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Updated: Mar 30, 2026

Assessment of Vascular Function in Patients With Chronic Kidney Disease
Published on: June 16, 2014
Clinical Considerations for the Association between Vascular Damage and Chronic Kidney Disease
Hirofumi Tomiyama1, Akira Yamashina1
1Department of Cardiology, Tokyo Medical University, Tokyo, Japan.
Insights
Chronic kidney disease (CKD) is linked to cardiovascular disease and vascular damage. Noninvasive methods like ABI can predict kidney function decline, suggesting a vicious cycle.
Area of Science:
- Nephrology
- Cardiology
- Vascular Biology
Background:
- Chronic kidney disease (CKD) is an independent risk factor for cardiovascular disease.
- Noninvasive methods for assessing atherosclerotic vascular damage are increasingly available.
- Understanding the link between CKD and vascular damage is crucial for patient outcomes.
Purpose of the Study:
- To review the association between CKD and vascular damage using noninvasive morphological and functional methods.
- To explore the predictive value of these vascular markers for renal function decline.
- To investigate the potential vicious cycle between renal dysfunction and atherogenic states.
Main Methods:
- Review of prospective studies assessing carotid intima-media thickness (IMT), coronary artery calcium score (CACS), and ankle-brachial index (ABI).
- Evaluation of pulse wave velocity (PWV) as a marker of arterial stiffness.
- Analysis of the predictive value of vascular markers for renal function decline.
Main Results:
- CKD is associated with increased IMT, increased CACS, and decreased ABI.
- A reduced ABI predicts accelerated renal function decline.
- PWV is a marker of arterial stiffness, and CKD may accelerate its progression; functional markers like PWV predict renal function decline rate.
Conclusions:
- Renal dysfunction and atherogenic states may form a vicious cycle, accelerated by vascular abnormalities.
- Reduced ABI is a predictor of accelerated renal function decline.
- Functional vascular markers may predict the rate of renal function decline, suggesting potential therapeutic targets.
Abstract:
Chronic kidney disease (CKD) is an independent risk factor for cardiovascular disease. Recently, noninvasive and simple morphological and functional methods have been introduced to assess atherosclerotic vascular damage. This review describes the association of CKD with vascular damage as assessed by these methods. Carotid intima-media thickness (IMT) and coronary artery calcium score (CACS) are morphological parameters of vascular damage, and an ankle-brachial index (ABI) <0.90 suggests the presence of peripheral arterial disease (i.e., it represents advanced atherosclerosis). Several prospective studies have demonstrated that CKD is a risk factor for an increased IMT, an increased CACS and a decreased ABI. While it has not been clarified whether measuring the IMT or CACS might be useful to predict the progression of renal function decline, a reduced ABI has been demonstrated as a predictor of accelerated renal function decline. On the other hand, pulse wave velocity (PWV) is a marker of arterial stiffness rather than atherosclerosis, reflecting functional abnormalities caused by vascular damage, and moderate-to-severe CKD may be a risk factor for the progression of arterial stiffness. The measurement of functional markers, especially of PWV or pulse pressure, has been demonstrated to be useful to predict the rate of progression of renal function decline. Thus, renal dysfunction and atherogenic states may be components of a vicious cycle, and vascular function abnormalities associated with atherosclerosis may accelerate this cycle. As the next step, we propose to examine whether improvement of vascular function abnormalities can interrupt this vicious cycle.
Related Concept Videos
Chronic Kidney Disease I: Introduction
Chronic Kidney Disease II: Clinical Manifestations
Chronic Kidney Disease IV: Nursing Management
Chronic Kidney Disease III: Interprofessional Care
Acute Kidney Injury IV: Diagnostic Studies and Prevention
Acute Kidney Injury II: Pathophysiology

