Résumé
Oxidative stress, which results from an imbalance between reactive oxygen species (ROS) production and antioxidant defense mechanisms, is now a well recognized pathogenic process in hemodialysis (HD) patients that could be involved in dialysis-related pathologies such as accelerated atherosclerosis, amyloidosis and anemia. This review is aimed at evaluating the rationale for preventive intervention against oxidative damage during HD as well as the putative causal factors implicated in this imbalance. The antioxidant system is severely impaired in uremic patients and impairment increases with the degree of renal failure. HD further worsens this condition mainly by losses of hydrophilic unbound small molecular weight substances such as vitamin C, trace elements and enzyme regulatory compounds. Moreover, inflammatory state due to the hemo-incompatibility of the dialysis system plays a critical role in the production of oxidants contributing further to aggravate the pro-oxidant status of uremic patients. Prevention of ROS overproduction can be achieved by improvement of dialysis biocompatibility, a main component of adequate dialysis, and further complimented by antioxidant supplementation. This could be achieved either orally or via the extracorporeal circuit. Antioxidants such as vitamin E could be bound on dialyzer membranes. Alternatively, hemolipodialysis consisting of loading HD patients with vitamin C or E via an ancillary circuit made of vitamin E-rich liposomes may be used.Oxidative stress, which results from an imbalance between reactive oxygen species (ROS) production and antioxidant defense mechanisms, is now a well recognized pathogenic process in hemodialysis (HD) patients that could be involved in dialysis-related pathologies such as accelerated atherosclerosis, amyloidosis and anemia. This review is aimed at evaluating the rationale for preventive intervention against oxidative damage during HD as well as the putative causal factors implicated in this imbalance. The antioxidant system is severely impaired in uremic patients and impairment increases with the degree of renal failure. HD further worsens this condition mainly by losses of hydrophilic unbound small molecular weight substances such as vitamin C, trace elements and enzyme regulatory compounds. Moreover, inflammatory state due to the hemo-incompatibility of the dialysis system plays a critical role in the production of oxidants contributing further to aggravate the pro-oxidant status of uremic patients. Prevention of ROS overproduction can be achieved by improvement of dialysis biocompatibility, a main component of adequate dialysis, and further complimented by antioxidant supplementation. This could be achieved either orally or via the extracorporeal circuit. Antioxidants such as vitamin E could be bound on dialyzer membranes. Alternatively, hemolipodialysis consisting of loading HD patients with vitamin C or E via an ancillary circuit made of vitamin E-rich liposomes may be used.