• 1 January 1980
    • journal article
    • research article
    • Vol. 98  (2) , 339-+
Abstract
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 mo. 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 .ANG. at birth and increased to 4800 .ANG. by 24 mo. of age. GBM thickening correlated very closely with age (correlation coefficient r = 0.90, P < 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. The lesion of spontaneous glomerular sclerosis of aging rats may result not from proteinuria but from the natural process of abiotrophic involution. This lesion is but a more obvious indicator of the alterations occurring simultaneously in other portions of the kidney.