镁在慢性肾脏病(chronic kidney disease，CKD)中既可作为风险标志物，也被视为潜在治疗靶点。近年来系统评价显示，较低血镁与CKD患者不良结局相关，但观察性关联不能直接证明补镁能够改善预后。基础研究提示镁可能通过干扰钙磷晶体形成、延缓钙化蛋白颗粒成熟及调节血管平滑肌细胞表型等途径降低钙化倾向。然而，临床干预研究结果并不一致：口服补镁和提高透析液镁浓度虽可升高血镁并改善部分钙化倾向指标，但其对冠状动脉钙化进展的影响尚无一致结论，且现有证据不足以证明镁干预能够改善患者相关结局；部分口服补镁试验还观察到胃肠道不良反应增加。上述差异可能与患者基线血镁水平及钙化负荷、CKD分期、镁制剂与剂量、组织有效暴露、随访时间、终点选择及安全窗有关。现有证据支持结合临床情境监测血镁、识别可逆性低镁原因并防范不可控镁蓄积，但尚不支持对CKD患者无差别补镁。未来研究应采用风险分层设计，并同时评价机制性指标、影像学血管钙化及患者相关结局。

Magnesium serves both as a risk marker and as a potential therapeutic target in chronic kidney disease (CKD). Recent systematic reviews have shown that lower serum magnesium is associated with adverse outcomes in CKD patients, but observational associations cannot directly prove that magnesium supplementation improves prognosis. Basic research suggests that magnesium may reduce the tendency toward calcification by interfering with calcium-phosphate crystal formation, delaying the maturation of calcifying protein particles, and modulating the phenotype of vascular smooth muscle cells. However, the results of clinical intervention studies are inconsistent: although oral magnesium supplementation and increasing dialysate magnesium concentration can raise serum magnesium and improve some indicators of calcification tendency, their effects on the progression of coronary artery calcification remain inconclusive, and current evidence is insufficient to demonstrate that magnesium intervention can improve patient-related outcomes; some oral magnesium supplementation trials have also observed an increase in gastrointestinal adverse effects. These discrepancies may be related to patients' baseline serum magnesium levels and calcification burden, CKD stage, magnesium formulation and dose, effective tissue exposure, follow-up duration, endpoint selection, and safety window. Current evidence supports monitoring serum magnesium in the clinical context, identifying reversible causes of hypomagnesemia, and preventing uncontrollable magnesium accumulation, but it does not yet support indiscriminate magnesium supplementation in CKD patients. Future studies should adopt risk-stratified designs and simultaneously evaluate mechanistic indicators, imaging-based vascular calcification, and patient-related outcomes.