Podocytopathy in diabetes: A metabolic and endocrine disorder Article

Diez-Sampedro, A, Lenz, O, Fornoni, A. (2011). Podocytopathy in diabetes: A metabolic and endocrine disorder . AMERICAN JOURNAL OF KIDNEY DISEASES, 58(4), 637-646. 10.1053/j.ajkd.2011.03.035

cited authors

  • Diez-Sampedro, A; Lenz, O; Fornoni, A


  • 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. © 2011 National Kidney Foundation, Inc.

publication date

  • October 1, 2011

published in

Digital Object Identifier (DOI)

start page

  • 637

end page

  • 646


  • 58


  • 4