Changes in total and segmental extracellular and intracellular volumes with hypotension during hemodialysis measured with bioimpedance spectroscopy.

BACKGROUND: Bioelectrical impedance analysis (BIA) devices have been advocated to guide volume management in hemodialysis (HD) patients. We hypothesized that understanding the dynamics of fluid shifts in different body segments may provide additional insight on preventive measures to reduce the risk of intradialytic hypotension. METHODS: A prospective observational study was conducted among 42 HD patients at risk of hypotension who were admitted as emergencies inpatient. RESULTS: A total of 191 BIA measurements were made during the 42 HD sessions, and hypotension occurred during 52 measurements (27%). The extracellular water (ECW) to intracellular water ratio (EIR) was measured in different body segments and declined significantly only in the non-access arm with increasing HD session duration (ß = -0.04; 95% confidence interval (CI): -0.05 to -0.03, p < 0.01). There was no significant association between EIR and hypotension with respect to the different body segments. Only pre-HD N-terminal-pro b-type natriuretic peptide was significantly associated with hypotension (ß = 0.20, 95% CI: 0.04 to 0.89, p = 0.04). There was no association between relative blood volume monitoring change and EIR. CONCLUSION: In summary, we found that segmental BIA during HD was unable to detect or predict hypotension during dialysis. Although BIA is able to provide information about ECW and guide clinical assessment of volume in HD patients prior to dialysis, our findings did not suggest the use of serial measurements of changes in EIR in different body segments during HD provided sufficient information to predict intradialytic hypotension. Similarly, changes in EIR did not provide information on changes in plasma volume that could potentially trigger interventions to prevent or reduce intra-dialytic hypotension.

Randomized Controlled Clinical Trial of the Effect of Treatment with Vitamin K2 on Vascular Calcification in Hemodialysis Patients (Trevasc-HDK).

Introduction: Vitamin K deficiency among patients on hemodialysis (HD) affects the function of matrix GLA protein (MGP), a potent vitamin K-dependent inhibitor of vascular calcification (VC). Methods: We conducted a single-center randomized controlled trial (RCT) on maintenance HD patients to examine if vitamin K2 supplementation can reduce progression of coronary artery calcification (CAC) over an 18-month study period. Patients were randomized to vitamin K2 group receiving menaquinone-7360 µg 3 times/wk or control group. The primary outcome was CAC scores at the end of the study period. The secondary outcomes were aortic valve calcification (AVC), carotid-femoral pulse wave velocity (cfPWV), aortic augmentation index (AIx), dephosphorylated undercarboxylated MGP (dp-ucMGP) levels, major adverse cardiac events (MACE), and vascular access events. Results: Of the 178 patients randomized, follow-up was completed for 138 patients. The CAC scores between the 2 groups were not statistically different at the end of 18 months (relative mean difference [RMD] 0.85, 95% CI 0.55-1.31). The secondary outcomes did not differ significantly in AVC (RMD 0.82, 95% CI 0.34-1.98), cfPWV (absolute mean difference [AMD] 0.55, 95% CI -0.50 to 1.60), and AIx (AMD 0.13, 95% CI -3.55 to 3.80). Supplementation with vitamin K2 did reduce dp-ucMGP levels (AMD -86, 95% CI -854 to -117). The composite outcome of MACE and mortality was not statistically different between the 2 groups (Hazard ratio = 0.98, 95% CI 0.50-1.94). Conclusion: Our study did not demonstrate a beneficial effect of vitamin K2 in reducing progression of VC in this population at the studied dose and duration.

Selective reporting of fluoroquinolone susceptibility as a stewardship measure is of marginal benefit.

A retrospective time series analysis was conducted to compare inpatient fluoroquinolone use when susceptibilities were masked and after susceptibilities were unmasked. Although inappropriate culture-directed prescriptions increased, overall fluoroquinolone usage decreased. Culture-directed therapy was a small part of fluoroquinolone usage; hence, efforts should target empiric use to reduce overall consumption.

Treatment to reduce vascular calcification in hemodialysis patients using vitamin K (Trevasc-HDK): A study protocol for a randomized controlled trial.

INTRODUCTION: End stage renal failure patients on hemodialysis have significant vascular calcification This is postulated to be related to sub-clinical vitamin K deficiency, which is prevalent in hemodialysis patients. Vitamin K deficiency result in the failure of the matrix GLA protein (MGP) to undergo carboxylation. MGP is a natural local inhibitor of vascular calcification and the lack of functional carboxylated MGP may contribute to increase vascular calcification. Vitamin K supplement should therefore correct this anomaly and decrease the rate or severity of vascular calcification in this population of patients on long-term maintenance hemodialysis. Our study seeks to evaluate the prevalence and the progression of vascular calcification in a cohort of maintenance hemodialysis patients. It will also evaluate the efficacy of vitamin K supplementation in reducing the progression of vascular calcification in this group of patients. METHODS: This will be a single-center randomized, prospective and open-label interventional clinical trial of end stage renal failure patients on hemodialysis. We aim to recruit 200 patients. Eligible patients will be randomized to either the standard care arm or active treatment arm. Active treatment arm patients will receive standard care plus supplementation with oral vitamin K2 isoform 360 mcg 3 times weekly for a total duration of 18 months. Primary outcome measured will be absolute difference in coronary artery calcification score at 18-month between control and intervention arms. Secondary outcomes will be to compare absolute difference in aortic valve calcification, percentage of patients with regression of coronary artery calcification of at least 10%, absolute difference in aortic and systemic arterial stiffness, mortality from any cause and major adverse cardiovascular over the same period. DISCUSSION: Evidence of successful regression or retardation of vascular calcification will support the conduct of larger and longer-term trials aimed at reducing cardiovascular disease mortality and major adverse cardiovascular events in this high-risk population using a safe and inexpensive strategy TRIAL REGISTRATION:: ClinicalTrials.gov NCT02870829. Registered on 17 August 2016 - Retrospectively registered, https://clinicaltrials.gov/ct2/show/NCT02870829National University Hospital's Institutional Review Board (2015/01000).