Receptor activator of nuclear factor κB ligand/osteoprotegerin axis and vascular calcifications in patients with chronic kidney disease

Abstract

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.Spartalis M, Papagianni A. Receptor activator of nuclear factor κB ligand/osteoprotegerin axis and vascular calcifications in patients EDITORIAL 1 January 6, 2016|Volume 5|Issue 1|

Serum Osteoprotegerin Is a Potential Biomarker of Insulin Resistance in Chinese Postmenopausal Women with Prediabetes and Type 2 Diabetes

“…The serum OPG was significantly increased in patients with chronic kidney disease. Recent evidences suggest that inflammation, secondary hyperparathyroidism, disorder of bone metabolism, vascular calcifications, and atherosclerosis may play important roles in this process [ 47 ].…”

Elevated Circulating Osteoprotegerin Levels in the Plasma of Hemodialyzed Patients With Severe Artery Calcification

“…It is involved in the regulation of tissue calcification, controls bone resorption by inhibiting osteoclastogenesis and is highly expressed in many different cell types such as osteoblasts, heart, lung, kidney, liver, spleen, bone marrow, articular chondrocytes and lymph nodes . As a decoy receptor for the receptor activator of nuclear factor κB ligand (RANKL), OPG inhibits differentiation of osteoclasts . While OPG acts as a soluble bone protector, RANKL is considered to be a stimulator of bone resorption through the induction of osteoclastic differentiation and activation of mature osteoclasts.…”