Dietary fatty acids intake and all-cause and cardiovascular mortality in patients on peritoneal dialysis.

BACKGROUND & AIMS: The relationship between dietary fatty acids (FA) and clinical outcomes are relatively lacking in non-dialyzed and dialyzed chronic kidney disease (CKD) population, resulting in insufficient guide about the dietary FA intake in this population. In this study, we aimed to observe the association between the intake of total or different types of FA and all-cause and cardiovascular (CV) mortality in patients undergoing peritoneal dialysis (PD). METHODS: This is a prospective cohort study with data retrospectively analyzed in 881 patients undergoing PD. Dietary FA intake measured by 3-day dietary records. The outcomes were defined as all-cause and CV death. Baseline FA intake and time-averaged FA intake were categorized by tertiles based on the distribution among the study population. We used univariate and multivariate Cox proportional regression models to determine the association between amounts and types of FA and all-cause and CV mortality. RESULTS: During a median follow up of 45 months, 93 patients were still being maintained on PD, 467 had died, including 189 (40.5%) attributable to CV death. Compared to patients in the low tertile of total FA (TFA) intake at baseline group, the middle or/and high tertile groups were more likely to be male, younger, well-educated and better nutritional status (P < 0.05). At the baseline, no association was found between all-cause and CV death in either total or different types of FA after adjusting for nutritional variables. As for time-averaged analyses, the associations of TFA, saturated FA (SFA), monounsaturated FA (MUFA), ω-3 and ω-6 polyunsaturated FA (PUFA) and all-cause mortality were weakened after adjustment for laboratory and nutrients variables. However, PUFA independently reduced 5% of mortality even after adjustment for laboratory and nutrients variables [HR 0.95 (0.91, 0.99), P = 0.023], and the ratio of MUFA/PUFA was positively associated with the risk for all-cause mortality [HR 1.05 (1.01, 1.09), P = 0.008]. Furthermore, each 10% increase of the ratio of ω-6/ω-3 was only weakly associated with the risk for all-cause mortality [HR 1.02 (1.00, 1.04), P = 0.034]. As for CVD mortality, the impacts of total and each type of FA disappeared after adjustment for laboratory or nutrients variables. CONCLUSIONS: Time-averaged PUFA intake was independently associated with a lower risk for all-cause mortality in our PD cohort, while the higher ratio of MUFA/PUFA and ω-6/ω-3 increased all-cause mortality. More observational and interventional researches are needed to determine these associations.