Advanced glycation in uraemic toxicity.
The Maillard reaction involves the non enzymatic combination of carbohydrates such as glucose with protein aminogroups to yield schiff bases and Amadori protein adducts evolving into irreversible advanced glycation end products (AGEs). This phenomenon, part of normal ageing, is accelerated in diabetes, as a result of hyperglycaemia, and in renal failure, as a consequence of the accumulation of reactive carbonyl compounds (RCOs). AGEs and RCOs are implicated in uraemic toxicity both at the biochemical and the clinical level (dialysis amyloidosis, atherosclerosis, alterations of peritoneal membrane permeability). Reduction of plasma AGEs and RCOs is an interesting avenue to reduce uraemic toxicity. Therapeutic strategies involve dialysis technique (haemodialysis membranes, daily haemodialysis, ultrapure dialysate, RCO free peritoneal dialysate) as well as drugs inhibiting AGE formation (aminoguanidine and the less toxic angiotensin converting enzyme inhibitors or angiotensin receptor blockers).
van Ypersele de Strihou
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University of Louvain Medical School, Cliniques Universitaires St. Luc, Brussels, Belgium.
D000368:Aged; D000375:Aging / Q000378:metabolism; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D003920:Diabetes Mellitus / Q000378:metabolism; D017127:Glycation End Products, Advanced / Q000037:antagonists & inhibitors / Q000097:blood; D006031:Glycosylation; D006146:Guanidines / Q000627:therapeutic use; D006801:Humans; D007676:Kidney Failure, Chronic / Q000378:metabolism* / Q000628:therapy; D015227:Lipid Peroxidation; D015416:Maillard Reaction; D006435:Renal Dialysis; D012545:Schiff Bases / Q000378:metabolism; D014511:Uremia / Q000378:metabolism* / Q000628:therapy
D000806:Angiotensin-Converting Enzyme Inhibitors; D017127:Glycation End Products, Advanced; D006146:Guanidines; D012545:Schiff Bases; C004479:pimagedine