Korean J Med.  2009 Dec;77(6):670-677.

Pathogenesis of diabetic nephropathy

Affiliations
  • 1Department of Internal Medicine, Yonsei University College of Medicine, Seoul, Korea.

Abstract

Diabetic nephropathy, the leading cause of end stage renal disease in many countries, is pathologically characterized by glomerular and tubular hypertrophy, extracellular matrix accumulation, inflammatory cell infiltration, and podocytopenia associated with foot process effacement, which eventually results in glomerulosclerosis and tubular atrophy. The pathogenesis of diabetic nephropathy comprises both metabolic and hemodynamic factors related to diabetes. Hemodynamic factors include intraglomerular hypertension which is associated with the activation of both systemic and local renin-angiotensin system. Hyperglycemia per se, advanced glycation end-products and glucose-dependent aldose reductase pathways, as metabolic factors, is also known to contribute to the development and progression of diabetic nephropathy. All of these factors induce various cytokines and activate intracellular signal transduction pathways such as protein kinase C and mitogen-activated protein kinase, ultimately leading to diabetic nephropathy.

Keyword

Diabetic nephropathy; Advanced glycated end-products; Renin-angiotensin system; Reactive oxygen species

MeSH Terms

Aldehyde Reductase
Atrophy
Cytokines
Diabetic Nephropathies
Extracellular Matrix
Foot
Hemodynamics
Hyperglycemia
Hypertension
Hypertrophy
Kidney Failure, Chronic
Protein Kinase C
Protein Kinases
Reactive Oxygen Species
Renin-Angiotensin System
Signal Transduction
Aldehyde Reductase
Cytokines
Protein Kinase C
Protein Kinases
Reactive Oxygen Species
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