Peer-review started: June 4, 2015
First decision: August 14, 2015
Revised: September 23, 2015
Accepted: October 20, 2015
Article in press: October 27, 2015
Published online: January 6, 2016
Processing time: 220 Days and 16.8 Hours
Vascular calcifications are commonly observed in patients with chronic kidney disease (CKD) and contribute to the excessive cardiovascular morbidity and mortality rates observed in these patients populations. Although the pathogenetic mechanisms are not yet fully elucidated, recent evidence suggests a link between bone metabolism and the development and progression of vascular calcifications. Moreover, accumulating data indicate that receptor activator of nuclear factor κB ligand/osteoprotegerin axis which plays essential roles in the regulation of bone metabolism is also involved in extra-osseous bone formation. Further studies are required to establish the prognostic significance of the above biomarkers as predictors of the presence and severity of vascular calcifications in CKD patients and of cardiovascular morbidity and mortality. Moreover, randomized clinical trials are needed to clarify whether inhibition of osteoclast activity will protect from vascular calcifications.
Core tip: Vascular calcifications are commonly observed in chronic kidney disease patients and recently mounting evidence suggest that Receptor activator of nuclear factor κB ligand/osteoprotegerin axis controls both bone metabolism and extra-osseous bone formation. Further studies are required to establish the role of these biomarkers as predictors of the presence and severity of vascular calcifications and of cardiovascular morbidity and mortality. Moreover, randomized clinical trials are needed to clarify whether inhibition of osteoclast activity will protect from vascular calcifications.