NDT Advance Access originally published online on November 25, 2008
Nephrology Dialysis Transplantation 2009 24(3):710-713; doi:10.1093/ndt/gfn634
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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
AGEs, autofluorescence and renal function
1 Diabetes Center, Isala Clinics, Zwolle 2 Department of Medicine, University Medical Center Groningen, University of Groningen, the Netherlands
Correspondence and offprint requests to: Esther G. Gerrits, Isala Clinics, PO Box 10400, 8000 GK Zwolle, The Netherlands. Tel: +31384242518; E-mail: e.g.gerrits@isala.nl
Keywords: fluorescence; glycation end products; renal function
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| Introduction |
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Accelerated formation and accumulation of AGEs occur under circumstances of hyperglycaemic or oxidative stress in age-related and chronic diseases like diabetes mellitus, chronic renal failure, neurodegenerative diseases, osteoarthritis and non-diabetic atherosclerosis [1–5]. Accumulation of irreversibly formed and chemically stable AGEs occurs on long-lived proteins such as collagen in the skin, but also in vascular basement membranes. This affects their structure and function resulting in vascular damage. Adequate renal clearance capacity is an important factor in the effective removal of AGEs. In renal failure, there is a profound decrease in clearance of AGE free adducts, which are formed mainly from proteolysis of glycated proteins. Plasma levels of these products are up to 40-fold higher in haemodialysis patients compared to healthy subjects. Increased levels of AGE-free adducts in plasma is also a characteristic of acute and chronic renal failure, whereas accumulation of AGE residues on plasma proteins appears to be
The autofluorescence reader
Clinical evidence
AGEs and renal disease
Skin AF and renal function in a screening setting: are skin AF levels directly related to the degree of renal failure?
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