Carstens P H, Karalakulasingam R
Virchows Arch A Pathol Anat Histol. 1975 Aug 12;367(3):171-9. doi: 10.1007/BF00430705.
The clinico-pathological data from a patient with irreversible post-partum renal failure (IPRF) are presented. The electron microscopy of the late changes are described for the first time and consists of: 1. Thickening of the basement membrane. 2. Interposition of mesangial cells and matrix between the thickened basement membrane and the endothelial cell encircling the periphery of the tuft. 3. Multiplication of basal lamina material between mesangial cells and endothelial cells. 4. Proliferation of endothelial cells. All of the above changes tend to obliterate the glomerular tufts and transform the vascular lumina into slit-like spaces. They explain morphologically why most patients with IPRF terminate in chronic renal failure, if they survive the early changes. The late occurring hypertension is regarded as a secondary stimulation of the renin-angiotension system caused by partial or complete occlusion of arteries and arterioles.
本文报告了一例产后不可逆性肾衰竭（IPRF）患者的临床病理资料。首次描述了晚期病变的电子显微镜检查结果，包括：1. 基底膜增厚。2. 系膜细胞和基质插入增厚的基底膜与围绕肾小球丛周边的内皮细胞之间。3. 系膜细胞和内皮细胞之间基底膜物质增多。4. 内皮细胞增殖。上述所有变化往往会使肾小球丛闭塞，并将血管腔转变为裂隙样间隙。从形态学上解释了为什么大多数IPRF患者如果能度过早期变化，最终会发展为慢性肾衰竭。晚期出现的高血压被认为是由动脉和小动脉部分或完全闭塞引起的肾素 - 血管紧张素系统的继发性刺激。
