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.