Extract

Introduction

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 limited to chronic renal failure [ 6–8 ]. Generally, AGE residues on plasma proteins are not decreased during a dialysis session, while AGE-free adducts are indeed removed by haemodiafiltration or other dialysis procedures [ 7 ]. Little is known about tissue accumulation of AGEs on long-lived proteins in patients with chronic renal failure and patients on haemodialysis.

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