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(Hypertension. 2006;48:519.)
© 2006 American Heart Association, Inc.

Brief Reviews

Mechanisms of Diabetic Nephropathy

Role of Hypertension

From the Danielle Alberti Memorial Center for Diabetic Complications, Diabetes and Metabolism Division, Baker Heart Research Institute, Melbourne, Australia.

Correspondence to Mark Cooper, Baker Medical Research Institute, 75 Commercial Rd, Prahran VIC 3181, Melbourne, Australia. E-mail mark.cooper@baker.edu.au

An extract of the first 250 words of the full text is provided, because this article has no abstract.

	Introduction

 
Diabetic nephropathy is a major microvascular complication of diabetes, representing the leading cause of end-stage renal disease in the Western world, and a major cause of morbidity and mortality in both type 1 and type 2 diabetic subjects. Clinical hallmarks of diabetic nephropathy include a progressive increase in urinary albumin excretion and a decline in glomerular filtration rate (GFR), which occur in association with an increase in blood pressure, ultimately leading to end-stage renal failure.¹ These renal functional changes develop as a consequence of structural abnormalities, including glomerular basement membrane thickening, mesangial expansion with extracellular matrix accumulation, changes in glomerular epithelial cells (podocytes), including a decrease in number and/or density, podocyte foot process broadening and effacement, glomerulosclerosis, and tubulointerstitial fibrosis.

Diabetic nephropathy occurs only in a minority of subjects with either type 1 or type 2 diabetes and seems to result from the interaction between genetic susceptibility and environmental insults, primarily metabolic and hemodynamic in origin. Over the last decade, the cellular and molecular mechanisms by which these insults translate to structural and functional abnormalities leading to diabetic nephropathy have been increasingly delineated. In particular, it has been determined that both metabolic and hemodynamic stimuli lead to the activation of key intracellular signaling pathways and transcription factors, thus triggering the production/release of cytokines, chemokines, and growth factors, which mediate and/or amplify renal damage.

In the present review, we summarize molecular and cellular mechanisms that seem to be responsible for hypertension-induced renal injury in diabetes, with particular focus on the role . . . [Full Text of this Article]

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