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首页> 外文期刊>Journal of Pathology: Journal of the Pathological Society of Great Britain and Ireland >Glomerular prolapse as precursor of one type of segmental sclerosing lesions.
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Glomerular prolapse as precursor of one type of segmental sclerosing lesions.

机译:肾小球脱垂是一种类型的节段性硬化性病变的前体。

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A distinctive segmental glomerular abnormality is confined to the region of the tubular opening. The hypothesis was that this followed prolapse of the tuft into the tubule. Analysis was made of 39 renal biopsy specimens with acute postinfective glomerulonephritis, later material from ten cases, four specimens from three women with pre-eclampsia, and 21 control specimens, with morphometry of glomeruli and immunohistological examination for immunoproteins and monocytes/macrophages. Prolapse was found in 14 specimens with acute postinfective glomerulonephritis, associated in eight with adhesion to Bowman's capsule and local alterations in the tuft, which together constitute early tip changes. Another three had early tip changes only and eight others had thin adhesions between the tuft and capsule next to the tubular opening. Later material confirmed this order of development and showed another late change, with sclerosed and hyaline material in the tuft and adhesion at the tubular origin. Findings in pre-eclampsia were comparable. Glomeruli were significantly larger in acute postinfective glomerulonephritis than in controls and were shown by others to be larger in pre-eclampsia than in normal pregnancy. Immunohistology showed IgM and a few foamy monocytes/macrophages in early tip changes but not in prolapsed loops. Glomerular prolapse appears to be a temporary consequence of acute enlargement of the tuft, probably causes mechanical damage to epithelial cells, and is a precursor of permanent structural changes near the tubular origin. This gives a unifying hypothesis to explain how these changes can be seen in acute postinfective glomerulonephritis, pre-eclampsia, and many other human and experimental renal disorders. Copyright 2000 John Wiley & Sons, Ltd.
机译:独特的节段性肾小球异常仅限于管状开口区域。假设是,这是由于簇绒向小管中脱出所致。分析了39例急性感染后肾小球肾炎的肾活检标本,10例后来的材料,3例先兆子痫妇女的4例标本和21例对照标本,分析了肾小球的形态,并对免疫蛋白和单核细胞/巨噬细胞进行了免疫组织学检查。在14例急性感染后肾小球肾炎标本中发现了脱垂,其中8例与鲍曼氏囊的粘附和簇中的局部改变相关,一起构成了早期的尖端改变。另外三个只有早期的尖端改变,而另外八个则在簇簇和靠近管状开口的囊之间有较薄的粘附。后来的材料证实了这种发展的顺序,并显示出另一个较晚的变化,簇状和透明的材料出现在簇中,并在管状起源处粘附。先兆子痫的发现是可比的。急性感染后肾小球肾炎的肾小球明显大于对照组,子痫前期的肾小球比正常妊娠的大。免疫组织学研究显示,IgM和一些泡沫状单核细胞/巨噬细胞在早期尖端改变中没有,但在脱垂循环中没有。肾小球脱垂似乎是簇的急性扩大的暂时结果,可能对上皮细胞造成机械损伤,并且是肾小管起点附近永久性结构变化的先兆。这提供了一个统一的假设,以解释在急性感染后肾小球肾炎,先兆子痫以及许多其他人类和实验性肾脏疾病中如何观察到这些变化。版权所有2000 John Wiley&Sons,Ltd.

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