Els, and baseline AoACS were significantly associated with AoAC progression. In

Els, and baseline AoACS were significantly associated with AoAC progression. In multivariate binary logistic regression models, baseline AoACS (OR: 1.234, 95 CI: 1.104?.197, P = 0.027) and hs-CRP levels (OR: 2.238, 95 CI: 1.051?.767, P = 0.037) were independent predictors of AoAC progression after adjustment for confounders. On the other hand, in patients without baseline AoAC, age, previous cardiovascular disease, the use of lipid-lowering drugs, and hs-CRP levels were Pleuromutilin supplier significant predictors of AoAC progression in univariate analysis. Multivariate binary logistic regression models demonstrated that age (OR: 1.063, 95 CI: 1.014?.113, P = 0.002) and hs-CRP Fexinidazole biological activity concentrations (OR: 1.294, 95 CI: 1.019?.581, P = 0.035) were significant risk factors for AoAC progression. However, peritoneal membrane transport characteristics, weekly Kt/V urea, Ca x P products, iPTH concentrations, and the use of phosphate binders were not 1326631 significantly associated with AoAC progression in both subgroups.Progression of AoAC as an Independent Risk Factor for MortalityIn patients with AoAC at baseline, all-cause and cardiovascular death rates were significantly higher in the AoAC progression group (19.8 vs. 8.6 and 11.0 vs. 3.8 per 100 Person-Years, respectively, P,0.001). Results were similar even when the analysis was performed using only patients without baseline AoAC. In the progression groups, all-cause and cardiovascular death rates were 11.1 and 4.4 per 100 Person-Years, respectively. These rates were significantly higher than those of the nonprogression group (2.2 and 0.6 per 100 Person-Years, respectively, P,0.001) (Table 3). Kaplan-Meier analysis and Cox proportional hazard models (Figure 2 and Table 4) were used to determine the prognosticvalue of AoAC progression on mortality. In patients with baseline AoAC, patients with AoAC progression had significantly lower allcause and cardiovascular mortality-free survival rates compared to patients without progression (log-rank test, P = 0.002 and 0.016, respectively). In addition, AoAC progression along with previous history of cardiovascular disease and hs-CRP levels was found to be significantly associated with all-cause and cardiovascular mortality in univariate Cox analysis. However, multivariate Cox proportional hazard analysis revealed that AoAC progression was an independent predictor of all-cause (HR: 2.625, 95 CI: 1.15?5.991, P = 0.022) and cardiovascular mortality (HR: 4.008, 95 CI: 1.079?4.890, P = 0.038). Similarly, in the subgroup of patients without baseline AoAC, Kaplan-Meier analysis showed that patients with AoAC progression had significantly higher risks for all-cause (P,0.001) and cardiovascular mortality (P = 0.003). Moreover, in univariate analysis, age, previous history of cardiovascular 1326631 disease, the use of lipid-lowering drugs, and hsCRP concentrations as well as AoAC progression were demonstrated to be significant risk factors for all-cause and cardiovascular mortality. However, subsequent multivariate Cox proportional hazard models found that AoAC progression was a significant independent predictor of all-cause mortality (HR: 3.408, 95 CI: 1.028?1.300, P = 0.045), but not of cardiovascular mortality (HR: 5.935, 95 CI: 0.912?6.995, P = 0.057).DiscussionVascular calcification is common in ESRD patients and closely linked with cardiovascular disease, the leading cause of death in this population [1,5,8,9,10,11]. In this study, we demonstrate that AoAC presence at the initiation of d.Els, and baseline AoACS were significantly associated with AoAC progression. In multivariate binary logistic regression models, baseline AoACS (OR: 1.234, 95 CI: 1.104?.197, P = 0.027) and hs-CRP levels (OR: 2.238, 95 CI: 1.051?.767, P = 0.037) were independent predictors of AoAC progression after adjustment for confounders. On the other hand, in patients without baseline AoAC, age, previous cardiovascular disease, the use of lipid-lowering drugs, and hs-CRP levels were significant predictors of AoAC progression in univariate analysis. Multivariate binary logistic regression models demonstrated that age (OR: 1.063, 95 CI: 1.014?.113, P = 0.002) and hs-CRP concentrations (OR: 1.294, 95 CI: 1.019?.581, P = 0.035) were significant risk factors for AoAC progression. However, peritoneal membrane transport characteristics, weekly Kt/V urea, Ca x P products, iPTH concentrations, and the use of phosphate binders were not 1326631 significantly associated with AoAC progression in both subgroups.Progression of AoAC as an Independent Risk Factor for MortalityIn patients with AoAC at baseline, all-cause and cardiovascular death rates were significantly higher in the AoAC progression group (19.8 vs. 8.6 and 11.0 vs. 3.8 per 100 Person-Years, respectively, P,0.001). Results were similar even when the analysis was performed using only patients without baseline AoAC. In the progression groups, all-cause and cardiovascular death rates were 11.1 and 4.4 per 100 Person-Years, respectively. These rates were significantly higher than those of the nonprogression group (2.2 and 0.6 per 100 Person-Years, respectively, P,0.001) (Table 3). Kaplan-Meier analysis and Cox proportional hazard models (Figure 2 and Table 4) were used to determine the prognosticvalue of AoAC progression on mortality. In patients with baseline AoAC, patients with AoAC progression had significantly lower allcause and cardiovascular mortality-free survival rates compared to patients without progression (log-rank test, P = 0.002 and 0.016, respectively). In addition, AoAC progression along with previous history of cardiovascular disease and hs-CRP levels was found to be significantly associated with all-cause and cardiovascular mortality in univariate Cox analysis. However, multivariate Cox proportional hazard analysis revealed that AoAC progression was an independent predictor of all-cause (HR: 2.625, 95 CI: 1.15?5.991, P = 0.022) and cardiovascular mortality (HR: 4.008, 95 CI: 1.079?4.890, P = 0.038). Similarly, in the subgroup of patients without baseline AoAC, Kaplan-Meier analysis showed that patients with AoAC progression had significantly higher risks for all-cause (P,0.001) and cardiovascular mortality (P = 0.003). Moreover, in univariate analysis, age, previous history of cardiovascular 1326631 disease, the use of lipid-lowering drugs, and hsCRP concentrations as well as AoAC progression were demonstrated to be significant risk factors for all-cause and cardiovascular mortality. However, subsequent multivariate Cox proportional hazard models found that AoAC progression was a significant independent predictor of all-cause mortality (HR: 3.408, 95 CI: 1.028?1.300, P = 0.045), but not of cardiovascular mortality (HR: 5.935, 95 CI: 0.912?6.995, P = 0.057).DiscussionVascular calcification is common in ESRD patients and closely linked with cardiovascular disease, the leading cause of death in this population [1,5,8,9,10,11]. In this study, we demonstrate that AoAC presence at the initiation of d.