Background: Heart failure is a highly prevalent cardiovascular complication among patients receiving long‐term hemodialysis, but the benefits of carvedilol, bisoprolol, and metoprolol controlled release/extended release on the outcomes of these patients remain unclear. In this study, we address the use of these 3 β‐blockers and their associations with mortality. Methods and Results: Long‐term hemodialysis patients, aged ≥35 years, with new‐onset heart failure and receiving various medications were identified through the use of 1999–2010 data from the Taiwan National Health Insurance Research Database. From the total of 4435 heart failure patients, we selected 1700 new users of the 3 β‐blockers (study group) and 1700 nonusers (control group), by using matched cohorts according to their propensity scores, and then compared the 5‐year all‐cause mortality rates by using Cox proportional hazard regressions and time‐dependent covariate adjustment. During 3944 person‐years of follow‐up, 666 (39.2%) deaths occurred within the study group, compared with 918 (54%) deaths during 2893 person‐years of follow‐up in the control group. The 5‐year mortality rate for the study (control) group was 54.5% (70.3%); P <0.001. Adjusted hazard regression analyses revealed that the therapeutic effects of β‐blockers remained significant for all‐cause mortality (hazard ratio 0.80, 95% CI 0.72 to 0.90). Subgroup analyses revealed that patients in the study group receiving β‐blockers plus renin‐angiotensin system antagonists exhibited the lowest mortality rate, while the highest mortality rate was found among patients in the control group receiving neither β‐blockers nor renin‐angiotensin system antagonists. Conclusions: This study demonstrates that the 3 β‐blockers were associated with improved survival in long‐term hemodialysis patients with heart failure.

Objectives The total medical (economic) costs of haemodialysis (HD) and peritoneal dialysis (PD), including direct medical costs, out-of-pocket (OOP) costs and productivity losses, have become an important issue. This study aims to compare the direct non-medical costs and indirect medical costs of both modalities in Taiwan. Design and setting This multicentre study included cross-sectional interviews of patients over 20 years old and articulate, who had been continuously receiving long-term HD or PD for more than 3 months between April 2015 and March 2016. Mann-Whitney U test, Wilcoxon rank-sum test and 1000 bootstrap procedures with replacement were used for analysis. Outcome measures Differences in OOP costs and productivity losses. Results There were 308 HD and 246 PD patients available for analysis. HD patients had significantly higher monthly OOP costs than PD patients after bootstrap procedures (NTD 5912 vs NTD 5225, p<0.001; NTD, new Taiwan dollars; 1 US dollar=30 NTD). Compared with PD patients, HD patients had higher monthly productivity losses after bootstrap procedures (NTD 14 150 vs NTD 11 611, p<0.001), resulting from more time spent seeking outpatient care (HD, 70.4 hours vs PD, 4.4 hours, p<0.001) and time spent by family caregivers for outpatient care (HD, 66.1 hours vs PD, 6.1 hours, p<0.001). The total costs per patient–month of HD and PD modalities, including OOP costs and productivity losses, were NTD 20 062 and NTD 16 836, respectively. Conclusions The HD modality has higher OOP costs and productivity losses than the PD modality in Taiwan.

Aims: Heart failure is among the most frequent complications of patients on long-term haemodialysis. The benefits of renin–angiotensin system (RAS) blockade on the outcomes of these patients have yet to be determined. Methods and results: We conducted a nationwide observational study using data from the Taiwan National Health Insurance claims database, between 1999 and 2010. We enrolled patients aged ≥35 years with new-onset heart failure [diagnosed by International Classification of Diseases, 9th revision, clinical modification (ICD-9-CM) codes] under treatment with medications. New users of a RAS blocker (RASB; i.e. an ACE inhibitor or an ARB used as monotherapy or dual therapy) were selected to compare with non-RASB users. We used Cox proportional hazards regression with and without propensity score adjustment to compare the risk of 3-year all-cause and cardiovascular mortality. Stratified analyses and RASB therapy duration as a time-dependent covariate were also performed. In all, 4771 were treated with an RASB (n = 3024) or without an RASB (n = 1747). RASB users had a higher prevalence of hypertension and diabetes, and a higher number of hospitalization. Among RASB users, 1148 deaths (38.0%) occurred during 5272 person-years of follow-up compared with 734 deaths (42.0%) among non-RASB users during 2683 person-years of follow-up. Three-year mortality rates were 45.4% and 49.1% for patients receiving and those not receiving an RASB, respectively (log-rank test, P < 0.001). Adjusted hazard analysis revealed that RASB therapeutic effects remained significant on all-cause [hazard ratio (HR) 0.8; 95% confidence interval (CI) 0.72–0.89; P < 0.001] and cardiovascular mortality (HR 0.76; 95% CI 0.64–0.90; P < 0.01). Conclusions: RASB therapy reduced all-cause and cardiovascular mortality in heart failure patients on long-term haemodialysis.

Chronic kidney disease–mineral bone disorder (CKD–MBD), comprising mineral, hormonal, and bone metabolic imbalance, is a major CKD-related issue; it causes osteoporosis prevalence in CKD patients. Osteocyte-derived sclerostin inhibits the osteogenic Wnt/β-catenin signaling pathway; its levels rise when kidney function declines. Exercise modulates the physiological functions of osteocytes, potentially altering sclerostin production. It may aid bone and mineral electrolyte homeostasis in CKD. Mild CKD was induced in rats by partial nephrectomy. They were divided into: sham (no CKD), CKD, and CKD + exercise (8 weeks of treadmill running) groups. Micro-CT scanning demonstrated that the CKD + exercise-group rats had a higher bone mineral density (BMD) of the spine and femoral metaphysis and higher femoral trabecular bone volume than the CKD-group rats. Bone formation rates were not significantly different. The CKD + exercise-group rats had lower serum sclerostin (157.1 ± 21.1 vs 309 ± 38.1 pg/mL, p < 0.05) and CTX-1 (bone resorption marker) levels. Immunohistochemistry revealed higher tibial β-catenin concentrations in the CKD + exercise-group rats. Serum FGF-23, intact parathyroid hormone (iPTH), alkaline phosphatase (ALP), calcium, and phosphate levels showed no significant differences between these groups. Thus, exercise improves BMD and bone microstructure in mild CKD by inhibiting sclerostin production, but does not alter serum minerals.