Vascular calcification.

PURPOSE OF REVIEW

This review presents new evidence related to molecular mechanisms involved in the process of cardiovascular calcification, as well as to discuss new biomarkers and novel therapeutic strategies related to vascular calcification in chronic kidney disease (CKD) patients.

RECENT FINDINGS

microRNAs have emerged as potential players in the genesis of osteo-chondrogenic transformation, depending on the stimulus and the localization of vascular calcification. The disturbances of the fibroblast growth factor-23 (FGF23)/alpha-Klotho (Klotho) axis observed in CKD appear to play an important role in CKD-associated vascular calcification. Numerous studies have identified circulating biomarkers potentially responsible for vascular calcification and have evaluated their link with this process. The respective role of these biomarkers is not yet elucidated. Beyond phosphate binders, modulation of calcium-sensing receptor and vitamin K supplementation come into sight as new potential strategies to prevent cardiovascular calcification.

CONCLUSION

A better understanding of the molecular mechanisms which are responsible for cardiovascular calcification have led to a better detection and more adequate follow-up of this pathologic process, as well as the identification of novel therapeutic targets. Whether these new insights will lead to improved care and better survival of CKD patients with cardiovascular calcification remains to be demonstrated.