title: Study of oxidative stress in patients with advanced renal disease and undergoing either hemodialysis or peritoneal dialysis.
abstract: Oxidative stress (OS) is directly involved in the formation of atheroma plaque and has been shown to be present since the early stages of Chronic Kidney Disease (CKD); however, the net role that dialytica techniques may play in OS process is yet to be determined. We studied three groups: hemodialysis (HD, n = 30), peritoneal dialysis (PD, n = 31), predialysis (pre-D, n = 32), and one control group (C, n = 67). Using highresolution liquid chromatography columns (HPLC), the superoxide dismutase (SOD), glutathione oxidized/reduced ratio (GSSG/GSH), and nuclear, as well as mitochondrial 8-oxo-dG (8-oxo-dG mit) were measured in lymphocytes. Protein carbonyls and F2-isoprostanes were measured in plasma. The antioxidant enzyme activity was evaluated by a spectrophotometric assay of catalase, glutathione peroxidase (GPX), glutathione reductase (GSR), and superoxide dismutase (SOD). Compared to the control group, all groups had significantly higher levels of products derived from molecular oxidation with a significant decrease in antioxidant enzymes. Patients in the pre-D group showed higher values for most of the oxidized molecules. The PD group showed a better oxidative balance, with no significant differences in levels of mitochondrial 8-oxo-dG when compared to the control group. We speculated that the better control of OS observed in patients receiving PD might be explained by the fact that this technique is more biocompatible, and this might help reduce the risk of cardiovascular events.
authors.forename: Maria J
authors.initials: MJ
authors.lastname: Puchades
authors.forename: Guillermo
authors.initials: G
authors.lastname: Saez
authors.forename: M Carmen
authors.initials: MC
authors.lastname: Muñoz
authors.forename: Miguel
authors.initials: M
authors.lastname: Gonzalez
authors.forename: Isidro
authors.initials: I
authors.lastname: Torregrosa
authors.forename: Isabel
authors.initials: I
authors.lastname: Juan
authors.forename: Alfonso
authors.initials: A
authors.lastname: Miguel
mesh_terms: D000080242:8-Hydroxy-2'-Deoxyguanosine; D000328:Adult; D000368:Aged; D015415:Biomarkers / Q000097:blood; D016022:Case-Control Studies; D002374:Catalase / Q000097:blood; D016009:Chi-Square Distribution; D002851:Chromatography, High Pressure Liquid; D003430:Cross-Sectional Studies; D004249:DNA Damage; D003849:Deoxyguanosine / Q000031:analogs & derivatives / Q000097:blood; D028441:F2-Isoprostanes / Q000097:blood; D005260:Female; D005978:Glutathione / Q000097:blood; D005979:Glutathione Peroxidase / Q000097:blood; D005980:Glutathione Reductase / Q000097:blood; D006801:Humans; D007674:Kidney Diseases / Q000097:blood / Q000628:therapy*; D016014:Linear Models; D015227:Lipid Peroxidation; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D018384:Oxidative Stress; D010530:Peritoneal Dialysis; D050050:Protein Carbonylation; D006435:Renal Dialysis; D013482:Superoxide Dismutase / Q000097:blood; D016896:Treatment Outcome; D015854:Up-Regulation
chemical_list: D015415:Biomarkers; D028441:F2-Isoprostanes; D000080242:8-Hydroxy-2'-Deoxyguanosine; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D005980:Glutathione Reductase; D003849:Deoxyguanosine; D005978:Glutathione