TSUCHIYA Ken
   Department   School of Medicine(Tokyo Women's Medical University Hospital), School of Medicine
   Position   Professor (Fixed Term)
Article types Original article
Language English
Peer review Non peer reviewed
Title Eicosapentaenoic Acid (EPA) Decreases the All-Cause Mortality in Hemodialysis Patients
Journal Formal name：Internal medicine (Tokyo, Japan)
Abbreviation：Intern Med
ISSN code：1349-7235(Electronic)0918-2918(Linking)
Domestic / ForeginForegin
Volume, Issue, Page 54(24),pp.3133-7
Author and coauthor Inoue Tomoko, Okano Kazuhiro, Tsuruta Yuki, Tsuruta Yukio, Tsuchiya Ken, Akiba Takashi, Nitta Kosaku
Publication date 2015/12/15
Summary Objective Atherosclerosis, which causes cardiovascular disease, is a major cause of death in hemodialysis (HD) patients. Eicosapentaenoic acid (EPA), an anti-hyperlipidemic agent, is known to have antioxidative or anti-inflammatory effects, resulting in improvements in atherosclerosis. In the present study, we examined whether EPA improves the all-cause mortality in patients receiving regular HD therapy. Methods We enrolled 176 patients treated with maintenance HD therapy and performed a longitudinal observational cohort study for three years. We divided the patients into two groups based on whether or not the received EPA treatment [EPA(+) and EPA(-), respectively]. The primary end-point was all-cause death. We also matched the two groups using propensity score matching and examined the effect of EPA. Results Before matching, the all-cause mortality rates were 24.0% in the EPA(+) and 11.8% in the EPA(-) groups, which were significantly different (p=0.044). After propensity score matching, the EPA(+) group still showed a significantly better prognosis than the EPA(-) group (p=0.038). A multivariate analysis showed that EPA treatment significantly reduced the risk of all-cause mortality both before and after propensity score matching. Conclusion EPA treatment is independently associated with lower mortality in HD patients.
DOI 10.2169/internalmedicine.54.4931
PMID 26666599