Chronic kidney disease (CKD) can develop mineral and bone disorder (CKD-MBD), characterized by abnormal bone remodelling and mineralization. Exploring therapeutic strategies for CKD-MBD is challenging due to complex interplays between multiple organs and limited clinical evidence arising from the risks of drug administration in patients with impaired kidney function. This study aims to establish a mathematical model to describe bone disorders in CKD-MBD and validate the model through computational simulations. We incorporated a model of osteoid mineralization into our established in silico platform (V-Bone), which enables voxel-based bone remodelling simulations coupling molecular/cellular-level biochemical regulations with tissue-level mechanics. Mineralization of osteoid was modelled as a process where hydroxyapatite (HA) density increases linearly after a specific time delay, defined as the mineralization lag time (MLT). Local bone stiffness is assumed to be proportional to the HA density. To reproduce bone disorders in CKD-MBD, we conducted 100-week simulations using a voxel-FE cancellous model reconstructed from micro-CT images of a swine femoral head. Given that bone remodelling and mineralization are key factors of bone disorders in CKD-MBD, the following pathological conditions were simulated: elevated RANKL levels, representing abnormal bone remodelling, and prolonged MLT, representing impaired mineralization. Increased RANKL resulted in enhanced bone resorption and decreased bone mass, reproducing the osteoporotic phenotype. In contrast, prolonged MLT resulted in the accumulation of osteoid. As MLT increased, osteoid volume increased and the overall stiffness of the cancellous bone decreased accordingly, reproducing the phenotype of osteomalacia. These findings demonstrate that the present model can represent the diverse pathological spectrum of CKD-MBD by perturbing remodelling and mineralization parameters. In conclusion, we established a mathematical model that describes the bone disorders in CKD-MBD. Expanding this multi-scale model into a multi-organ crosstalk model will enable the exploration of therapeutic strategies for CKD-MBD by simultaneously considering complex systemic interplays.