Magnesium (Mg) plays a crucial role in various biological processes, and its homeostasis is primarily regulated by the kidneys. Chronic kidney disease (CKD) patients often experience disturbances in Mg balance, leading to either hyper- or hypomagnesemia. Hypomagnesemia is particularly prevalent and associated with increased vascular calcification, a significant risk factor for cardiovascular morbidity and mortality in CKD patients. Vascular calcification involves the transformation of vascular smooth muscle cells (VSMCs) into an osteoblast-like phenotype, characterized by the formation of hydroxyapatite crystals and calciprotein particles (CPPs). Mg has been shown to protect against vascular calcification through several mechanisms, including inhibiting hydroxyapatite and CPP formation, limiting osteogenic differentiation of VSMCs, and modulating signaling pathways such as Wnt/β-catenin and microRNA expression. In vitro and animal studies have demonstrated the protective effects of Mg, but clinical trials have produced contradictory results, creating a state of equipoise. This review provides an overview of the current understanding of Mg's role in vascular calcification in CKD, the underlying mechanisms, and the need for further research to evaluate the efficacy of Mg supplementation.Magnesium (Mg) plays a crucial role in various biological processes, and its homeostasis is primarily regulated by the kidneys. Chronic kidney disease (CKD) patients often experience disturbances in Mg balance, leading to either hyper- or hypomagnesemia. Hypomagnesemia is particularly prevalent and associated with increased vascular calcification, a significant risk factor for cardiovascular morbidity and mortality in CKD patients. Vascular calcification involves the transformation of vascular smooth muscle cells (VSMCs) into an osteoblast-like phenotype, characterized by the formation of hydroxyapatite crystals and calciprotein particles (CPPs). Mg has been shown to protect against vascular calcification through several mechanisms, including inhibiting hydroxyapatite and CPP formation, limiting osteogenic differentiation of VSMCs, and modulating signaling pathways such as Wnt/β-catenin and microRNA expression. In vitro and animal studies have demonstrated the protective effects of Mg, but clinical trials have produced contradictory results, creating a state of equipoise. This review provides an overview of the current understanding of Mg's role in vascular calcification in CKD, the underlying mechanisms, and the need for further research to evaluate the efficacy of Mg supplementation.