Department of Comprehensive Kidney Disease Research, Osaka University Graduate School of Medicine, Suita, Japan and Department of Nephrology, Osaka University Graduate School of Medicine, Suita, Japan.
Department of Comprehensive Kidney Disease Research, Osaka University Graduate School of Medicine, Suita, Japan and Department of Nephrology, Osaka University Graduate School of Medicine, Suita, Japan.
Adv Chronic Kidney Dis. 2018 May;25(3):274-280. doi: 10.1053/j.ackd.2017.11.001.
Experimental and clinical studies have demonstrated that magnesium deficiency leads to hypertension, insulin resistance, and endothelial dysfunction, and is associated with an increased risk of cardiovascular events. Given that cardiovascular disease and CKD share similar risk factors, the low magnesium status may also contribute to CKD progression. In fact, lower serum magnesium levels and lower dietary magnesium intake are associated with an increased risk of incident CKD and progression to end-stage kidney disease. Because these associations are independent of traditional risk factors, other pathways might be involved in the relationship between magnesium deficiency and the risk of CKD progression. Recent evidence has shown that magnesium suppresses phosphate-induced vascular calcification. Magnesium impairs the crystallization of calcium phosphate-more specifically, the maturation of calciprotein particles. Considering that phosphate overload causes kidney damage, magnesium might counteract the phosphate toxicity to the kidney, as in the case of vascular calcification. This hypothesis is supported by an in vitro observation that magnesium alleviates proximal tubular cell injury induced by high phosphate. Potential usefulness of magnesium as a treatment option for phosphate toxicity in CKD should be further investigated by intervention studies.
实验和临床研究表明，镁缺乏可导致高血压、胰岛素抵抗和内皮功能障碍，并增加心血管事件的风险。鉴于心血管疾病和 CKD 具有相似的危险因素，低镁状态也可能导致 CKD 进展。事实上，血清镁水平较低和镁摄入较低与 CKD 事件的风险增加和进展至终末期肾病有关。由于这些关联独立于传统危险因素，因此镁缺乏与 CKD 进展风险之间的关系可能涉及其他途径。最近的证据表明，镁可抑制磷酸盐诱导的血管钙化。镁可破坏磷酸钙的结晶——更具体地说，可破坏钙磷蛋白颗粒的成熟。考虑到磷酸盐过载会导致肾脏损伤，镁可能会拮抗磷酸盐对肾脏的毒性，就像在血管钙化的情况下一样。体外观察结果支持这一假设，即镁可减轻高磷酸盐引起的近端肾小管细胞损伤。通过干预研究进一步探讨镁作为 CKD 中磷酸盐毒性治疗选择的潜在用途是合适的。
