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NDT Advance Access originally published online on November 18, 2006
Nephrology Dialysis Transplantation 2007 22(2):318-321; doi:10.1093/ndt/gfl655
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© The Author [2006]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

The link between mechanical stretch and glucose metabolism—a conceptual advance in understanding diabetic (and non diabetic?) renal disease

Luigi Gnudi and Giancarlo Viberti

Cardiovascular Division, King's College London School of Medicine, Guy's Hospital, London, UK

Correspondence and offprint requests to: Luigi Gnudi, MD, PhD, FRCP, FASN, Department of Diabetes, Endocrinology and Internal Medicine, 5th floor, Thomas Guy House, Guy's Hospital, St Thomas Street, London SE1 9RT, UK. Email: luigi.gnudi@kcl.ac.uk

Keywords: diabetes; facilitative glucose transporter-1; hypertension; TGF-ß1

The first 10% of the full text of this article appears below.



   Diabetic nephropathy—a tale of two hits?
 
Diabetic kidney disease is today the most common cause of end-stage renal failure in many countries of the world and the number of diabetic patients in need of renal replacement therapy has increased over the last two decades [1].

Haemodynamic forces are major contributors to the development of renal damage in diabetes [2] and in other chronic glomerulopathies characterized by increased intraglomerular capillary pressure [3]. In most renal diseases, the increased glomerular pressure affects surviving glomeruli following an initial disease-induced nephron loss.

In diabetes, intraglomerular hypertension occurs early as a result of hyperglycaemia-induced disruption of glomerular capillary autoregulatory mechanisms [4]. Under physiological euglycaemic conditions the pressure within the glomerular circulation is maintained stable by vasoregulatory mechanisms at the afferent and efferent . . . [Full Text of this Article]



   The facilitative glucose transporter GLUT-1—a link between haemodynamic and metabolic perturbations in glomerular injury
 

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