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NDT Advance Access originally published online on November 21, 2008
Nephrology Dialysis Transplantation 2009 24(2):361-369; doi:10.1093/ndt/gfn583
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© The Author [2008]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org


Myogenic tone and small artery remodelling: insight into diabetic nephropathy

Kaivan Khavandi1, Adam S. Greenstein1,2, Kazuhiko Sonoyama1, Sarah Withers1, Anna Price1, Rayaz A. Malik1 and Anthony M. Heagerty1,2

1 Cardiovascular Research Group, Department of Medicine, University of Manchester 2 Wellcome Trust Clinical Research Facility, Manchester Royal Infirmary, Manchester, UK

Correspondence and offprint requests to: Prof. Anthony M. Heagerty, Cardiovascular Research Group, Department of Medicine, University of Manchester, Manchester, UK. Tel: +44-161-275-1199; Fax: +44-161-275-1183; E-mail: tony.heagerty@manchester.ac.uk

Keywords: diabetic nephropathy; hypertension; myogenic tone; target organ damage; small artery remodelling

The first 150 words of the full text of this article appear below.



   Introduction
 
Diabetic nephropathy is the single most frequent cause of end-stage renal disease (ESRD) in the western world, with an estimated cost in excess of $15.6 billion per annum in the United States alone [1]. In anticipation of an obesity-related diabetes epidemic, coupled with progressively growing rates of hypertension, these figures are forecast to rise exponentially. As both diabetes and renal disease are increasingly recognized as generalized vasculopathic states, there has been renewed interest in identifying potential vascular mechanisms influencing renal damage.

The relationship between diabetes, hypertension and kidney disease is complex, progressive and reciprocal. In type 1 diabetes, the prevalence of microalbuminuria increases from the onset of disease, reaching 50% after 20 years [2], whilst in type 2 diabetes, it is stable at 20–25% [3]. Microalbuminuria is a powerful marker for progression to overt nephropathy [4–6] and renal function continues to decline . . . [Full Text of this Article]

Renal haemodynamics: clinical correlates
Small artery structure and function: fundamental principles
Is myogenic tone responsible for autoregulation of RBF?
Mechanisms responsible for wall remodelling and myogenic tone
Therapeutic and clinical implications
Future directions for research

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