首页> 美国卫生研究院文献>Journal of the Boston Society of Medical Sciences >Spontaneous glomerular sclerosis in aging Sprague-Dawley rats. II. Ultrastructural studies.
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Spontaneous glomerular sclerosis in aging Sprague-Dawley rats. II. Ultrastructural studies.

机译:Sprague-Dawley衰老大鼠的自发性肾小球硬化症。二。超微结构研究。

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摘要

Increased protein filtration and work overload have been proposed to account for the development of glomerular sclerosis in old rats. Sprague-Dawley rat kidneys were examined ultrastructurally from birth through 24 months of age to further delineate pathogenetic factors. There was progressive thickening of all basement membranes with lamination, intramembranous pseudolinear deposits, and degeneration. The glomerular basement membrane (GBM) was 1300 A at birth and increased to 4800 A by 24 months of age. GBM thickening correlated very closely with age (r = 0.90, P less than 0.001), correlated roughly with mesangial sclerosis, but did not correlate at all with proteinuria. Obliteration of podocytes and degenerative changes in the cytoplasm occurred in all cell types and was present in both proteinuric and nonproteinuric rats. These findings suggest that the lesion of spontaneous glomerular sclerosis of aging rats results not from proteinuria but from the natural process of abiotrophic involution. Further, this lesion is but a more obvious indicator of the alterations occurring simultaneously in other portions of the kidney.
机译:已经提出增加蛋白质过滤和工作负荷以解释老年大鼠肾小球硬化的发展。从出生到24个月大,对Sprague-Dawley大鼠肾脏进行超微结构检查,以进一步描述病因。层状,膜内假线性沉积和变性使所有基底膜逐渐增厚。肾小球基底膜(GBM)出生时为1300 A,到24个月大时增加到4800A。 GBM增厚与年龄密切相关(r = 0.90,P小于0.001),与肾小球膜硬化大致相关,但与蛋白尿完全不相关。在所有细胞类型中均发生足细胞闭塞和细胞质退行性变化,并且在蛋白尿和非蛋白尿大鼠中均存在。这些发现表明,衰老大鼠的自发性肾小球硬化病变不是由蛋白尿引起的,而是由生物营养退化的自然过程引起的。此外,该病变只是肾脏其他部分同时发生变化的更明显的指示。

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