Omega-3 fatty acids inhibit the up-regulation of endothelial chemokines in
maintenance hemodialysis patients.
Author(s): Hung AM(1), Booker C(2), Ellis CD(2), Siew ED(1), Graves AJ(3), Shintani A(3),
Abumrad NN(4), Himmelfarb J(5), Ikizler TA(1).
Affiliation(s): Author information:
(1)CSR&D, Veterans Administration Tennessee Valley Healthcare System, Nashville,
TN, USA Division of Nephrology, Vanderbilt University Medical Center, Nashville,
TN, USA. (2)Division of Nephrology, Vanderbilt University Medical Center,
Nashville, TN, USA. (3)Division of Biostatistics, Vanderbilt University,
Nashville, TN, USA. (4)Department of Surgery, Vanderbilt University, Nashville,
TN, USA. (5)Kidney Research Institute, University of Washington, Seattle, WA,
USA.
Publication date & source: 2015, Nephrol Dial Transplant. , 30(2):266-74
BACKGROUND: Chronic systemic inflammation is common in patients with chronic
kidney disease on dialysis (CKD5D) and has been considered a key mediator of the
increased cardiovascular risk in this patient population. In this study, we
tested the hypothesis that supplementation of omega-3 polyunsaturated fatty acids
(ω-3 PUFAs) will attenuate the systemic inflammatory process in CKD5D patients.
METHODS: The design was a randomized, double-blinded, placebo controlled pilot
trial (NCT00655525). Thirty-eight patients were randomly assigned in a 1 : 1
fashion to receive 2.9 g of eicosapentaenoic acid (C20:5, n-3) plus
docosahexaenoic acid (C22:6, n-3) versus placebo for 12 weeks. The primary
outcome was change in pro-inflammatory chemokines measured by lipopolysaccharide
(LPS)-stimulated peripheral blood mononuclear cells (PBMCs). Secondary outcomes
were changes in systemic inflammatory markers. Analysis of covariance was used to
compare percent change from baseline to 12 weeks.
RESULTS: Thirty-one patients completed 12 weeks and three patients completed 6
weeks of the study. Median age was 52 (interquartile range 45, 60) years, 74%
were African-American and 79% were male. Supplementation of ω-3 PUFAs effectively
decreased the LPS-induced PBMC expression of RANTES (Regulated upon Activation,
Normal T cell Expressed and Secreted) and MCP-1 (Monocyte Chemotactic Protein-1;
unadjusted P = 0.04 and 0.06; adjusted for demographics P = 0.02 and 0.05,
respectively). There was no significant effect of the intervention on serum
inflammatory markers (C-reactive protein, interleukin-6 and procalcitonin).
CONCLUSIONS: The results of this pilot study suggest that supplementation of ω-3
PUFAs is beneficial in decreasing the levels of endothelial chemokines, RANTES
and MCP-1. Studies of larger sample size and longer duration are required to
further evaluate effects of ω-3 PUFAs on systemic markers of inflammation, other
metabolic parameters and clinical outcomes, particularly cardiovascular outcomes
in CKD5D patients.
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