{"title":"Vitamin K and vascular calcification in chronic kidney disease: An update of current evidence.","authors":"Yu-Li Lin, Bang-Gee Hsu","doi":"10.4103/tcmj.tcmj_100_22","DOIUrl":null,"url":null,"abstract":"<p><p>Vascular calcification, characterized by calcium deposition in the intimal and medial layers of the arterial wall, is frequently encountered in patients with chronic kidney disease (CKD) and leads to an enhanced risk of adverse cardiovascular (CV) outcomes. However, the underlying complex pathophysiology remains incompletely understood. Recently, Vitamin K supplementation aimed at correcting Vitamin K deficiency highly prevalent in CKD holds great promise to mitigate the progression of vascular calcification. This article discusses the functional Vitamin K status in CKD, the pathophysiology linking Vitamin K deficiency and vascular calcification, and reviews current literature from animal models, observational studies, and clinical trials across the different spectrum of CKD. While favorable effects of Vitamin K on vascular calcification and CV outcomes are suggested in animal and observational studies, most recently published clinical trials investigating the effects of Vitamin K on vascular health failed to support the beneficial role of Vitamin K supplementation, despite improving the functional status of Vitamin K. We address the potential reasons for these discrepancies and provide further perspective on Vitamin K research in CKD.</p>","PeriodicalId":45873,"journal":{"name":"Tzu Chi Medical Journal","volume":"35 1","pages":"44-50"},"PeriodicalIF":1.4000,"publicationDate":"2022-07-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/36/2a/TCMJ-35-44.PMC9972925.pdf","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Tzu Chi Medical Journal","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.4103/tcmj.tcmj_100_22","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2023/1/1 0:00:00","PubModel":"eCollection","JCR":"Q2","JCRName":"MEDICINE, GENERAL & INTERNAL","Score":null,"Total":0}
引用次数: 0
Abstract
Vascular calcification, characterized by calcium deposition in the intimal and medial layers of the arterial wall, is frequently encountered in patients with chronic kidney disease (CKD) and leads to an enhanced risk of adverse cardiovascular (CV) outcomes. However, the underlying complex pathophysiology remains incompletely understood. Recently, Vitamin K supplementation aimed at correcting Vitamin K deficiency highly prevalent in CKD holds great promise to mitigate the progression of vascular calcification. This article discusses the functional Vitamin K status in CKD, the pathophysiology linking Vitamin K deficiency and vascular calcification, and reviews current literature from animal models, observational studies, and clinical trials across the different spectrum of CKD. While favorable effects of Vitamin K on vascular calcification and CV outcomes are suggested in animal and observational studies, most recently published clinical trials investigating the effects of Vitamin K on vascular health failed to support the beneficial role of Vitamin K supplementation, despite improving the functional status of Vitamin K. We address the potential reasons for these discrepancies and provide further perspective on Vitamin K research in CKD.
血管钙化的特点是钙沉积在动脉内壁和内侧层,慢性肾脏病(CKD)患者经常会出现血管钙化,并导致不良心血管(CV)后果的风险增加。然而,人们对其背后复杂的病理生理学仍然知之甚少。最近,旨在纠正慢性肾脏病患者普遍存在的维生素 K 缺乏症的维生素 K 补充剂有望缓解血管钙化的进展。本文讨论了 CKD 中维生素 K 的功能状态、维生素 K 缺乏与血管钙化之间的病理生理学联系,并回顾了目前来自动物模型、观察性研究和临床试验等不同 CKD 领域的文献。虽然动物模型和观察性研究表明维生素 K 对血管钙化和心血管疾病的预后有有利影响,但最近发表的大多数调查维生素 K 对血管健康影响的临床试验却未能支持维生素 K 补充剂的有利作用,尽管维生素 K 的功能状态有所改善。我们探讨了这些差异的潜在原因,并对 CKD 中的维生素 K 研究提供了进一步的视角。
期刊介绍:
The Tzu Chi Medical Journal is the peer-reviewed publication of the Buddhist Compassion Relief Tzu Chi Foundation, and includes original research papers on clinical medicine and basic science, case reports, clinical pathological pages, and review articles.