The renal vascular response to diabetes

Curr Opin Nephrol Hypertens. 2010 Jan;19(1):85-90. doi: 10.1097/MNH.0b013e32833240fc.


Purpose of review: Diabetes mellitus is the primary cause of end-stage renal disease, yet the mechanisms underlying diabetic nephropathy remain ill-defined. The widely accepted opinion holds that events occurring early during the course of diabetes engender the eventual decline in renal function. This review will summarize recent advances (published January 2008 through June 2009) regarding the renal vascular and glomerular functional changes that occur during the early stage of diabetes.

Recent findings: Reduced C-peptide levels and increased cyclooxygenase-2 activity both seem to promote diabetic hyperfiltration, presumably via effects on afferent arteriolar tone. In addition, exaggerated tonic influences of K+ channels on afferent arteriolar function likely act in concert with impaired Ca2+ influx responses to changes in membrane potential to promote vasodilation. Mechanisms underlying these changes remain largely speculative. Diabetes may also alter autoregulation of renal blood flow and glomerular filtration rate, as well as provoke afferent arteriolar dilation secondary to alterations in proximal tubular reabsorption; however, conflicting evidence continues to flood the literature concerning these events.

Summary: New evidence has expanded our appreciation of the complexity of events that promote preglomerular vasodilation during the early stage of diabetes; however, it seems that the more we know, the less we understand.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Diabetes Mellitus / physiopathology*
  • Diabetic Nephropathies / etiology
  • Diabetic Nephropathies / physiopathology
  • Glomerular Filtration Rate
  • Homeostasis
  • Humans
  • Ion Channels / metabolism
  • Kidney / blood supply*
  • Kidney / physiopathology
  • Microcirculation / physiology
  • Models, Biological
  • Receptors, Purinergic P1 / metabolism
  • Renal Circulation
  • Vasodilation


  • Ion Channels
  • Receptors, Purinergic P1