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

2. 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  , DOI: ( /ki )
Copyright © 2014 International Society of Nephrology Terms and Conditions