title: Oxidant stress in nephrotic syndrome: comparison of F(2)-isoprostanes and plasma antioxidant potential.
abstract: BACKGROUND
  The nephrotic syndrome (NS) is associated with an increased risk of coronary heart disease. Increased oxidant stress may contribute to this by means of hyperlipidaemia and/or hypoalbuminaemia. In this study we assessed the contributory role of oxidant stress, as measured by F(2)-isoprostanes and plasma oxygen radical absorbance capacity (ORAC), in subjects with NS.
  
  
  METHODS
  We studied 14 subjects with NS and 17 age- and sex-matched healthy non-proteinuric controls. Measurement of plasma and urinary F(2)-isoprostanes was carried out using a combination of silica and reverse-phase cartridges, high-performance liquid chromatography, and gas chromatography mass spectrometry using electron-capture negative ionization. The plasma ORAC assay measured the decrease in fluorescence of phycoerythrin added to plasma in the presence of a free-radical generator. The ORAC value (microM) was calculated as the ratio of the area under the fluorescence decay curve for plasma to the area under the fluorescence decay curve for a Trolox standard.
  
  
  RESULTS
  Plasma ORAC was significantly lower in NS patients compared with controls: mean (standard error) NS patients 3306 microM (286); controls 4882 microM (496), P=0.011. In univariate linear regression analysis, plasma albumin was significantly positively correlated with plasma ORAC (r=0.40, P=0.03). Plasma and urinary F(2)-isoprostanes did not differ significantly between NS and control groups.
  
  
  CONCLUSIONS
  This study demonstrates that in the NS there is decreased free-radical trapping capacity of plasma that is inversely correlated with hypoalbuminaemia, but no increase in plasma and urinary F(2)-isoprostanes. Decreased total plasma antioxidant potential in combination with hyperlipidaemia may contribute to the increased risk of cardiovascular disease seen in NS.
authors.affiliation: Department of Medicine and Western Australian Heart Research Institute, University of Western Australia, Perth, Western Australia, Australia.
authors.forename: G
authors.initials: G
authors.lastname: Dogra
authors.forename: N
authors.initials: N
authors.lastname: Ward
authors.forename: K D
authors.initials: KD
authors.lastname: Croft
authors.forename: T A
authors.initials: TA
authors.lastname: Mori
authors.forename: P H
authors.initials: PH
authors.lastname: Barrett
authors.forename: S E
authors.initials: SE
authors.lastname: Herrmann
authors.forename: A B
authors.initials: AB
authors.lastname: Irish
authors.forename: G F
authors.initials: GF
authors.lastname: Watts
mesh_terms: D000042:Absorption; D000328:Adult; D000368:Aged; D001790:Blood Physiological Phenomena; D003430:Cross-Sectional Studies; D015237:Dinoprost / Q000031:analogs & derivatives / Q000097:blood* / Q000652:urine*; D028441:F2-Isoprostanes; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009404:Nephrotic Syndrome / Q000378:metabolism*; D018384:Oxidative Stress; D017382:Reactive Oxygen Species / Q000378:metabolism; D012016:Reference Values
chemical_list: D028441:F2-Isoprostanes; D017382:Reactive Oxygen Species; D015237:Dinoprost