title: Overproduction of reactive oxygen species in end-stage renal disease patients: a potential component of hemodialysis-associated inflammation.
abstract: During the past decade, hemodialysis (HD)-induced inflammation has been linked to the development of long-term morbidity in end-stage renal disease (ESRD) patients on regular renal replacement therapy. Because interleukins and anaphylatoxins produced during HD sessions are potent activators for nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, an example of an enzyme that is responsible for overproduction of reactive oxygen species (ROS), this may constitute a link between leukocyte activation and cell or organ toxicity. Oxidative stress, which results from an imbalance between oxidant production and antioxidant defense mechanisms, has been documented in ESRD patients using lipid and/or protein oxidative markers. Characterization of HD-induced oxidative stress has included identification of potential activators for NADPH oxidase. Uremia per se could prime phagocyte oxidative burst. HD, far from improving the oxidative status, results in an enhancement of ROS owing to hemoincompatibility of the dialysis system, hemoreactivity of the membrane, and trace amounts of endotoxins in the dialysate. In addition, the HD process is associated with an impairment in antioxidant mechanisms. The resulting oxidative stress has been implicated in long-term complications including anemia, amyloidosis, accelerated atherosclerosis, and malnutrition. Prevention of oxidative stress in HD might focus on improving the hemocompatibility of the dialysis system, supplementation of deficient patients with antioxidants, and modulation of NADPH oxidase by pharmacologic approaches.
authors.affiliation: Biochemistry Laboratory, Lapeyronie University Hospital, 371 Avenue Doyen Gaston Giraud, 34295 Montpellier, France.
authors.forename: Marion
authors.initials: M
authors.lastname: Morena
authors.forename: Sandrine
authors.initials: S
authors.lastname: Delbosc
authors.forename: Anne-Marie
authors.initials: AM
authors.lastname: Dupuy
authors.forename: Bernard
authors.initials: B
authors.lastname: Canaud
authors.forename: Jean-Paul
authors.initials: JP
authors.lastname: Cristol
mesh_terms: D000706:Anaphylatoxins / Q000096:biosynthesis; D015415:Biomarkers / Q000378:metabolism; D016207:Cytokines / Q000096:biosynthesis; D004789:Enzyme Activation; D006801:Humans; D007249:Inflammation / Q000150:complications / Q000209:etiology / Q000378:metabolism; D007676:Kidney Failure, Chronic / Q000150:complications* / Q000503:physiopathology / Q000628:therapy; D007962:Leukocytes / Q000378:metabolism; D015227:Lipid Peroxidation; D019255:NADPH Oxidases / Q000378:metabolism; D010084:Oxidation-Reduction; D018384:Oxidative Stress; D017382:Reactive Oxygen Species / Q000378:metabolism*; D006435:Renal Dialysis / Q000009:adverse effects*
chemical_list: D000706:Anaphylatoxins; D015415:Biomarkers; D016207:Cytokines; D017382:Reactive Oxygen Species; D019255:NADPH Oxidases