Skip to main content
Log in

Regulation of podocyte structure during the development of nephrotic syndrome

  • REVIEW
  • Published:
Journal of Molecular Medicine Aims and scope Submit manuscript

Abstract

 Nephrotic syndrome is a common kidney disease seen in both children and adults. The clinical syndrome includes massive proteinuria, hypoalbuminemia, edema, and usually hypercholesterolemia. Development of these clinical changes is closely correlated with profound structural changes in glomerular epithelial cells, or podocytes, which together with the glomerular basement membrane and endothelium comprise the kidney’s blood filtration barrier. Although relatively little is known about the cellular or molecular changes which occur within podocytes during the development of nephrotic syndrome, cytoskeletal proteins very likely play a central role in these changes since they are primarily responsible for the maintenance of cell structure in almost all cells. This review focuses on: (a) the structure and function of podocytes in both the normal state and during nephrotic syndrome and (b) the potential roles of several cytoskeleton-associated proteins identified in podocytes in the development of and/or recovery from the pathophysiological cytoskeletal changes which occur in podocytes during nephrotic syndrome.

This is a preview of subscription content, log in via an institution to check access.

Access this article

Price excludes VAT (USA)
Tax calculation will be finalised during checkout.

Instant access to the full article PDF.

Similar content being viewed by others

Author information

Authors and Affiliations

Authors

Additional information

Received: 18 April 1997 / Accepted: 18 July 1997

Rights and permissions

Reprints and permissions

About this article

Cite this article

Smoyer, W., Mundel, P. Regulation of podocyte structure during the development of nephrotic syndrome. J Mol Med 76, 172–183 (1998). https://doi.org/10.1007/s001090050206

Download citation

  • Issue Date:

  • DOI: https://doi.org/10.1007/s001090050206

Navigation