Editorial comment on Vitamin K and vascular calcification in chronic kidney disease: An update of current evidence – The role of Vitamin K in managing chronic kidney disease–mineral bone disorder

Yi‑Chou Hou^a, Kuo‑Cheng Lu^b,c*

 

^aDivision of Nephrology, Department of Medicine, Cardinal‑Tien Hospital, School of Medicine, Fu‑Jen Catholic University, New Taipei, Taiwan; ^bDivision of Nephrology, Department of Medicine, Taipei Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, New Taipei, Taiwan; ^cSchool of Medicine, Tzu Chi University, Hualien, Taiwan

 

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Open Access funded by Buddhist Compassion Relief Tzu Chi Foundation

 

Cardiovascular disease poses the major cause of mortality in chronic kidney disease (CKD) patients. Vascular calcification (VC) is the most pathogenesis of cardiovascular morbidities in CKD patients. Beyond the traditional risk factors, secondary hyperparathyroidism and sequential osteodystrophy accelerate the VC by increasing the extraosseous deposition of calcium apatite [1]. The excessive osteoclastic activity with uncoupled bone formation increased the calcium and phosphorus release under the high bone turnover status, and the deficiency of calcifying inhibitors such as fetuin‑A or matrix Gla protein worsens the extraosseous calcification [2]. Therefore, the nutrients supplement for enhancing bone formation and the calcifying inhibition should be regarded as the preventive strategy for lowering the incidence of cardiovascular complications in CKD subjects. Vitamin K, as the main factor for carboxylation, might be an important niche for treating CKD–mineral bone disorder (CKD–MBD) and VC. In this issue, Lin and Hsu made an extensive review of Vitamin K and VC in CKD [3].