Bolton W K, Sturgill B C
Am J Pathol. 1980 Feb;98(2):339-56.
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.
蛋白质滤过增加和工作负荷过重被认为是老年大鼠肾小球硬化发展的原因。对出生至24月龄的Sprague-Dawley大鼠肾脏进行超微结构检查，以进一步明确致病因素。所有基底膜均有进行性增厚，伴有分层、膜内假线性沉积物和变性。肾小球基底膜（GBM）在出生时为1300埃，到24月龄时增加到4800埃。GBM增厚与年龄密切相关（r = 0.90，P < 0.001），与系膜硬化大致相关，但与蛋白尿完全无关。所有细胞类型均出现足细胞消失和细胞质变性改变，蛋白尿大鼠和非蛋白尿大鼠均有此现象。这些发现表明，老年大鼠自发性肾小球硬化病变并非由蛋白尿引起，而是由营养障碍性退化的自然过程所致。此外，这种病变只是肾脏其他部分同时发生改变的一个更明显指标。
