Podocytopathy in diabetes: A metabolic and endocrine disorder

Ana Diez-Sampedro, Oliver Lenz, Alessia Fornoni

Research output: Contribution to journalArticle

59 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)637-646
Number of pages10
JournalAmerican Journal of Kidney Diseases
Volume58
Issue number4
DOIs
StatePublished - Oct 1 2011

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Keywords

  • Diabetic nephropathy
  • hormones
  • podocytes
  • proteinuria

ASJC Scopus subject areas

  • Nephrology

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