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Acute effects of haemodialysis on biochemical modulators of endothelial function
Author(s) -
Hewitson C. L.,
Whiting M. J.,
Barbara J. A.,
Mangoni A. A.
Publication year - 2007
Publication title -
journal of internal medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.625
H-Index - 160
eISSN - 1365-2796
pISSN - 0954-6820
DOI - 10.1111/j.1365-2796.2007.01848.x
Subject(s) - medicine , hemodialysis , function (biology) , intensive care medicine , pharmacology , microbiology and biotechnology , biology
. Objectives. To assess the acute effects of haemodialysis (HD) on biochemical factors modulating endothelial function. Setting. Academic medical centre. Subjects. Forty patients (age 63.5 ± 2.2 years, mean ± SEM) undergoing HD. Interventions. 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 μmol L −1 , P < 0.001) and ADMA (0.64 ± 0.02 vs. 0.47 ± 0.02 μmol 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.