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Author(s): Akash Jain 1*, Sunil Sharma 2, Ashok Kumar

Journal: International Journal of Drug Formulation and Research
ISSN 2229-5054

Volume: 1;
Issue: 1;
Start page: 144;
Date: 2010;
Original page

Keywords: Nephropathy | Diabetes | Angiotensin

Diabetic nephropathy is a leading cause of chronic kidney disease and end stage renal disease and accountsfor significant morbidity and mortality in diabetic patients. Hyperglycemia may lead to end stage renal damagethrough both metabolic and non metabolic pathways. The non-enzymatic glycation of proteins with irreversibleformation and deposition of reactive advanced glycation end products (AGE) have been noted to play a major role inthe pathogenesis of diabetic nephropathy. Further, diabetic nephropathy is associated with hyperactivity of sorbitolaldosereductase pathway, hyperactivity of hexosamine biosynthetic pathway, activation of protein kinase C andMAPK and overexpression of growth factors and cytokines i.e. transforming growth factor-β, vascular endothelialgrowth factor, platelet-derived growth factor and insulin-like growth factor. Moreover, high glucose concentration indiabetes has been noted to induce oxidative and nitrosative stress, activate intracellular RAAS and releaseendothelin-1 and prostaglandins to deteriorate the function of kidney. In addition, up-regulation of transforminggrowth factor-β (TGF-β) and consequent overproduction of extracellular matrix molecules have been implicated inthe progression of diabetic nephropathy. The present review study the various cellular mechanisms involved indiabetic nephropathy.

Tango Jona
Tangokurs Rapperswil-Jona

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