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Background The results remain controversial with regards to the impact of serum uric acid on clinical outcomes from peritoneal dialysis population. The aim of our study was to investigate the influence of serum uric acid levels on mortality in peritoneal dialysis patients. Methods Data on 9405 peritoneal dialysis patients from the Zhejiang Renal Data system were retrospectively analyzed. All demographic and laboratory data were recorded at baseline. The study cohort was divided into quintiles according to baseline uric acid level (mg/dL): Q1 (< 6.06), Q2 (6.06–6.67), Q3 (6.68–7.27) (reference), Q4 (7.28–8.03), and Q5 (≥8.04). Hazards ratio (HR) of all-cause and cardiovascular mortality was calculated. Results Mean serum uric acid was 7.07 ± 1.25 mg/dL. During a median follow-up of 29.4 (range, 3.0 to 115.4) months, 1226 (13.0%) patients died, of which 515 (5.5%) died of cardiovascular events. The Kaplan-Meier survival curves showed that patients in the middle uric acid quintile (Q3: 6.68–7.27) exhibited the highest patient and cardiovascular survival rates (log-rank test P < 0.05). Multivariate Cox regression analysis showed that, using Q3 as the reference, in the fully adjusted model, a higher uric acid level (Q4: 7.28–8.03, and Q5: ≥8.04) was significantly associated with higher all-cause mortality (Model 3; Q4: HR, 1.335, 95% CI, 1.073 to 1.662, P = 0.009; Q5: HR, 1.482, 95% CI, 1.187 to 1.849, P = 0.001), but not with cardiovascular mortality. The adverse effect of higher uric acid level (≥7.28 mg/dL) on all-cause mortality was more prominent in groups such as male, hypoalbuminemia, normal weight, non-diabetes mellitus at baseline rather than in their counterparts respectively. Conclusions A higher uric acid level was an independent risk factor for all-cause mortality in peritoneal dialysis patients. Electronic supplementary material The online version of this article (10.1186/s12986-019-0379-y) contains supplementary material, which is available to authorized users.

Tea (Camellia sinensis) flower saponins (TFS) have various biological properties. However, the anti-cancer effects of TFS have not been investigated in any detail. Here, we evaluated the anticancer effects of TFS using human ovarian cancer cell lines. TFS (1.5 μg/ml) produced significant antiproliferative effects against A2780/CP70 and OVCAR-3 cells by inducing p53-dependent apoptosis and S phase arrest. Further study showed that TFS decreased mitochondrial membrane potential, activated Caspase-3/7, Caspase-8 and Caspase-9 activities, and that the p53 inhibitor PFT-α reversed the TFS-induced cell growth inhibition and apoptosis. In addition, TFS inhibited the expression of Cdc25A, Cdk2, and CyclinD1 and upregulated Cyclin E and Cyclin A, suggesting that the Cdc25A-Cdk2-Cyclin E/A pathway was involved in TFS-induced S phase arrest. Furthermore, the S phase arrest was associated with a Chk2-Cdc25A DNA damage response. These results demonstrated that TFS has promising potential serving as functional food components for prevention of ovarian cancer.