Exploring the role of vascular frailty in understanding blood pressure variability and mortality risk among end-stage kidney disease patients undergoing hemodialysis

Abstract

Dong et al. investigated the relationship between interdialytic home blood pressure variability (BPV) and mortality in individuals with end-stage kidney disease (ESKD) undergoing hemodialysis.¹ Their study revealed a notable correlation between increasing home BPV and a stepwise escalation in the risk of all-cause mortality among this population. In the discussion, the authors attributed this association to comorbid cardiovascular diseases, diabetes, systemic inflammation, and higher vascular stiffness. We believe that a more comprehensive characterization of vascular integrity impairment is needed to explain this BPV-outcome association.

Our team previously introduced the concept of vascular frailty, which elucidates vascular structural and functional degeneration leading to physical frailty or the coexistence of both phenotypes.² Vascular tissues are exquisitely susceptible to adverse consequences related to tissue senescence from chronological aging and metabotoxic stimuli, particularly uremic toxins. Vascular frailty manifests through structural degenerations such as vascular calcification and atherosclerosis, as well as functional perturbations like increased stiffness and vasomotor dysfunction. Uremic toxins predispose individuals with chronic kidney disease to developing physical frailty³ and contribute to the pathogenesis of vascular frailty by inducing vascular calcification and increasing vascular stiffness,⁴ thereby leading to higher BPV. It is widely acknowledged that ESKD patients are prone to developing vascular calcification over time. Moreover, individuals with ESKD exhibit accelerated aging and heightened tissue wear, culminating in physical frailty that significantly elevates mortality risk. Our previous findings demonstrated that ESKD patients with frailty faced a significantly higher risk of mortality compared with those without.⁵

From this perspective, we recommend that the authors consider incorporating additional features of vascular frailty, such as measurements of vascular calcification severity and evidence of autonomic dysfunction, in their assessments of these patients. Doing so will facilitate a more thorough understanding of the mechanisms underlying the BPV-outcome association.

Szu-Ying Lee and Chia-Ter Chao are responsible for drafting of this manuscript.

The authors declare no conflict of interest.