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Vitamin K deficiency: an emerging player in the pathogenesis of vascular calcification and an iatrogenic consequence of therapies in advanced renal disease.
Am J Physiol Renal Physiol. 2020 10 01; 319(4):F618-F623.AJ

Abstract

Vascular calcification is a known complication of chronic kidney disease (CKD). The prevalence of vascular calcification in patients with non-dialysis-dependent CKD stages 3-5 has been shown to be as high as 79% (20). Vascular calcification has been associated with increased risk for mortality, hospital admissions, and cardiovascular disease (6, 20, 50, 55). Alterations in mineral and bone metabolism play a pivotal role in the pathogenesis of vascular calcification in CKD. As CKD progresses, levels of fibroblast growth factor-23, parathyroid hormone, and serum phosphorus increase and levels of 1,25-(OH)2 vitamin D decrease. These imbalances have been linked to the development of vascular calcification. More recently, additional factors have been found to play a role in vascular calcification. Matrix G1a protein (MGP) in its carboxylated form (cMGP) is a potent inhibitor of vascular calcification. Importantly, carboxylation of MGP is dependent on the cofactor vitamin K. In patients with CKD, vitamin K deficiency is prevalent and is exacerbated by warfarin, which is frequently used for anticoagulation. Insufficient bioavailability of vitamin K reduces the amount of cMGP available, and, therefore, it may lead to increased risk of vascular calcification. In vitro studies have shown that in the setting of a high-phosphate environment and vitamin K antagonism, human aortic valve interstitial cells become calcified. In this article, we discuss the pathophysiological consequence of vitamin K deficiency in the setting of altered mineral and bone metabolism, its prevalence, and clinical implications in patients with CKD.

Authors+Show Affiliations

University of Rochester School of Medicine, Rochester, New York.University of Rochester School of Medicine, Rochester, New York.University of Rochester School of Medicine, Rochester, New York.

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

32830534

Citation

Levy, David S., et al. "Vitamin K Deficiency: an Emerging Player in the Pathogenesis of Vascular Calcification and an Iatrogenic Consequence of Therapies in Advanced Renal Disease." American Journal of Physiology. Renal Physiology, vol. 319, no. 4, 2020, pp. F618-F623.
Levy DS, Grewal R, Le TH. Vitamin K deficiency: an emerging player in the pathogenesis of vascular calcification and an iatrogenic consequence of therapies in advanced renal disease. Am J Physiol Renal Physiol. 2020;319(4):F618-F623.
Levy, D. S., Grewal, R., & Le, T. H. (2020). Vitamin K deficiency: an emerging player in the pathogenesis of vascular calcification and an iatrogenic consequence of therapies in advanced renal disease. American Journal of Physiology. Renal Physiology, 319(4), F618-F623. https://doi.org/10.1152/ajprenal.00278.2020
Levy DS, Grewal R, Le TH. Vitamin K Deficiency: an Emerging Player in the Pathogenesis of Vascular Calcification and an Iatrogenic Consequence of Therapies in Advanced Renal Disease. Am J Physiol Renal Physiol. 2020 10 1;319(4):F618-F623. PubMed PMID: 32830534.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Vitamin K deficiency: an emerging player in the pathogenesis of vascular calcification and an iatrogenic consequence of therapies in advanced renal disease. AU - Levy,David S, AU - Grewal,Rickinder, AU - Le,Thu H, Y1 - 2020/08/24/ PY - 2020/8/25/pubmed PY - 2020/11/25/medline PY - 2020/8/25/entrez KW - carboxylated form of matrix G1a protein KW - dephosphorylated uncarboxylated form of matrix G1a protein KW - matrix G1a protein KW - vascular calcification KW - vitamin K SP - F618 EP - F623 JF - American journal of physiology. Renal physiology JO - Am J Physiol Renal Physiol VL - 319 IS - 4 N2 - Vascular calcification is a known complication of chronic kidney disease (CKD). The prevalence of vascular calcification in patients with non-dialysis-dependent CKD stages 3-5 has been shown to be as high as 79% (20). Vascular calcification has been associated with increased risk for mortality, hospital admissions, and cardiovascular disease (6, 20, 50, 55). Alterations in mineral and bone metabolism play a pivotal role in the pathogenesis of vascular calcification in CKD. As CKD progresses, levels of fibroblast growth factor-23, parathyroid hormone, and serum phosphorus increase and levels of 1,25-(OH)2 vitamin D decrease. These imbalances have been linked to the development of vascular calcification. More recently, additional factors have been found to play a role in vascular calcification. Matrix G1a protein (MGP) in its carboxylated form (cMGP) is a potent inhibitor of vascular calcification. Importantly, carboxylation of MGP is dependent on the cofactor vitamin K. In patients with CKD, vitamin K deficiency is prevalent and is exacerbated by warfarin, which is frequently used for anticoagulation. Insufficient bioavailability of vitamin K reduces the amount of cMGP available, and, therefore, it may lead to increased risk of vascular calcification. In vitro studies have shown that in the setting of a high-phosphate environment and vitamin K antagonism, human aortic valve interstitial cells become calcified. In this article, we discuss the pathophysiological consequence of vitamin K deficiency in the setting of altered mineral and bone metabolism, its prevalence, and clinical implications in patients with CKD. SN - 1522-1466 UR - https://www.unboundmedicine.com/medline/citation/32830534/Vitamin_K_deficiency:_an_emerging_player_in_the_pathogenesis_of_vascular_calcification_and_an_iatrogenic_consequence_of_therapies_in_advanced_renal_disease_ DB - PRIME DP - Unbound Medicine ER -