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The causes of long-term complications of uraemia are yet to be fully elucidated. It has recently been demonstrated that renal failure is associated with a dramatic elevation of advanced glycation end products (AGEs). These products are the result of the non-enzymatic Maillard reaction linking a protein amino group with a glucose-derived aldehyde group. A mild rise of AGEs is associated with normal ageing. Proteins with a slow turnover such as matrix proteins are thus modified and removed by an AGE-specific receptor-mediated process thought to be a part of normal tissue remodelling. A more striking rise of AGEs is observed in diabetic patients as a result of sustained hyperglycaemia. A greater variety of proteins is thus modified leading to tissue damage through alteration of tissue protein structure and function, stimulation of several cellular responses, or generation of reactive oxygen species. In uraemia, the rise of AGEs is even more marked than in diabetics and is associated with a variety of tissue disorders including vascular damage, dyslipidaemia, and beta 2-microglobulin amyloidosis. AGE accumulation in uraemia does not result from hyperglycaemia. Identification of its cause as well as of the involved precursors should contribute to the understanding of uraemic toxicity and open new therapeutic approaches. In this presentation, we propose the hypothesis that AGE generation is enhanced by an increased oxidative stress associated with uraemia. Under these conditions, a variety of compounds, both related and unrelated to glucose, may contribute to the advanced glycoxidation of proteins. In uraemia, AGEs could be taken as a marker of oxidative stress damage to proteins.

Hypothesis. Oxidation conspires with glycation to generate noxious advanced glycation end products in renal failure