Abstract: PUB040
Vascular Stiffness in CKD: Pathophysiology, Prognostic Significance, and Therapeutic Implications
Session Information
Category: Cardiovascular-Kidney-Metabolic Health
- 602 Cardiovascular-Kidney-Metabolic Health: Clinical
Authors
- Adel, Edris, MedStar Georgetown University Hospital, Washington, District of Columbia, United States
- Pourafshar, Negiin, MedStar Georgetown University Hospital, Washington, District of Columbia, United States
Background
Cardiovascular disease (CVD) is the leading cause of morbidity and mortality in chronic kidney disease (CKD). Traditional risk models, including the Framingham Risk Score, underestimate the excess cardiovascular burden of CKD. Vascular stiffness has emerged as a surrogate marker reflecting endothelial dysfunction, inflammation, oxidative stress, vascular smooth muscle cell transformation, extracellular matrix remodeling, and vascular calcification. These changes reduce arterial compliance and contribute to hypertension, widened pulse pressure, left ventricular hypertrophy, and adverse cardiovascular outcomes.
Methods
This narrative review summarizes the pathophysiology, prognostic significance, and therapeutic modulation of vascular stiffness in CKD. Studies evaluating carotid-femoral pulse wave velocity (cfPWV), central blood pressure, and augmentation index were reviewed. Interventions included renin-angiotensin-aldosterone system blockade, calcium channel blockers, mineralocorticoid receptor antagonists, dialysis optimization, statins, exercise, and kidney transplantation.
Results
Arterial stiffness is independently associated with cardiovascular events, CKD progression, and mortality in non-dialysis and dialysis populations. cfPWV is the gold-standard noninvasive measure and consistently predicts adverse outcomes. Several therapies improve vascular stiffness beyond blood pressure reduction. RAAS blockade, calcium channel blockers, and mineralocorticoid receptor antagonists reduce vascular remodeling and fibrosis. Optimized dialysis improves volume control and lowers uremic toxin exposure. Statins, exercise, and kidney transplantation also improve vascular stiffness. Limitations include lack of standardized measurement techniques, uncertain therapeutic targets, and few large randomized trials linking PWV reduction to improved outcomes.
Conclusion
Vascular stiffness is a clinically relevant and potentially modifiable biomarker that provides prognostic information beyond traditional cardiovascular risk factors in CKD. Noninvasive measures such as cfPWV may improve risk stratification and treatment monitoring. Further randomized studies are needed to standardize assessment methods, define treatment thresholds, and determine whether reducing vascular stiffness improves cardiovascular and renal outcomes.