A glimpse of various pathogenetic mechanisms of diabetic nephropathy

Yashpal S. Kanwar, Lin Sun, Ping Xie, Fu You Liu, Sheldon Chen

Research output: Contribution to journalArticlepeer-review

577 Scopus citations


Diabetic nephropathy is a well-known complication of diabetes and is a leading cause of chronic renal failure in the Western world. It is characterized by the accumulation of extracellular matrix in the glomerular and tubulointerstitial compartments and by the thickening and hyalinization of intrarenal vasculature. The various cellular events and signaling pathways activated during diabetic nephropathy may be similar in different cell types. Such cellular events include excessive channeling of glucose intermediaries into various metabolic pathways with generation of advanced glycation products, activation of protein kinase C, increased expression of transforming growth factor β? and GTP-binding proteins, and generation of reactive oxygen species. In addition to these metabolic and biochemical derangements, changes in the intraglomerular hemodynamics, modulated in part by local activation of the renin-angiotensin system, compound the hyperglycemia-induced injury. Events involving various intersecting pathways occur in most cell types of the kidney.

Original languageEnglish (US)
Pages (from-to)395-423
Number of pages29
JournalAnnual Review of Pathology: Mechanisms of Disease
StatePublished - Feb 28 2011


  • GTP-binding proteins
  • advanced glycation products
  • hyperglycemia
  • hypertension
  • protein kinase C
  • reactive oxygen species
  • tubulointerstitial fibrosis

ASJC Scopus subject areas

  • Pathology and Forensic Medicine


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