Mineral and bone disorders are the most common pathology in patients with chronic kidney disease (CKD) resulting in 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 for ligand of receptor activator of nuclear factor NF- kappaB (RANKL), preventing it from binding to receptor (RANKL) 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 circulating levels of OPG characterize patients with severe atherosclerotic lesions. Experimental studies suggest that OPG does not stimulate, 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. Results of these studies revealed accumulation of OPG in the circulation in CKD patients. Additionally, OPG is rather a marker and not the factor involved in the pathogenesis of vascular calcification development o in this group of patients.