Editorial
Copyright ©The Author(s) 2016. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Nephrol. Jan 6, 2016; 5(1): 1-5
Published online Jan 6, 2016. doi: 10.5527/wjn.v5.i1.1
Receptor activator of nuclear factor κB ligand/osteoprotegerin axis and vascular calcifications in patients with chronic kidney disease
Michalis Spartalis, Aikaterini Papagianni
Michalis Spartalis, Aikaterini Papagianni, Department of Nephrology, Aristotle University of Thessaloniki, “Hippokration” General Hospital, 54642 Thessaloniki, Greece
Author contributions: Sartalis M made the literature search and wrote the first draft of the manuscript; Papagianni A critically reviewed the literature and wrote the final form of the manuscript.
Conflict-of-interest statement: The authors declare no conflict of interest.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Aikaterini Papagianni, MD, PhD, Associate Professor, Department of Nephrology, Aristotle University of Thessaloniki, “Hippokration” General Hospital, Papanastasiou 50 Str, 54642 Thessaloniki, Greece. aikpapag@otenet.gr
Telephone: +30-2310-992856 Fax: +30-2310-892382
Received: May 31, 2015
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
Core Tip

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.