Acute effects of haemodialysis on biochemical modulators of endothelial function.
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.
Hewitson
C L
CL
Department of Clinical Pharmacology, Flinders University and Flinders Medical Centre, Adelaide, Australia.
Whiting
M J
MJ
Barbara
J A
JA
Mangoni
A A
AA
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
C487735:dimethylarginine; D006710:Homocysteine; D008315:Malondialdehyde; D002097:C-Reactive Protein; D005492:Folic Acid; D001120:Arginine