Wuyts Julie, Dhondt Annemieke
a Department of Internal Medicine, Renal Division , Ghent University Hospital , Ghent , Belgium.
Acta Clin Belg. 2016 Dec;71(6):462-467. doi: 10.1080/17843286.2016.1180770. Epub 2016 May 25.
Patients with chronic kidney disease (CKD) are prone to vascular calcification. Pathogenetic mechanisms of vascular calcifications have been broadly studied and discussed such as the role of hyperphosphatemia, hypercalcemia, parathormone, and vitamin D. In recent years, new insights have been gained pointing to vitamin K as a main actor. It has been discovered that vitamin K is an essential cofactor for the activation of matrix Gla protein (MGP), a calcification inhibitor in the vessel wall. Patients with CKD often suffer from vitamin K deficiency, resulting in low active MGP and eventually a lack of inhibition of vascular calcification. Vitamin K supplementation and switching warfarin to new oral anticoagulants are potential treatments. In addition, MGP may have a role as a non-invasive biomarker for vascular calcification.
慢性肾脏病(CKD)患者易于发生血管钙化。血管钙化的发病机制已得到广泛研究和讨论,如高磷血症、高钙血症、甲状旁腺激素和维生素D的作用。近年来,有新的见解指出维生素K是主要因素。已发现维生素K是血管壁钙化抑制剂基质Gla蛋白(MGP)激活的必需辅助因子。CKD患者常存在维生素K缺乏,导致活性MGP水平降低,最终缺乏对血管钙化的抑制作用。补充维生素K以及将华法林换用新型口服抗凝剂是潜在的治疗方法。此外,MGP可能作为血管钙化的一种非侵入性生物标志物。