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Updated: May 8, 2026
Assessment of Vascular Function in Patients With Chronic Kidney Disease
Published on: June 16, 2014
Impaired renal function impacts negatively on vascular stiffness in patients with coronary artery disease
Insights
Impaired kidney function increases vascular stiffness, a key indicator of cardiovascular risk, even in patients with coronary artery disease. This link appears driven by inflammation and cell adhesion markers.
Area of Science:
- Cardiovascular Medicine
- Nephrology
- Vascular Biology
Background:
- Chronic kidney disease (CKD) and coronary artery disease (CAD) are independent risk factors for increased vascular stiffness.
- Vascular stiffness is a predictor of cardiovascular events.
Purpose of the Study:
- To investigate if renal function impacts vascular stiffness independently of CAD.
- To explore the relationship between renal function, vascular stiffness, and inflammatory markers.
Main Methods:
- 160 patients with CAD and 169 controls were studied.
- Estimated glomerular filtration rate (eGFR) assessed renal function; impaired function defined as eGFR <60 mL/min.
- Carotid-femoral pulse wave velocity (PWV) measured vascular stiffness; plasma biomarkers analyzed.
Main Results:
- Patients with CAD and impaired renal function exhibited significantly higher PWV than those with CAD and normal renal function (10.2 vs 7.3 m/s).
- PWV was inversely correlated with eGFR (β = -0.293, P < 0.001) after adjusting for multiple clinical factors.
- Impaired renal function in CAD patients was associated with elevated E-selectin and osteopontin, markers of cell adhesion and inflammation.
Conclusions:
- Renal function is a significant determinant of vascular stiffness, even in severe atherosclerotic disease.
- Inflammatory processes and cell adhesion molecule expression may mediate the link between impaired renal function and increased vascular stiffness.
- These findings suggest vascular remodeling due to inflammation contributes to stiffness in CKD patients, irrespective of CAD.
Background:
Chronic kidney disease (CKD) and coronary artery disease (CAD) are independently associated with increased vascular stiffness. We examined whether renal function contributes to vascular stiffness independently of CAD status.
Methods:
We studied 160 patients with CAD and 169 subjects without CAD. The 4-variable MDRD formula was used to estimate glomerular filtration rate (eGFR); impaired renal function was defined as eGFR <60 mL/min. Carotid-femoral pulse wave velocity (PWV) was measured with the SphygmoCor® device. Circulating biomarkers were assessed in plasma using xMAP® multiplexing technology.
Results:
Patients with CAD and impaired renal function had greater PWV compared to those with CAD and normal renal function (10.2 [9.1;11.2] vs 7.3 [6.9;7.7] m/s; P < 0.001). In all patients, PWV was a function of eGFR (β = -0.293; P < 0.001) even after adjustment for age, sex, systolic blood pressure, body mass index and presence or absence of CAD. Patients with CAD and impaired renal function had higher levels of adhesion and inflammatory molecules including E-selectin and osteopontin (all P < 0.05) compared to those with CAD alone, but had similar levels of markers of oxidative stress.
Conclusions:
Renal function is a determinant of vascular stiffness even in patients with severe atherosclerotic disease. This was paralleled by differences in markers of cell adhesion and inflammation. Increased vascular stiffness may therefore be linked to inflammatory remodeling of the vasculature in people with impaired renal function, irrespective of concomitant atherosclerotic disease.
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