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The podocyte: A major player in the development of diabetic nephropathy?

Lookup NU author(s): Emerita Professor Sally Marshall


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Although abnormalities in the glomerular epithelial cell, the podocyte, have been appreciated for some time, it is only recently that their significance and the underlying mechanisms for the changes have begun to be explored. There is a decrease in podocyte number early in diabetes, with further decreases as albuminuria increases. The number of podocytes is inversely related to the degree of albuminuria in both cross-sectional and longitudinal studies. Foot process width is increased in proteinuria, the width correlating with albuminuria. Loss of nephrin - both mRNA and protein - occurs some time after the onset of diabetes and is also inversely related to proteinuria. The amount of the α3β1 integrin on the basement-membrane surface of the foot process of the podocyte is also reduced in diabetes. Loss of nephrin and α3β1 integrin is induced by both hyperglycaemia and mechanical stretch. Agents that inhibit the renin-angiotensin system, but not other agents that reduce proteinuria, restore nephrin expression and prevent the structural changes seen in the podocyte in diabetes. Thus, changes in the podocyte contribute to the proteinuria of diabetic nephropathy and can be ameliorated by inhibition of the renin-angiotensin system. © Georg Thieme Verlag KG Stuttgart.

Publication metadata

Author(s): Marshall SM

Publication type: Conference Proceedings (inc. Abstract)

Publication status: Published

Conference Name: Hormone and Metabolic Research

Year of Conference: 2005

Pages: S9-S16

ISSN: 0018-5043

Publisher: Hormone and Metabolic Research, Georg Thieme Verlag


DOI: 10.1055/s-2005-861397

PubMed id: 15918105

Library holdings: Search Newcastle University Library for this item

ISBN: 14394286