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人类肾移植中的肾小球疾病

Glomerulopathies in human renal allografts.

作者信息

Rossmann P, Jirka J, Málek P, Hejnal J

出版信息

Beitr Pathol. 1975 May;155(1):18-35. doi: 10.1016/s0005-8165(75)80056-4.

Abstract

The present study discusses the light, electron and immunofluorescence microscopy as well as some clinicopathologic correlations of rejection change in human renal allograft glomeruli. It is based on examination of 126 tissue specimens from 54 grafts obtained from 50 patients (1966-1973). The most frequent and characteristic lesion was membranous transplant glomerulopathy (MG) with irregular fibrillar thickening of capillary walls but without conspicuous hypercellularity. This thickening was caused by subendothelial depositsdifferent from classical fibrinoid lesions. During further progression, widening and peripheral extension of mesangium with degenerative changes became apparent. Advanced MG was encountered most frequently in the 2nd year after transplantation (TPL) at moderate to medium proteinuria and hypertension. It was accompanied by endarteristic rejection changes, and renal insufficiency set on usually in the course of the 3rd year. Nevertheless, the course, symptoms, and graft survival exhibited considerable variations. - The morphology and manifestations of destructive segmental transplant glomerulopathy (SG) depended on the time of its development. In the early stage (within about 3 months after TPL), the lesion was characterized by areas of fibrinoid insudation and necro(bio)sis associated with severe vascular changes, most frequently obliterative arterio(lo)pathy (OA). The ultrastructure was characterized by endothelial defects with host's polynuclear reaction and focal intravascular coagulation. The grafts thus affected failed soon, their function usually subsiding within the first trimester at a moderate, but gradually increasing proteinuria and severe persistent hypertension. The late from of destructive SG presenting as fibrohyaline obliteration of the loops with foam cells always accompanied advanced MG with severe arterial lesions. - Fluorescence microscopy revealed both linear and focal fixation of antisera, which, however had no apparent correlation with the microscopical and clinical presentations.

摘要

本研究探讨了人肾移植肾小球排斥反应变化的光镜、电镜和免疫荧光显微镜检查以及一些临床病理相关性。该研究基于对50例患者(1966 - 1973年)的54个移植肾的126份组织标本的检查。最常见且具有特征性的病变是膜性移植肾小球病(MG),其毛细血管壁有不规则的纤维状增厚,但无明显的细胞增多。这种增厚是由内皮下沉积物引起的,与经典的纤维蛋白样病变不同。在进一步发展过程中,系膜增宽并向周边延伸,同时出现退行性改变。晚期MG最常出现在移植后第2年,伴有中度至中度蛋白尿和高血压。它伴有动脉性排斥反应变化,肾功能不全通常在第3年出现。然而,病程、症状和移植肾存活情况存在相当大的差异。 - 破坏性节段性移植肾小球病(SG)的形态和表现取决于其发展时间。在早期(移植后约3个月内),病变的特征是纤维蛋白样渗出和坏死(生物)区域,伴有严重的血管变化,最常见的是闭塞性动脉(小动脉)病(OA)。超微结构的特征是内皮缺陷伴有宿主多核反应和局灶性血管内凝血。受此影响的移植肾很快就会失败,其功能通常在孕早期内减退,伴有中度但逐渐增加的蛋白尿和严重的持续性高血压。晚期破坏性SG表现为袢的纤维透明样闭塞并伴有泡沫细胞,总是与伴有严重动脉病变的晚期MG同时出现。 - 荧光显微镜检查显示抗血清呈线性和局灶性固定,然而,这与显微镜检查和临床表现无明显相关性。

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