Foellmer H G, Sterzel R B, Kashgarian M
Am J Kidney Dis. 1986 Jan;7(1):5-11. doi: 10.1016/s0272-6386(86)80050-6.
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-GBM anti-body 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-aminohippuric 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.
在Wistar大鼠中建立了实验性抗肾小球基底膜(anti-GBM)肾小球肾炎慢性进行性肾小球硬化模型。给予加速形式抗GBM抗体肾小球肾炎的Wistar大鼠最初出现明显蛋白尿和肾功能不全,主要与肾小球滤过率(GFR)降低有关,对氨基马尿酸肾清除率正常,滤过分数明显降低。肾小球功能异常与由于白细胞浸润以及固有肾小球细胞增殖伴新月体形成导致的明显肾小球细胞增多有关。在疾病后期,到第21天时,GFR进一步下降,同时对氨基马尿酸清除率平行下降,滤过分数正常。在此阶段,肾小球细胞增多已减少,并被肾小球硬化所取代。该模型似乎是慢性肾小球硬化的一种可重复形式,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环境来研究独立于初始炎症变化的肾小球硬化过程。