Vitamin K and cardiovascular calcification in CKD: is patient supplementation on the horizon?  Maurizio Gallieni, Maria Fusaro  Kidney International  Volume 86, Issue 2, Pages 232-234 (August 2014) DOI: 10.1038/ki.2014.24 Copyright © 2014 International Society of Nephrology Terms and Conditions

Figure 1 Vitamin K cycle. Conversion of glutamate (Glu) to γ-carboxyglutamate (Gla) residues by γ-glutamyl carboxylase (GGCX) (1) is essential for the activation of vitamin K–dependent (VKD) proteins. γ-Carboxylation transforms undercarboxylated (ucVKD) into carboxylated (cVKD) proteins. Vitamin K hydroquinone (KH2) is oxidized to vitamin K epoxide (KO). KO is converted to vitamin K quinone by vitamin K epoxide reductase (2). A similar reductase enzymatic reaction (2) converts vitamin K quinone back into KH2. Another reductase, NAD(P)H-dependent vitamin K reductase (3), or DT-diaphorase, can also catalyze the same conversion into KH2. Warfarin inhibits the reductase activity (2) that is dithiol dependent but not the NADPH-dependent reductase (3), whose substrate can be dietary vitamin K. Kidney International 2014 86, 232-234DOI: (10.1038/ki.2014.24) Copyright © 2014 International Society of Nephrology Terms and Conditions