Horm Metab Res 2005; 37: 9-16
DOI: 10.1055/s-2005-861397
Review
© Georg Thieme Verlag KG Stuttgart · New York

The Podocyte: A Major Player in the Development of Diabetic Nephropathy?

S.  M.  Marshall1
  • 1Diabetes Research Group, University of Newcastle upon Tyne
Further Information

Publication History

Received 13 December 2004

Accepted after Revision 13 January 2005

Publication Date:
25 May 2005 (online)

Abstract

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.

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Prof. Sally M. Marshall

Diabetes Research Group · School of Clinical Medical Sciences · 4th Floor · Leech Building

The Medical School · Framlington Place · Newcastle upon Tyne · NE2 4HH · UK ·

Phone: + 44(191)2227019

Fax: + 44(191)2220723

Email: s.m.marshall@ncl.ac.uk

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