RESUMO
Advanced glycation end-products (AGEs) are found in excess during diabetes mellitus, uremia and aging. Non enzymatique glycation, glycoxidation with glucose auto-oxidation and the polyol pathway are involved in the production of AGEs. Tissue accumulation of AGEs and their binding to cell receptors are critical steps in the deleterious consequences of AGE excess. AGE-receptor interaction altered endothelial cells, macrophages, mesangial and mesothelial cell functions. AGEs appear to be involved in the genesis of diabetic micro but also macro-angiopathy. Reduction of AGE clearance and permanent oxidative stress are responsible for AGE excess during uremia. High-flux hemodialysis and peritoneal dialysis reduce AGE level but kidney transplantation is the best treatment to restore homeostasis. New drugs are tested to reduce AGEs or AGE deleterious effects but the best treatment remains the prevention of AGE formation by a strict glycemic control.
