Key result
Endothelial dysfunction is linked to exaggerated systolic BP responses to maximal exercise in CKD.
Why the study?
Exaggerated exercise systolic BP increases are common in CKD, but whether endothelial dysfunction assessed by the simpler, operator-independent EndoPAT method relates to these responses was untested.
Is endothelial dysfunction assessed by EndoPAT associated with exaggerated systolic blood pressure responses during maximal exercise in patients with CKD?
Observational (n=23)
Is endothelial dysfunction assessed by EndoPAT associated with exaggerated systolic blood pressure responses during maximal exercise in patients with CKD?
Endothelial dysfunction measured by EndoPAT is associated with exaggerated systolic blood pressure responses to maximal exercise in patients with CKD, suggesting RHI may serve as a practical biomarker for cardiovascular risk.
Answers are grounded in this paper and cite their sources.
Exaggerated exercise systolic BP rise may signal endothelial dysfunction; leaves open its role in risk stratification pending validation.
Exaggerated increases in systolic blood pressure (BP) during exercise are common in patients with chronic kidney disease (CKD) and may reflect underlying vascular dysfunction. Prior work has shown that endothelial function measured using the gold-standard brachial artery flow-mediated dilation (FMD) is correlated with exaggerated BP responses during cardiopulmonary exercise testing (CPET) in CKD. Endothelial function can also be assessed using peripheral arterial tonometry (EndoPAT) that is simpler and faster to use, not operator-dependent and calculates the reactive hyperemia index (RHI) with low measures indicating endothelial dysfunction. Therefore, we tested the hypothesis that endothelial dysfunction assessed by EndoPAT relates to exaggerated BP responses during CPET in CKD. We studied 23 patients with CKD (stages III–IV; 63 ± 10 years) who completed a CPET with brachial BP measured every 2 minutes and underwent endothelial function testing via EndoPAT on separate days. The change in systolic BP from baseline to peak exercise (∆SBP) was calculated, and its relationship with endothelial function (RHI) was examined using correlation analyses. Patients with CKD showed a wide inter-individual variability in BP responses to exercise. RHI values were consistent with reduced endothelial function in many of the participants. We found a significant negative correlation between ∆SBP and RHI (R= -0.533; P = 0.025), indicating that individuals with poorer endothelial function exhibited larger rises in systolic BP during exercise. In contrast, traditional markers of kidney function such creatinine and eGFR were not significantly correlated with ∆SBP (R = 0.128, P = 0.601; and R = −0.073, P = 0.768, respectively). In patients with CKD, endothelial dysfunction measured by EndoPAT was associated with exaggerated systolic BP responses to maximal exercise. These findings suggest that impaired endothelial-dependent vasodilation may contribute to abnormal hemodynamic responses during exercise in CKD, and that EndoPAT-derived RHI may serve as a practical biomarker for identifying patients at higher cardiovascular risk from exercise-induced BP increases. This abstract was presented at the American Physiology Summit 2026 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.
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Niu et al. (2026) conducted an observational in Chronic kidney disease (CKD) (n=23). EndoPAT (reactive hyperemia index) was evaluated on Relationship between change in systolic BP from baseline to peak exercise (∆SBP) and endothelial function (RHI) (R= -0.533, p=0.025). Endothelial dysfunction measured by EndoPAT (RHI) was significantly and inversely correlated with exaggerated systolic BP responses to maximal exercise in patients with CKD (R= -0.533; P=0.025).
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