Pathogenesis of diabetic nephropathy.
- Author:
Jung Tak PARK
1
;
Shin Wook KANG
Author Information
1. Department of Internal Medicine, Yonsei University College of Medicine, Seoul, Korea.
- Publication Type:Review
- Keywords:
Diabetic nephropathy;
Advanced glycated end-products;
Renin-angiotensin system;
Reactive oxygen species
- MeSH:
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
- From:Korean Journal of Medicine
2009;77(6):670-677
- CountryRepublic of Korea
- Language:Korean
-
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.
