Key result
Estimated pulse wave velocity (ePWV1) correlated strongly with carotid-femoral pulse wave velocity (r = 0.729, p = 0.002) and was significantly elevated in CKD patients compared to controls.
Why the study?
The clinical relevance, accuracy, and effectiveness of blood pressure-estimated pulse wave velocity (ePWV) in relation to renal function and cardiometabolic conditions in CKD patients remain unclear.
Does estimated pulse wave velocity (ePWV) accurately reflect measured arterial stiffness and correlate with cardiometabolic parameters in patients with chronic kidney disease?
Cross-Sectional (n=230)
Does estimated pulse wave velocity (ePWV) accurately reflect measured arterial stiffness and correlate with cardiometabolic parameters in patients with chronic kidney disease?
Effect estimate: r = 0.729
p-value: p=0.002
Estimated pulse wave velocity calculated from blood pressure correlates strongly with measured carotid-femoral pulse wave velocity and identifies early vascular and cardiac alterations in CKD patients.
Objective: In chronic kidney disease (CKD), including IgA nephropathy (IgAN) and autosomal dominant polycystic kidney disease (ADPKD), carotid-femoral pulse wave velocity (cfPWV) has important prognostic value. Recent studies indicate that pulse wave velocity can also be estimated using blood pressure values (ePWV); however, the clinical relevance, accuracy, and effectiveness of ePWV in relation to renal function and cardiometabolic conditions in CKD patients remain unclear. Design and method: A total of 130 IgAN patients (mean age 54.9 years), 50 ADPKD patients, and 50 controls were included. ePWV was calculated by two formulas (ePWV1 and ePWV2) and compared with three arterial stiffness measures: photoplethysmographic stiffness index (SI), oscillometric aortic PWVao, and applanation tonometry cfPWV. NT-proBNP levels were measured via enzyme-linked immunoassay, and echocardiography was performed for further cardiac assessment. Results: Results indicated a strong correlation between ePWV1 and cfPWV (r = 0.729, p = 0.002) and ePWV2 and cfPWV (r = 0.332, p = 0.002), but no correlation with SI and PWVao. IgAN patients were categorized into CKD1-2 and CKD3-5 groups; the CKD3-5 group exhibited higher ePWV1 (p = 0.001) and ePWV2 (p = 0.001) than CKD1-2. In comparison to a control group with preserved eGFR, IgAN CKD1-2 and CKD3-5 demonstrated significantly elevated ePWV1 and ePWV2 (p < 0.001; p = 0.001). In ADPKD patients, ePWV1 and ePWV2 were also significantly higher than in IgAN patients (p = 0.001; p = 0.003). Then we divided the patients into two groups based on the ePWV1 median results (9 m/s). Higher ePWV1 groups (> 9.0 m/s) exhibited significantly lower E/A ratios (0.9 vs. 1.16; p < 0.001), higher LVMI (112.87 vs. 100.95 g/m2; p = 0.01), NT-proBNP (313.76 vs. 137.43; p = 0.009), and SBPao (131.87 vs. 111.91; p < 0.001). The independent predictors of ePWV1 were age, waist/hip ratio, aortic pulse pressure, E/A, NT-proBNP, cfPWV and PWVao by multivariate regression analysis. Conclusions: Simple ePWV1 calculation correlates strongly with cfPWV, indicating its effectiveness for estimating vascular stiffness linked to renal function in CKD patients, highlighting early vascular alterations compared to controls.
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Sági et al. (2026) conducted a cross-sectional in Chronic kidney disease (IgA nephropathy and ADPKD) (n=230). Estimated pulse wave velocity (ePWV) vs. Controls with preserved eGFR / Lower ePWV was evaluated on Correlation between ePWV1 and cfPWV (r = 0.729, p=0.002). Estimated pulse wave velocity (ePWV1) correlated strongly with carotid-femoral pulse wave velocity (r = 0.729, p = 0.002) and was significantly elevated in CKD patients compared to controls.
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