (PBM and BMLM) in the glomerular tuft are considered as two different expressions of a fundamental BM abnormality. The two locations present different conditions for quantitation, may have a different biochemical make-up, and immediate functional implications of the abnormalities may differ as well. In the long run, however, the two in concert lead to the ultimate solidification of the glomerular tuft with loss of capillary surface. The end-stage is glomerular closure, with elimination of glomerular function. A very close correlation has been found between the total remnant surface area of the glomerular capillaries and the level of GFR. Along with the classical changes of the diabetic glomerulopathy, changes in glomerular size are detectable. In early diabetes during the stages of glomerular hyperfunction, hypertrophy develops acutely at the onset of diabetes, leading to an increase in capillary surface corresponding to the increase in filtration rate. In the advanced stages when glomerular closure involves a proportion of the nephrons compensatory hypertrophy develops, thereby probably helping to preserve capillary surface for a period of time. The exact mechanisms that may influence these developments are not known, but underlying them all are the metabolic abnormalities of diabetes.

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