Coagulation meets calcification: the vitamin K system

Int J Artif Organs. 2009 Feb;32(2):67-74. doi: 10.1177/039139880903200202.


Morbidity and mortality are massively increased in patients with chronic kidney disease (CKD) and patients with end-stage renale disease (ESRD). Bone disease (renal osteodystrophy) and vascular disease (accelerated arteriosclerosis) are two typical entities contributing to this excess morbidity and mortality. Vitamin K and vitamin K-dependent-proteins play pivotal roles in the physiology of mineralization and in preventing ectopic calcification: two of these vitamin K-dependent-proteins are osteocalcin (regulating bone mineralization) and matrix-Gla protein (MGP, local calcification inhibitor in the vessel wall). Vitamin K deficiency impairs the physiological function of osteocalcin and MGP and, therefore, presumably contributes to bone demineralisation and vascular calcification (the so-called calcification paradox). In this context, the usage of vitamin K antagonists for long-term oral anticoagulation therapy might be risky especially in CKD patients exhibiting a high background level of vascular calcification. We present a summary of data describing the potential role of vitamin K deficiency and supplementation in bone and vascular disease in patients with CKD or ESRD.

Publication types

  • Review

MeSH terms

  • Blood Coagulation Factors / physiology
  • Calcinosis / etiology*
  • Calcinosis / metabolism
  • Calcinosis / pathology
  • Calcium-Binding Proteins / physiology
  • Cardiovascular Diseases / etiology*
  • Cardiovascular Diseases / metabolism
  • Cardiovascular Diseases / prevention & control
  • Extracellular Matrix Proteins / physiology
  • Humans
  • Kidney Failure, Chronic / complications*
  • Kidney Failure, Chronic / metabolism
  • Kidney Failure, Chronic / pathology
  • Vitamin K / physiology*


  • Blood Coagulation Factors
  • Calcium-Binding Proteins
  • Extracellular Matrix Proteins
  • matrix Gla protein
  • Vitamin K