Krueger Thilo, Westenfeld Ralf, Schurgers Leon, Brandenburg Vincent
Department of Nephrology and Clinical Immunology, University Hospital of the RWTH Aachen, Aachen - Germany.
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.
慢性肾脏病(CKD)患者和终末期肾病(ESRD)患者的发病率和死亡率大幅增加。骨病(肾性骨营养不良)和血管疾病(加速动脉粥样硬化)是导致这种额外发病率和死亡率的两个典型情况。维生素K和维生素K依赖性蛋白在矿化生理过程以及预防异位钙化中起关键作用:其中两种维生素K依赖性蛋白是骨钙素(调节骨矿化)和基质Gla蛋白(MGP,血管壁局部钙化抑制剂)。维生素K缺乏会损害骨钙素和MGP的生理功能,因此,可能会导致骨质脱矿和血管钙化(所谓的钙化悖论)。在这种情况下,使用维生素K拮抗剂进行长期口服抗凝治疗可能存在风险,尤其是在血管钙化背景水平较高的CKD患者中。我们总结了描述维生素K缺乏和补充在CKD或ESRD患者的骨和血管疾病中的潜在作用的数据。