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Revista de Osteoporosis y Metabolismo Mineral

versión On-line ISSN 2173-2345versión impresa ISSN 1889-836X


MARTINEZ ARIAS, L. et al. Effect of RANK/RANKL/OPG pathway on bone demineralization and vascular calcification in chronic kidney disease. Rev Osteoporos Metab Miner [online]. 2016, vol.8, n.4, pp.105-114. ISSN 2173-2345.

Introduction: In cases of chronic kidney disease (CKD), bone and mineral metabolism changes occur which favor soft tissue calcification. Alterations in the RANK/RANKL/OPG system could also favor vascular calcification, a major cause of morbidity and mortality in CKD. Objective: In an in vivo experimental model of chronic renal failure progression, we assess the effect of CKD on vascular calcification and bone loss correlating these changes in the RANK/RANKL/OPG pathway. An in vitro system was used to confirm findings. Material and Methods: Two models of vascular calcification were used: an in vivo rat model with chronic renal failure fed on a diet with different phosphorus content, and an in vitro model in vascular smooth muscle cells (VSMC) subjected to different calcifying stimuli. Results: At 20 weeks, 50% of animals with a diet high in phosphorus presented aortic calcification accompanied by increased aortic expression of RANKL. In contrast, OPG decreased probably as a consequence of an inflammatory component. At 20 weeks, expression of RANKL and OPG in the tibia increased, while the increase in OPG occurred at earlier stages. In VSMC, the addition of uremic serum and calcification medium increased calcium content and expression of RANKL and OPG. The addition of OPG and silencing of RANK inhibited this increase. Conclusions: Our results confirm RANK/RANKL/OPG system involvement in the vascular calcification process.

Palabras clave : RANK; RANKL; OPG; chronic kidney disease; vascular calcification.

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