Chronic kidney disease (CKD) is associated with disturbances in bone and mineral metabolism, leading to osteoporosis and vascular calcification, which are significant contributors to mortality. Although denosumab, a monoclonal antibody targeting RANKL, has been shown to increase BMD, its effects on vascular calcification remain controversial. This retrospective study investigated the effects of denosumab on vascular calcification and BMD in 25 dialysis patients compared to the control group of 21 dialysis patients without denosumab over 2 yr. All patients underwent BMD assessments at 1-yr intervals, as well as evaluations of abdominal aortic vascular calcification using CT to determine changes in calcification volume and the Agatston score. Denosumab significantly increased BMD in the LS (8.5% vs 1.5%, p = .0079) compared with the control group. In contrast, the rate of increase from baseline in calcification volume and the Agatston score were significantly higher in the denosumab group compared with the controls (32.8% vs 19.3%, p = .0476; 34.6% vs 20.5%, p = .0483, respectively). Although denosumab is beneficial for bone health in patients on dialysis, its vascular effects warrant careful monitoring.