Abstract
Chronic kidney disease (CKD) is associated with excess cardiovascular mortality, resulting from both traditional and nontraditional, CKD-specific, cardiovascular risk factors. Nontraditional risk factors include the entity Chronic Kidney Disease–Mineral and Bone Disorder (CKD-MBD) which is characterised by disorders of bone and mineral metabolism, including biochemical abnormalities of hyperphosphatemia and hyperparathyroidism, renal osteodystrophy, and vascular calcification. Increased arterial stiffness in the CKD population can be attributed amongst other influences to progression of vascular calcification, with significant resultant contribution to the cardiovascular disease burden. Pulse wave velocity (PWV) measured over the carotid-femoral arterial segments is the noninvasive gold-standard technique for measurement of aortic stiffness and has been suggested as a surrogate cardiovascular end-point. A PWV value of 10 m/s or greater has been recommended as a suitable cut-off for an increased risk of cardiovascular mortality. CKD is a risk factor for an excessive rate of increase in aortic stiffness, reflected by increases in PWV, and increased aortic PWV in CKD shows faster progression than for individuals with normal kidney function. Patients with varying stages of CKD, as well as those on dialysis or with a kidney transplant, have different biological milieu which influence aortic stiffness and associated changes in PWV. This review discusses the pathophysiology of arterial stiffness with CKD and outlines the literature on PWV across the spectrum of CKD, highlighting that determination of arterial stiffness using aortic PWV can be a useful diagnostic and prognostic tool for assessing cardiovascular disease in the CKD population.
Highlights
Chronic kidney disease (CKD) is increasingly recognised globally as a major public health problem
This review briefly outlines the pathophysiology of increased arterial stiffness in patients with CKD and discusses the use of pulse wave velocity (PWV) to assess arterial stiffness, as well as PWV changes mediated by interventions in clinical trials, in this population
Elevated serum phosphate is a late manifestation of CKD and has been shown to accelerate mineral deposition in vessel walls leading to increased vascular calcification and arterial stiffness. α-Klotho and fibroblast growth factor 23 (FGF-23) are emerging factors in Chronic Kidney Disease–Mineral and Bone Disorder (CKD-MBD) and are thought to be involved in the pathogenesis of vascular calcification [16, 17]
Summary
Chronic kidney disease (CKD) is increasingly recognised globally as a major public health problem. Increased carotid-femoral aortic stiffness, as measured by segmental pulse wave velocity (PWV), is a strong, independent predictor of cardiovascular mortality in this population [5, 6]. Carotid-femoral PWV is utilised as the noninvasive gold standard measure of arterial stiffness, with assessment of changes in vascular stiffness having been advocated as a suitable surrogate cardiovascular end-point in clinical trials. Development of vascular calcification and arterial stiffness observed with progression of CKD results in a different age-related pattern of PWV change than in the disease-free normal population. This review briefly outlines the pathophysiology of increased arterial stiffness in patients with CKD and discusses the use of PWV to assess arterial stiffness, as well as PWV changes mediated by interventions in clinical trials, in this population
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
