title: Acute effects of haemodialysis on biochemical modulators of endothelial function.
abstract: OBJECTIVE
  To assess the acute effects of haemodialysis (HD) on biochemical factors modulating endothelial function.
  
  
  METHODS
  Academic medical centre.
  
  
  METHODS
  Forty patients (age 63.5 +/- 2.2 years, mean +/- SEM) undergoing HD.
  
  
  METHODS
  Folic acid (F), homocysteine (tHcy), asymmetric dimethylarginine (ADMA), high-sensitivity C-reactive protein (CRP) and malondialdehyde (MDA) were measured pre-HD, 1 h after commencing HD and within the last hour of HD (end-HD). Endothelium-dependent and -independent vasodilatation were measured by applanation tonometry (changes in augmentation index, AIx, postinhaled salbutamol and postsublingual nitroglycerin) in conjunction with biochemical measurements.
  
  
  RESULTS
  Marked reductions in serum F (616 +/- 73 vs. 273 +/- 30 nmol L(-1), P < 0.001), tHcy (16.3 +/- 0.7 vs. 11.2 +/- 0.5 micromol L(-1), P < 0.001) and ADMA (0.64 +/- 0.02 vs. 0.47 +/- 0.02 micromol L(-1), P < 0.001) occurred end-HD, whereas CRP and MDA levels did not significantly change. There was no significant change in endothelium-dependent vasodilatation, whereas endothelium-independent vasodilatation improved end-HD (-23.1 +/- 1.9 vs. -17.3 +/- 1.3%, P = 0.018). Regression analysis showed that both higher ADMA (P = 0.029) and lower F levels (P = 0.040) end-HD were determinants of reduced endothelium-dependent vasodilatation end-HD (R(2) = 0.23).
  
  
  CONCLUSIONS
  HD is associated with significant reductions in F, tHcy and ADMA serum concentrations. The lack of significant effects of HD on endothelium-dependent vasodilatation could be secondary to the concomitant loss of factors either enhancing (F) or impairing (ADMA) endothelial function.
authors.affiliation: Department of Clinical Pharmacology, Flinders University and Flinders Medical Centre, Adelaide, Australia.
authors.forename: C L
authors.initials: CL
authors.lastname: Hewitson
authors.forename: M J
authors.initials: MJ
authors.lastname: Whiting
authors.forename: J A
authors.initials: JA
authors.lastname: Barbara
authors.forename: A A
authors.initials: AA
authors.lastname: Mangoni
mesh_terms: D001120:Arginine / Q000031:analogs & derivatives / Q000097:blood; D001794:Blood Pressure / Q000502:physiology; D002097:C-Reactive Protein / Q000032:analysis; D004730:Endothelium, Vascular / Q000503:physiopathology*; D005260:Female; D005492:Folic Acid / Q000097:blood; D006339:Heart Rate / Q000502:physiology; D006710:Homocysteine / Q000097:blood; D006801:Humans; D007676:Kidney Failure, Chronic / Q000097:blood* / Q000503:physiopathology / Q000628:therapy; D008297:Male; D008315:Malondialdehyde / Q000097:blood; D008875:Middle Aged; D006435:Renal Dialysis / Q000009:adverse effects*; D014664:Vasodilation / Q000502:physiology
chemical_list: C487735:dimethylarginine; D006710:Homocysteine; D008315:Malondialdehyde; D002097:C-Reactive Protein; D005492:Folic Acid; D001120:Arginine