Journal of Endocrinological Investigation

, Volume 34, Issue 4, pp 317–323

Vitamin K, bone fractures, and vascular calcifications in chronic kidney disease: An important but poorly studied relationship


    • Department of Medical and Surgical Sciences, Clinica Medica 1University of Padova. Policlinico IV piano
  • G. Crepaldi
    • CNR Aging SectionInstitute of Neuroscience
  • S. Maggi
    • CNR Aging SectionInstitute of Neuroscience
  • F. Galli
    • Laboratory of Biochemistry and Nutrition, Department of Internal Medicine, School of PharmacyUniversity of Perugia
  • A. D’Angelo
    • Nephrology UnitUniversity of Padua
  • L. Calò
    • Department of Clinical and Experimental Medicine, Medical Clinic 4University of Padua
  • S. Giannini
    • Department of Medical and Surgical Sciences, Clinica Medica 1University of Padova. Policlinico IV piano
  • D. Miozzo
    • CNR Aging SectionInstitute of Neuroscience
  • M. Gallieni
    • Nephrology and Dialysis UnitOspedale San Carlo Borromeo
Review Article

DOI: 10.1007/BF03347093

Cite this article as:
Fusaro, M., Crepaldi, G., Maggi, S. et al. J Endocrinol Invest (2011) 34: 317. doi:10.1007/BF03347093


Vitamin K denotes a group of lipophilic vitamins determining post- translational modification of proteins. There are 2 main forms of vitamin K: vitamin K1 (phylloquinone, found in vegetables); vitamin K2 (menaquinone, produced by bacteria in the intestine and in fermented foods). Vitamin K stores are limited in humans, but it can be recycled. Vitamin K1 is principally transported to the liver, regulating the production of coagulation factors. Vitamin K2, instead, is also transported to extra- hepatic tissues, such as bone and arteries, regulating the activity of matrix Gla- protein (MGP) and osteocalcin [bone Gla- protein (BGP)]. In patients with chronic kidney disease (CKD), cardiovascular mortality is the first cause of death. Some pathogenetic mechanisms of vascular calcification (such as hyperparathyroidism, hyperphosphatemia, hypercalcemia, role of vitamin D) have been widely investigated, but the potential role of vitamin K is still uncertain. Vitamin K could play a key role, as it transforms glutamic acid residues into γ- carboxyglutamic acid, through a carboxylation process, makings both MGP (cMGP) and BGP (cBGP) biologically active. cMGP inhibits vascular calcifications (VC), while cBGP has an important role for a proper mineralization process. Uncarboxylated MGP and BGP (ucMGP and ucBGP) concentrations are indirect markers of vitamin K2 deficiency. The purpose of this review is to analyze the current literature to understand the relationship between vitamin K2 status, fragility fractures and VC in CKD patients. This analysis could be of help in planning investigations of Vitamin K status and its possible supplementation in CKD patients to avert fragility fractures and VC.


Dialysisfracturesmenaquinoneosteoporosisphylloquinonevascular calcifications

Copyright information

© Italian Society of Endocrinology (SIE) 2011