Progressive glomerular sclerosis in experimental antiglomerular basement membrane glomerulonephritis.
Progressive glomerular sclerosis in experimental antiglomerular basement membrane glomerulonephritis.
复制标题
实验性抗肾小球基底膜肾炎中的进行性肾小球硬化。
DOI：
10.1016/s0272-6386(86)80050-6
复制
发表时间：
1986
期刊：
影响因子：
--
通讯作者：
Kashgarian,M
中科院分区：
文献类型：
--
作者：
Foellmer,HG;Sterzel,RB;Kashgarian,M
用Wistar大鼠建立了实验性抗肾小球基底膜（anti-GBM）肾炎慢性进行性肾小球硬化模型。给予加速形式的抗GBIVI抗体肾小球肾炎的Wistar大鼠最初出现显著的蛋白尿和肾功能不全，主要与肾小球滤过率（GFR）降低相关，对氨基马尿酸的肾清除率正常，滤过分数显著降低。肾小球功能异常与白细胞浸润引起的显著肾小球细胞过多以及固有肾小球细胞增殖伴新月体形成相关。在病程后期，到第21天，GFR进一步下降，与对氨基马尿酸清除率和正常滤过分数的平行降低相关。在这个阶段，肾小球细胞增生减少，取而代之的是肾小球硬化。该模型似乎是慢性肾小球硬化症的可重复形式，并表明肾小球基底膜（GBM）肾小球肾炎的慢性期与急性期明显不同。它提供了一个可控的设置，以研究肾小球硬化过程的独立的初始炎症变化。
A model of chronic progressive glomerular sclerosis in experimental antiglomerular basement membrane (anti-GBM) glomerulonephritis was developed in Wistar rats. Wistar rats given the accelerated form of anti-GBIVI antibody glomerulonephritis initially developed significant proteinuria and renal insufficiency associated primarily with a decrease in glomerular filtration rate (GFR) with normal renal clearance of para-aminohippuric acid and with markedly reduced filtration fraction. The glomerular functional abnormalities were associated with marked glomerular hypercellularity due to leukocytic infiltration as well as proliferation of intrinsic glomerular cells with crescent formation. Late in the course of the disease, by day 21, GFR had fallen further, associated with a parallel decrease in the clearance of para-amminohippuric acid and a normal filtration fraction. At this stage, glomerular hypercellularity had diminished and was replaced by glomerular sclerosis. The model appears to be a reproducible form of chronic glomerulosclerosis and demonstrates that the chronic phase of glomerular basement membrane (GBM) glomerulonephritis is distinctly different from that of the acute phase. It provides a controllable setting to study the glomerular sclerotic process independent of the initial inflammatory changes.