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Updated: Dec 6, 2025

Assessment of Vascular Function in Patients With Chronic Kidney Disease
Published on: June 16, 2014
Associations Between Arterial Stiffness Indices and Chronic Kidney Disease Categories in Essential Hypertensive
Hiroshi Kusunoki1,2, Yoshio Iwashima2,3, Yuhei Kawano4
1Department of General Medicine, Hyogo College of Medicine, Nishinomiya, Hyogo, Japan.
Insights
Arterial stiffness, including aortic pulse wave velocity and renal resistive index, is linked to higher chronic kidney disease (CKD) risk in hypertensive patients. Circadian variations in blood pressure and stiffness may contribute to CKD progression.
Area of Science:
- Cardiovascular Medicine
- Nephrology
- Hypertension Research
Background:
- Essential hypertension is a significant risk factor for chronic kidney disease (CKD).
- Arterial stiffness is an independent predictor of cardiovascular events and mortality.
- Early detection of CKD risk in hypertensive patients is crucial for timely intervention.
Purpose of the Study:
- To investigate the association between arterial stiffness indices and asymptomatic chronic kidney disease (CKD) risk categories in hypertensive patients.
- To identify specific arterial stiffness parameters that predict higher CKD risk.
- To explore the role of circadian hemodynamic variations in the relationship between arterial stiffness and CKD.
Main Methods:
- 184 essential hypertensive patients were assessed for arterial stiffness using 24-hour ambulatory blood pressure monitoring, pulse wave velocity (PWV) measurements (aortic and brachial-ankle), and renal resistive index (RI) via ultrasonography.
- Chronic kidney disease (CKD) risk was categorized using Kidney Disease Improving Global Outcomes (KDIGO) criteria, based on estimated glomerular filtration rate and albuminuria.
- Multivariate logistic regression and multivariate regression models were employed to analyze the associations between arterial stiffness indices, circadian hemodynamics, and CKD risk categories.
Main Results:
- 24-hour aortic PWV (aPWV), brachial-ankle PWV (baPWV), and RI demonstrated a significant increase with worsening CKD risk categories (P < 0.01).
- Increased nighttime aortic systolic blood pressure (SBP), PWV, and RI were independently associated with higher CKD stages (ORs ranging from 1.52 to 4.80, P < 0.05).
- Disturbed day-to-night changes in brachial SBP and aPWV were observed, and these circadian variations were linked to intrarenal hemodynamics.
Conclusions:
- Hypertensive patients with higher CKD risk exhibit altered circadian hemodynamics, characterized by elevated nighttime aortic SBP and PWV, and impaired intrarenal hemodynamics.
- Blunted nocturnal blood pressure reduction in these patients may be influenced by disturbed intrarenal hemodynamics and circadian variations in aortic SBP and arterial stiffness.
- Arterial stiffness indices, particularly those reflecting aortic stiffness and intrarenal hemodynamics, are valuable markers for assessing CKD risk in hypertensive individuals.
Background:
This study investigated the association between arterial stiffness indices and asymptomatic chronic kidney disease (CKD) risk categories in hypertensive patients.
Methods:
Arterial stiffness indices, including 24-hour brachial and aortic systolic blood pressure (SBP) and pulse wave velocity (PWV), were measured by an oscillometric Mobil-O-Graph device, brachial-ankle PWV (baPWV) by a volume-plethysmographic method, and renal resistive index (RI) by ultrasonography, in 184 essential hypertensive patients (66.0 ± 17.1 years, 47.3% male). CKD was categorized into 3 stages based on the Kidney Disease Improving Global Outcomes (KDIGO) criteria, using a combination of estimated glomerular filtration and albuminuria.
Results:
The 24-hour aortic PWV (aPWV), baPWV, and RI increased with worsening severity of CKD risk category (all P < 0.01 for trend). Multivariate logistic regression analysis found that a 1 SD increase of nighttime aortic SBP (odds ratio [OR] 1.52), PWV (OR 4.80), or RI (OR 1.75) was an independent predictor of high or very-high CKD stage (all P < 0.05). After adjustment for potential confounders, day-to-night change in brachial SBP as well as in aPWV differed among groups (P < 0.05, respectively). In a multivariate regression model, day-to-night changes in aortic SBP and PWV, and RI were independently associated with day-to-night brachial SBP change.
Conclusions:
In hypertension, circadian hemodynamics in high CKD stage are characterized by higher nighttime values of aortic SBP and PWV and disturbed intrarenal hemodynamics. Further, the blunted nocturnal BP reduction in these patients might be mediated via disturbed intrarenal hemodynamics and circadian hemodynamic variation in aortic SBP and arterial stiffness.
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