Abstract: Chronic kidney disease (CKD) has a high prevalence rate. Its common complication, chronic kidney disease-mineral and bone disorder (CKD-MBD), has become an important factor affecting the long-term prognosis of patients. The pathogenesis of CKD-MBD is complex, involving multiple mechanisms such as dysregulation of the Klotho-fibroblast growth factor 23 (FGF23)-FGF receptor (FGFR) signaling pathway, calcium-phosphorus metabolism disorders, impaired synthesis of 1, 25-dihydroxyvitamin D₃1, 25-(OH)₂D₃, abnormal regulationof parathyroid hormone (PTH) secretion, and the involvement of the Wnt/β-catenin signaling pathway. Its pathological manifestations not only include renal osteodystrophy but also involve in extraskeletal complications, such as vascular calcification and increased risk of cardiovascular events. Diabetes, as the most common cause of CKD, further exacerbates the development of CKD-MBD through various mechanisms, including hyperglycemia, oxidative stress, activation of inflammatory factors, and bone microvascular disease. In the population undergoing maintenance hemodialysis, there are differences in calcium-phosphorus levels, PTH concentrations, and FGF23 expression patterns between diabetic nephropathy patients and non-diabetic CKD patients. However, the specific mechanisms underlying these changes have not been fully elucidated in large-scale epidemiological studies. This article aimed to review the basic research and clinical characteristics of CKD-MBD in diabetic nephropathy patients and non-diabetic CKD patients, with the hope of providing theoretical basis and practical guidance for future precision treatment.