title: Influence of hemodialysis membrane type on pentosidine plasma level, a marker of "carbonyl stress".
abstract: Influence of hemodialysis membrane type on pentosidine plasma level, a marker of "carbonyl stress."
  
  
  BACKGROUND
  The accumulation of advanced glycation end products (AGEs) in uremia has been ascribed to the retention of carbonyl precursors of AGEs. Pentosidine plasma level has been identified as a surrogate marker of carbonyl precursors ("carbonyl stress"). The influence of hemodialysis (HD) membrane type and residual diuresis on carbonyl stress has not been studied.
  
  
  METHODS
  We measured protein-linked and free plasma pentosidine (a surrogate marker of carbonyl stress) by high-performance liquid chromatography in patients on HD with low-flux cellulose (N = 29), high-flux polysulfone (PS; N = 57), polymethylmethacrylate (PMMA) (N = 25), and AN69 (N = 15).
  
  
  RESULTS
  Both protein-linked and free pentosidine were similar on low-flux cellulose, high-flux PMMA, and AN69, but were lower (P < 0.01) on high-flux PS. Pentosidine levels were virtually identical on Fresenius and Asahi PS in Japanese and Belgian patients. By multivariate analysis, only the type of HD membrane and residual diuresis proved to be independent determinants (P < 0.001) of pentosidine levels. During a single HD session, the clearance of free pentosidine was similar with all membranes. In three patients who were switched from AN69 to PS, the protein-linked pentosidine level dropped to the control level after resumption of the AN69 membrane.
  
  
  CONCLUSIONS
  Both HD membrane type and residual diuresis are independent determinants of pentosidine plasma level, which is a marker of carbonyl stress.
authors.affiliation: Department of Nephrology, University of Louvain Medical School, Brussels, Belgium. Jadoul@nefr.ucl.ac.be
authors.forename: M
authors.initials: M
authors.lastname: Jadoul
authors.forename: Y
authors.initials: Y
authors.lastname: Ueda
authors.forename: Y
authors.initials: Y
authors.lastname: Yasuda
authors.forename: A
authors.initials: A
authors.lastname: Saito
authors.forename: A
authors.initials: A
authors.lastname: Robert
authors.forename: N
authors.initials: N
authors.lastname: Ishida
authors.forename: K
authors.initials: K
authors.lastname: Kurokawa
authors.forename: C
authors.initials: C
authors.lastname: Van Ypersele De Strihou
authors.forename: T
authors.initials: T
authors.lastname: Miyata
mesh_terms: D000368:Aged; D001120:Arginine / Q000031:analogs & derivatives* / Q000097:blood; D001530:Belgium; D015415:Biomarkers / Q000097:blood; D001798:Blood Proteins / Q000378:metabolism; D005260:Female; D017127:Glycation End Products, Advanced / Q000097:blood*; D006801:Humans; D007564:Japan; D007688:Kidneys, Artificial; D008239:Lysine / Q000031:analogs & derivatives* / Q000097:blood; D008297:Male; D008567:Membranes, Artificial; D008875:Middle Aged; D011485:Protein Binding; D006435:Renal Dialysis; D014511:Uremia / Q000097:blood / Q000628:therapy
chemical_list: D015415:Biomarkers; D001798:Blood Proteins; D017127:Glycation End Products, Advanced; D008567:Membranes, Artificial; D001120:Arginine; C062187:pentosidine; D008239:Lysine