TY - JOUR
T1 - Vascular calcification and arterial stiffness in chronic kidney disease: implications and management
AU - Toussaint, Nigel David
AU - Kerr, Peter
PY - 2007
Y1 - 2007
N2 - Cardiovascular (CV) disease is the commonest cause of mortality in patients with chronic kidney
disease (CKD). Vascular calcification (VC), induced by calcium and phosphate excess and uraemia, is a major
risk factor and is independently associated with CV events and death. Local and systemic calcium-regulatory
proteins as well as inhibitory extracellular factors are involved in the pathogenesis of VC. In CKD the balance
becomes dysregulated leading to differentiation of vascular smooth muscle cells into phenotypically distinct
osteoblast-like cells with subsequent ossification of the arterial wall. Associated with imbalances in mineral
metabolism, VC has intimate interactions with bone mineralization and enhanced bone resorption. Arterial
stiffness represents the functional disturbance of VC, with reduced compliance of large arteries, and predominantly
results from greater medial calcification. As with VC, arterial stiffness is an independent predictor of CV
mortality and patients with CKD have greater arterial stiffness than the general population resulting in the principal
consequences of left ventricular hypertrophy and altered coronary perfusion. Both VC and arterial stiffness can
be measured through non-invasive techniques involving computed tomography, ultrasound, echocardiography,
and pulse wave velocity.
AB - Cardiovascular (CV) disease is the commonest cause of mortality in patients with chronic kidney
disease (CKD). Vascular calcification (VC), induced by calcium and phosphate excess and uraemia, is a major
risk factor and is independently associated with CV events and death. Local and systemic calcium-regulatory
proteins as well as inhibitory extracellular factors are involved in the pathogenesis of VC. In CKD the balance
becomes dysregulated leading to differentiation of vascular smooth muscle cells into phenotypically distinct
osteoblast-like cells with subsequent ossification of the arterial wall. Associated with imbalances in mineral
metabolism, VC has intimate interactions with bone mineralization and enhanced bone resorption. Arterial
stiffness represents the functional disturbance of VC, with reduced compliance of large arteries, and predominantly
results from greater medial calcification. As with VC, arterial stiffness is an independent predictor of CV
mortality and patients with CKD have greater arterial stiffness than the general population resulting in the principal
consequences of left ventricular hypertrophy and altered coronary perfusion. Both VC and arterial stiffness can
be measured through non-invasive techniques involving computed tomography, ultrasound, echocardiography,
and pulse wave velocity.
UR - http://www3.interscience.wiley.com.ezproxy.lib.monash.edu.au/cgi-bin/fulltext/118522634/PDFSTART
U2 - 10.1111/j.1440-1797.2007.00823.x
DO - 10.1111/j.1440-1797.2007.00823.x
M3 - Article
SN - 1320-5358
VL - 12
SP - 500
EP - 509
JO - Nephrology
JF - Nephrology
IS - 5
ER -