The role of osteoprotegerine in pathogenesis of mineral and bone disorders in chronic kidney disease (CKD-MBD)

Journal Title: Annales Academiae Medicae Silesiensis - Year 2014, Vol 68, Issue 4

Abstract

Mineral and bone disorders are the most common pathology in patients with chronic kidney disease (CKD) resulting in the development of accelerated atherosclerosis. Therefore, they are considered as non-traditional cardiovascular risk factors and the cause of increased morbidity and mortality, especially in patients on renal replacement therapy. Osteoprotegerin (OPG) is an important physiological regulator of osteoclastogenesis. As decoy receptor, it binds to the receptor activator of nuclear factor NF- kappaB ligand (RANKL), preventing it from binding to the (RANK) receptor and maturation of osteoclast precursors. The physiological role of OPG, beyond the regulatory function of bone turnover is the inhibition of cell apoptosis induced by inflammatory processes. Elevated levels of circulating OPG is observed in patients with severe atherosclerotic lesions. The experimental studies suggest that OPG does not stimulate, but on the contrary, inhibits the process of atherogenesis. This paper provides an overview of the available literature presenting the role of OPG in the pathogenesis of mineral and bone disorders in CKD. The results of these studies revealed the accumulation of circulating OPG in CKD patients. Additionally, OPG is rather a marker and not a factor involved in the pathogenesis of vascular calcification development in this group of patients.

Authors and Affiliations

Marzena Żelaźnicka-Wilk, Jarosław Wajda, Magdalena Olszanecka-Glinianowicz, Jerzy Chudek

Keywords

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  • EP ID EP376544
  • DOI -
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How To Cite

Marzena Żelaźnicka-Wilk, Jarosław Wajda, Magdalena Olszanecka-Glinianowicz, Jerzy Chudek (2014). The role of osteoprotegerine in pathogenesis of mineral and bone disorders in chronic kidney disease (CKD-MBD). Annales Academiae Medicae Silesiensis, 68(4), 255-260. https://europub.co.uk/articles/-A-376544