Background: Central venous oxygen saturation (ScvO₂) is correlated with cardiac output. In most patients, ScvO₂ declines during hemodialysis (HD) due to factors such as reduced preload, myocardial stunning, and intermittent arrhythmias. Previous research has shown that low ScvO₂ is associated with higher mortality in chronic HD patients. In this research, we tested the hypothesis that ScvO₂ variability is associated with all-cause mortality. Methods: We conducted a retrospective study in 232 chronic HD patients with central venous catheter as vascular access. ScvO₂ was recorded 1× per minute during dialysis using the Crit-Line monitor. A 6-month baseline comprising at least 10 dialysis treatments with ScvO₂ recordings preceded a follow-up period of up to 3 years. The coefficient of variation (CV) of ScvO₂ (100 times the ratio of the standard deviation and mean of ScvO₂) served as a measure of ScvO₂ stability during baseline. Patients were stratified by median population CV of ScvO₂ during baseline, and survival during follow-up was compared between the 2 groups by Kaplan Meier and multivariate Cox analysis. The association between CV of ScvO₂ and all-cause mortality during follow-up was further assessed by Cox analysis with a spline term for CV of ScvO₂. Results: The mean CV ± standard deviation of ScvO₂ in our population was 6.1 ± 2.7% and the median was 5.3%. Univariate Kaplan-Meier analysis (p = 0.043) and multivariate Cox analysis (hazard ratio [HR] 1.16; p = 0.0005) indicated that a CV of ScvO₂ > 5.3% was significantly associated with increased mortality. In Cox analysis with spline term, a CV of ScvO₂ >  11% was associated with a significantly increased HR for all-cause mortality. Conclusion: High ScvO₂ variability during dialysis is associated with increased all-cause mortality.

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Background Maintenance hemodialysis (MHD) patients are particularly vulnerable to COVID-19, a viral disease that may cause interstitial pneumonia, impaired alveolar gas exchange, and hypoxemia. We ascertained the time course of intradialytic arterial oxygen saturation (SaO2) in MHD patients between 4 weeks pre- and the week post-diagnosis of COVID-19. Methods We conducted a quality improvement project in confirmed COVID-19 in-center MHD patients from 11 dialysis facilities. In patients with an arterio-venous access SaO2 was measured 1x/minute during dialysis using the Crit-Line monitor (Fresenius Medical Care, Waltham, MA). We extracted demographic, clinical, treatment, and laboratory data and COVID-19 related symptoms from the patients’ electronic health records. Results Intradialytic SaO2 was available in 52 patients (29 males; age 66.5±15.7 years) contributing 338 hemodialysis treatments. Mean time between onset of symptoms indicative of COVID-19 and diagnosis was 1.1 days (median 0; range 0 to 9). Prior to COVID-19 diagnosis the rate of hemodialysis treatments with hypoxemia, defined as treatment-level average SaO2 < 90%, increased from 2.8% (2 to 4 weeks pre-diagnosis) to 12.2% (1 week) and 20.7% (3 days pre-diagnosis). Intradialytic oxygen supplementation increased sharply post-diagnosis. Eleven patients died from COVID-19 within 5 weeks. Compared to patients who recovered from COVID-19, demised patients showed a more pronounced decline in SaO2 prior to COVID-19 diagnosis. Conclusion In hemodialysis patients, hypoxemia may precede the onset of clinical symptoms and the diagnosis of COVID-19. A steep decline of SaO2 is associated with poor patient outcomes. Measurements of SaO2 may aid the pre-symptomatic identification of patients with COVID-19.

The aim of the paper is to summarize the current understanding of the molecular biology of arteriovenous fistula (AVF). It intends to encourage vascular access teams, care providers, and scientists, to explore new molecular tools for assessing the suitability of patients for AVF as vascular access for maintenance hemodialysis (HD). This review also highlights most recent discoveries and may serve as a guide to explore biomarkers and technologies for the assessment of kidney disease patients choosing to start kidney replacement therapy. Objective criteria for AVF eligibility are lacking partly because the underlying physiology of AVF maturation is poorly understood. Several molecular processes during a life cycle of an AVF, even before creation, can be characterized by measuring molecular fingerprints using newest “omics” technologies. In addition to hypothesis-driven strategies, untargeted approaches have the potential to reveal the interplay of hundreds of metabolites, transcripts, proteins, and genes underlying cardiovascular adaptation and vascular access-related adjustments at any given timepoint of a patient with kidney disease. As a result, regular monitoring of modifiable, molecular risk factors together with clinical assessment could help to reduce AVF failure rates, increase patency, and improve long-term outcomes. For the future, identification of vulnerable patients based on the assessment of biological markers of AVF maturation at different stages of the life cycle may aid in individualizing vascular access recommendations.

Background: Most hemodialysis patients without residual kidney function accumulate fluid between dialysis session that needs to be removed by ultrafiltration. Ultrafiltration usually results in a decline in relative blood volume (RBV). Recent epidemiological research has identified RBV ranges that were associated with significantly better survival. The objective of this work was to develop an ultrafiltration controller to steer a patient’s RBV trajectory into these favorable RBV ranges. Methods: We designed a proportional-integral feedback ultrafiltration controller that utilizes signals from a device that reports RBV. The control goal is to attain the RBV trajectory associated with improved patient survival. Additional constraints such as upper and lower bounds of ultrafiltration volume and rate were realized. The controller was evaluated in in silico and ex vivo bench experiments, and in a clinical proof-of-concept study in two maintenance dialysis patients. Results: In all tests, the ultrafiltration controller performed as expected. In the in silico and ex vivo bench experiments, the controller showed robust reaction toward deliberate disruptive interventions (e.g. signal noise; extreme plasma refill rates). No adverse events were observed in the clinical study. Conclusions: The ultrafiltration controller can steer RBV trajectories toward desired RBV ranges while obeying to a set of constraints. Prospective studies in hemodialysis patients with diverse clinical characteristics are warranted to further explore the controllers impact on intradialytic hemodynamic stability, quality of life, and long-term outcomes.