title: Oxidative stress and non-enzymatic glycation in IgA nephropathy.
abstract: OBJECTIVE
  Approximately 20-50% of IgA nephropathy patients develop end-stage renal disease. We have previously found enhanced oxidative stress and decreased antioxidant capacity in red blood cells of IgA nephropathy patients. In this study we assess oxidative stress, non-enzymatic glycation, oxidative resistance of low-density lipoprotein and its alpha-tocopherol content in these patients.
  
  
  METHODS
  Non-enzymatic glycation and oxidative stress were assessed in 88 IgA nephropathy patients by measuring advanced glycation end products, Nepsilon-carboxymethyl-lysine, thiobarbituric acid reactive substances, oxidative resistance of low-density lipoprotein and its alpha-tocopherol content.
  
  
  RESULTS
  Advanced glycation end products (2659 +/- 958 a.u.) and Nepsilon-carboxymethyl-lysine (563 +/- 215 ng/ml) were significantly higher in IgA nephropathy patients with decreased renal function compared to those with normal renal function (p < 0.002) or controls (p < 0.001). Thiobarbituric acid-reactive substances in plasma and associated with low-density lipoprotein were significantly elevated and oxidative resistance of low-density lipoprotein was significantly reduced in all groups of IgA nephropathy patients. There was no significant difference in circulating fluorescent advanced glycation end products, Nepsilon-carboxymethyl-lysine, thiobarbituric acid-reactive substances levels, oxidative resistance of low-density lipoprotein and its alpha-tocopherol content between patients with normal vs. impaired glucose metabolism. Low alpha-tocopherol content of low-density lipoprotein was accompanied with decreased oxidative resistance, depletion in polyunsaturated fatty acids, elevated saturated fatty acids and thiobarbituric acid-reactive substances within low-density lipoprotein suggesting enhanced lipid peroxidation.
  
  
  CONCLUSIONS
  Decreased oxidative resistance of low-density lipoprotein and enhanced oxidative stress are common features in IgA nephropathy, while increased non-enzymatic glycation occurs as renal function declines.
authors.affiliation: Second Department of Internal Medicine and Nephrological Center, Faculty of Medicine, University of Pécs, Pécs, Hungary.
authors.forename: T
authors.initials: T
authors.lastname: Vas
authors.forename: Z
authors.initials: Z
authors.lastname: Wagner
authors.forename: V
authors.initials: V
authors.lastname: Jenei
authors.forename: Z
authors.initials: Z
authors.lastname: Varga
authors.forename: T
authors.initials: T
authors.lastname: Kovács
authors.forename: I
authors.initials: I
authors.lastname: Wittmann
authors.forename: R
authors.initials: R
authors.lastname: Schinzel
authors.forename: G
authors.initials: G
authors.lastname: Balla
authors.forename: J
authors.initials: J
authors.lastname: Balla
authors.forename: A
authors.initials: A
authors.lastname: Heidland
authors.forename: J
authors.initials: J
authors.lastname: Nagy
mesh_terms: D000328:Adult; D005260:Female; D005922:Glomerulonephritis, IGA / Q000378:metabolism*; D017127:Glycation End Products, Advanced / Q000378:metabolism; D006031:Glycosylation; D006801:Humans; D008077:Lipoproteins, LDL / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D018384:Oxidative Stress; D024502:alpha-Tocopherol / Q000378:metabolism
chemical_list: D017127:Glycation End Products, Advanced; D008077:Lipoproteins, LDL; D024502:alpha-Tocopherol