title: Ultrapure dialysate decreases plasma pentosidine, a marker of "carbonyl stress".
abstract: BACKGROUND
  Advanced glycation end products (AGEs) and their reactive carbonyl precursors accumulate in renal failure ("carbonyl stress"). Carbonyl stress derives from a broad derangement in the nonenzymatic biochemistry of both carbohydrates and lipids. We tested the influence of dialysate quality on plasma level of pentosidine, an AGE moiety taken as a surrogate marker of carbonyl stress, in hemodialysis patients.
  
  
  METHODS
  Plasma pentosidine is measured by means of high-performance liquid chromatography in patients hemodialyzed successively with a conventional and an ultrapure endotoxin-free dialysate.
  
  
  RESULTS
  Dialysate endotoxin level decreased from 0.040 +/- 0.017 EU/mL before the switch to the new water supply system to less than the detection limit (<0.001 EU/mL) after the switch. Plasma pentosidine levels decreased from 1.55 +/- 0.61 nmol/mL before the switch to 1.38 +/- 0.52 nmol/mL (P < 0.0001) and 1.31 +/- 0.50 nmol/mL (P < 0.0001) 3 and 6 months after the switch to an ultrapure dialysate, respectively. Decreases in plasma pentosidine levels were similar regardless of dialyzer membrane type; ie, high-flux polysulfone, high-flux polymethylmethacrylate, and low-flux cellulose acetate membranes. Unexpectedly, plasma triglyceride levels decreased from 150 +/- 116 mg/dL (1.69 +/- 1.31 mmol/L) before the switch to 124 +/- 79 mg/dL (1.40 +/- 0.89 mmol/L; P < 0.01) and 119 +/- 75 mg/dL (1.34 +/- 0.85 mmol/L; P < 0.01) 3 and 6 months after the switch despite unchanged total cholesterol levels, respectively. Changes in pentosidine levels were unrelated to those in triglycerides, and both were unrelated to C-reactive protein levels, which remained stable throughout the study.
  
  
  CONCLUSIONS
  Ultrapure dialysate reduces plasma pentosidine levels and improves plasma triglyceride levels in hemodialysis patients through still undefined mechanisms.
authors.affiliation: Institute of Medical Sciences and Department of Medicine, Tokai University School of Medicine, Kanagawa, Japan.
authors.forename: Yuko
authors.initials: Y
authors.lastname: Izuhara
authors.forename: Toshio
authors.initials: T
authors.lastname: Miyata
authors.forename: Kazuhiro
authors.initials: K
authors.lastname: Saito
authors.forename: Naoyoshi
authors.initials: N
authors.lastname: Ishikawa
authors.forename: Takatoshi
authors.initials: T
authors.lastname: Kakuta
authors.forename: Masaomi
authors.initials: M
authors.lastname: Nangaku
authors.forename: Hiroaki
authors.initials: H
authors.lastname: Yoshida
authors.forename: Akira
authors.initials: A
authors.lastname: Saito
authors.forename: Kiyoshi
authors.initials: K
authors.lastname: Kurokawa
authors.forename: Charles
authors.initials: C
authors.lastname: van Ypersele de Strihou
mesh_terms: D001120:Arginine / Q000031:analogs & derivatives* / Q000097:blood* / Q000378:metabolism; D015415:Biomarkers / Q000097:blood / Q000378:metabolism; D002851:Chromatography, High Pressure Liquid / Q000379:methods; D015314:Dialysis Solutions / Q000737:chemistry* / Q000592:standards; D017127:Glycation End Products, Advanced / Q000378:metabolism; D006801:Humans; D007676:Kidney Failure, Chronic / Q000097:blood / Q000628:therapy; D008239:Lysine / Q000031:analogs & derivatives* / Q000097:blood* / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D018384:Oxidative Stress / Q000502:physiology*; D006435:Renal Dialysis / Q000295:instrumentation / Q000379:methods; D014280:Triglycerides / Q000097:blood
chemical_list: D015415:Biomarkers; D015314:Dialysis Solutions; D017127:Glycation End Products, Advanced; D014280:Triglycerides; D001120:Arginine; C062187:pentosidine; D008239:Lysine