Podocytopathy in diabetes: a metabolic and endocrine disorder

Am J Kidney Dis. 2011 Oct;58(4):637-46. doi: 10.1053/j.ajkd.2011.03.035. Epub 2011 Jun 29.


Diabetic nephropathy (DN) represents a major public health cost. Tight glycemic and blood pressure control can dramatically slow, but not stop, the progression of the disease, and a large number of patients progress toward end-stage renal disease despite currently available interventions. An early and key event in the development of DN is loss of podocyte function (or glomerular visceral epithelial cells) from the kidney glomerulus, where they contribute to the integrity of the glomerular filtration barrier. Recent evidence suggests that podocytes can be the direct target of circulating hormones, lipids, and adipokines that are affected in diabetes. We review the clinical and experimental evidence implicating novel endocrine and metabolic pathways in the pathogenesis of podocyte dysfunction and the development of DN.

Publication types

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

MeSH terms

  • Adipokines / physiology
  • Adult
  • Albuminuria / etiology
  • Albuminuria / physiopathology
  • Animals
  • Diabetes Mellitus, Type 2 / drug therapy
  • Diabetes Mellitus, Type 2 / metabolism
  • Diabetic Nephropathies / metabolism
  • Diabetic Nephropathies / pathology*
  • Diabetic Nephropathies / physiopathology
  • Diabetic Nephropathies / prevention & control
  • Hormones / physiology
  • Humans
  • Hypoglycemic Agents / therapeutic use
  • Kidney Glomerulus / physiopathology
  • Kidney Glomerulus / ultrastructure
  • Male
  • Mice
  • Models, Biological
  • Oxidative Stress
  • Podocytes / metabolism
  • Podocytes / pathology*
  • Renin-Angiotensin System / physiology
  • Vitamin D / physiology


  • Adipokines
  • Hormones
  • Hypoglycemic Agents
  • Vitamin D