Vascular calcification in chronic kidney disease: vitamin K deficiency and new mediators

This thesis discusses vascular calcification in chronic kidney disease. The deficiency of the vascular calcification inhibitor vitamin K in these patients was researched. In addition, new mediators in this pathological process were studied. In the first part of the thesis, it could be observed that intake of vitamin K2 is significantly reduced in the context of CKD. Furthermore, at the protein level, it was found that a decrease in vitamin K recycling and synthesizing enzymes was negatively correlated with the degree of calcification in the CKD rat model. The second part of the thesis discusses VIF, a novel inhibitor of vascular calcification. The underlying inhibitor mechanism has been described in this thesis, and calcium-sensing receptors were discovered to be a VIF binding partner, pointing to VIF as an endogenous calcimimetic. The results of this thesis revealed new reasons behind vitamin K deficiency in CDK patients. Supplementation approaches should be taken into account in clinical therapy for better outcomes. In addition, a new mediator of vascular calcification was found, and this could open new opportunities for the development of drugs in patients with a higher risk of this pathological mechanism, like in CDK patients.