Patients with chronic kidney disease (CKD) have a high risk of bone fracture owing to their low bone mineral density, which resembles that of postmenopausal osteoporosis. However, the mineral and bone disorder associated with CKD (CKD-MBD) is more complex than osteoporosis and the same treatments might not be appropriate. In particular, vascular calcifications are strongly associated with CKD-MBD, and must be taken into consideration. Post hoc analyses of data from pivotal osteoporosis studies suggest that in patients with mild stage 3 CKD and normal parathyroid hormone (PTH), calcium and phosphate measurements, conventional medications for osteoporosis (such as raloxifene, bisphosphonates, teriparatide and denosumab) are effective at reducing fracture rates. However, for patients with stage 4-5 CKD, or those with abnormal PTH and mineral values, the available data are insufficient to determine whether these commonly used medications are effective against fractures. Moreover, all medications used to treat osteoporosis have known or potential adverse effects in patients with CKD. Medicines that increase bone formation by upregulating Wnt signalling have shown promise in patients with osteoporosis and might be used to treat CKD-MBD in the future, but off-target effects could limit their use in in this setting.