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首页> 外文期刊>Clinical kidney journal. >Magnesium and outcomes in patients with chronic kidney disease: focus on vascular calcification, atherosclerosis and survival
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Magnesium and outcomes in patients with chronic kidney disease: focus on vascular calcification, atherosclerosis and survival

机译：慢性肾脏病患者的镁及其结局：关注血管钙化，动脉粥样硬化和生存

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Patients with chronic kidney disease (CKD) have a high prevalence of vascular calcification, and cardiovascular disease is the leading cause of death in this population. However, the molecular mechanisms of vascular calcification, which are multifactorial, cell-mediated and dynamic, are not yet fully understood. We need to address ways to improve outcomes in CKD patients, both in terms of vascular calcification and cardiovascular morbidity and mortality—and to these ends, we investigate the role of magnesium. Magnesium's role in the pathogenesis of vascular calcification has not been extensively studied. Nonetheless, several in vitro and animal studies point towards a protective role of magnesium through multiple molecular mechanisms. Magnesium is a natural calcium antagonist and both human and animal studies have shown that low circulating magnesium levels are associated with vascular calcification. Clinical evidence from observational studies of dialysis patients has shown that low-magnesium levels occur concurrently with mitral annular calcification, peripheral arterial calcification and increased carotid intima–media thickness. Few interventional studies have been performed. Two interventional studies suggest that there may be benefits such as retardation of arterial calcification and/or reductions in carotid intima–media thickness in response to magnesium supplementation in CKD patients, though both studies have limitations. Finally, observational studies have shown that low serum magnesium may be an independent risk factor for premature death in CKD patients, and patients with mildly elevated serum magnesium levels could have a survival advantage over those with lower magnesium levels.
机译：慢性肾脏病（CKD）患者的血管钙化患病率很高，心血管疾病是该人群死亡的主要原因。然而，血管钙化的分子机制是多因素的，细胞介导的和动态的，目前尚未完全了解。我们需要在血管钙化，心血管疾病的发病率和死亡率方面寻求改善CKD患者预后的方法，为此，我们研究了镁的作用。镁在血管钙化发病机制中的作用尚未得到广泛研究。然而，一些体外和动物研究指出镁通过多种分子机制具有保护作用。镁是一种天然的钙拮抗剂，人类和动物研究都表明，低水平的循环镁与血管钙化有关。透析患者观察性研究的临床证据表明，低镁水平与二尖瓣环钙化，外周动脉钙化和颈动脉内膜-中膜厚度增加同时发生。很少进行干预研究。两项干预性研究表明，尽管对CKD患者补充镁，但它们可能有益于诸如延迟动脉钙化和/或降低颈动脉内膜中膜厚度，尽管这两项研究都有局限性。最后，观察性研究表明，低血清镁可能是CKD患者过早死亡的独立危险因素，血清镁水平轻度升高的患者可能比低镁水平的患者具有生存优势。

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