The renal hemodynamic basis of diabetic nephropathy

Semin Nephrol. 1997 Mar;17(2):93-100.

Abstract

Diabetic nephropathy occurs in approximately one third of individuals with insulin-dependent diabetes mellitus (IDDM), recent studies suggest that a similar proportion of non-insulin-dependent diabetes mellitus (NIDDM) patients develop this serious complication as well. Of the many risk factors identified in the pathogenesis of nephropathy, hemodynamic alterations have been particularly well studied. Increases in glomerular filtration rate (GFR), largely driven by increases in plasma flow and glomerular capillary pressure, are apparent in early IDDM and NIDDM. Furthermore, the elevation in capillary pressure may be damaging to glomerular endothelial, epithelial and mesangial cells, thereby initiating and contributing to the progression of diabetic nephropathy. Numerous mediators of diabetic hyperfiltration have been proposed, and this phenomenon likely reflects a mutilfactorial etiology. The purpose of this article is to examine the hemodynamic alterations characteristic of diabetic nephropathy, their etiology, and their role in the development and progression of diabetic nephropathy.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • Animals
  • Diabetic Nephropathies / etiology
  • Diabetic Nephropathies / pathology
  • Diabetic Nephropathies / physiopathology*
  • Disease Progression
  • Glomerular Filtration Rate
  • Glomerular Mesangium / pathology
  • Glomerular Mesangium / physiopathology
  • Humans
  • Renal Circulation / physiology*