help button home button Am J Pathol International Conference on Pathology of Chest Diseases
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS

This Article
Right arrow Order Full text via Infotrieve
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Bolton, W. K.
Right arrow Articles by Sturgill, B. C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Bolton, W. K.
Right arrow Articles by Sturgill, B. C.

American Journal of Pathology, Vol 98, 339-356, Copyright © 1980 by American Society for Investigative Pathology


REGULAR ARTICLES

Spontaneous glomerular sclerosis in aging Sprague-Dawley rats. II. Ultrastructural studies

WK Bolton and BC Sturgill

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.


This article has been cited by other articles:


Home page
J. Histochem. Cytochem.Home page
P. Verbeke, M. Perichon, C. Borot-Laloi, J. Schaeverbeke, and H. Bakala
Accumulation of Advanced Glycation Endproducts in the Rat Nephron: Link with Circulating AGEs During Aging
J. Histochem. Cytochem., August 1, 1997; 45(8): 1059 - 1068.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1980 by the American Society for Investigative Pathology.