title: Oxidative stress in patients with end-stage renal disease prior to the start of renal replacement therapy.
abstract: OBJECTIVE
  In patients with end-stage renal disease (ESRD), cardiovascular complications are the main cause of death. Increased oxidative stress is one of the risk factors for enhanced atherosclerosis in this population. Literature data vary partially dependent on differences in methodology. The present study compares three different methods: plasma lipid peroxides, the newly developed measurement of circulating oxidized LDL (Ox-LDL) particles and the frequently used copper-induced LDL oxidation lag time.
  
  
  METHODS
  We assessed plasma lipid peroxides, circulating Ox-LDL and in vitro copper-induced LDL oxidation lag time in 47 non-diabetic patients with ESRD, at the start of renal replacement therapy, and compared these with 41 age- and sex-matched controls.
  
  
  RESULTS
  In ESRD, total cholesterol (4.6 +/- 1.1 vs. 5.6 +/- 0.9 mmol/l; p < 0.001), LDL cholesterol (2.8 +/- 0.8 vs. 3.5 +/- 0.7 mmol/l; p < 0.001) and HDL cholesterol (1.0 +/- 0.3 vs. 1.4 +/- 0.4 mmol/l; p < 0.001) were lower compared to controls. Plasma lipid peroxides were higher (1.1 +/- 0.5 vs. 0.8 +/- 0.5 micromol/l; p = 0.003) in ESRD. No differences were observed in plasma Ox-LDL (63.1 +/- 62.0 vs. 55.3 +/- 48.0 mg/l). However, due to the lower plasma LDL cholesterol in ESRD, LDL oxidation level was increased in ESRD (7.1 +/- 0.1 vs. 4.2 +/- 0.3%; p = 0.03). LDL lag time was slightly longer (89 +/- 11 vs. 84 +/- 11 min; p = 0.04) in ESRD. There were no significant differences regarding the amount and rate of dienes produced.
  
  
  CONCLUSIONS
  Elevated levels of lipid peroxides and higher LDL oxidation levels support the theory that ESRD is associated with increased oxidative stress, which may explain the accelerated atherosclerosis. The measured amount of oxidative stress is not reflected by in vitro oxidizability of LDL.
authors.affiliation: Department of Internal Medicine, University Medical Center Nijmegen, Nijmegen, The Netherlands. S.Diepeveen@nier.umcn.nl
authors.forename: Sabine H A
authors.initials: SH
authors.lastname: Diepeveen
authors.forename: Gertie H W E
authors.initials: GH
authors.lastname: Verhoeven
authors.forename: Job
authors.initials: J
authors.lastname: van der Palen
authors.forename: Bert L D
authors.initials: BL
authors.lastname: Dikkeschei
authors.forename: Lambertus J
authors.initials: LJ
authors.lastname: van Tits
authors.forename: Geert
authors.initials: G
authors.lastname: Kolsters
authors.forename: Joop J G
authors.initials: JJ
authors.lastname: Offerman
authors.forename: Henk J G
authors.initials: HJ
authors.lastname: Bilo
authors.forename: Anton F H
authors.initials: AF
authors.lastname: Stalenhoef
mesh_terms: D015415:Biomarkers / Q000032:analysis; D002318:Cardiovascular Diseases / Q000209:etiology; D008078:Cholesterol, LDL / Q000378:metabolism; D005260:Female; D006801:Humans; D007676:Kidney Failure, Chronic / Q000150:complications / Q000378:metabolism* / Q000628:therapy*; D015227:Lipid Peroxidation; D008297:Male; D008875:Middle Aged; D018384:Oxidative Stress; D017582:Renal Replacement Therapy; D014810:Vitamin E / Q000097:blood
chemical_list: D015415:Biomarkers; D008078:Cholesterol, LDL; D014810:Vitamin E