In 2005, Moe et al coined the term chronic kidney disease–mineral and bone disorder (CKD-MBD) to describe a complex clinical syndrome encompassing disorders of calcium, phosphate, parathyroid hormone (PTH), vitamin D, and fibroblast growth factor-23 (FGF23) metabolism. These disruptions lead to alterations in bone morphology  (renal osteodystrophy), vascular calcification, and cardiovascular death in patients with chronic kidney disease (CKD). These abnormalities can potentially lead to high mortality rates, mainly from cardiovascular complications. Since the term CKD-MBD was introduced, various clinical guidelines have been developed, recommending specific laboratory targets and management options to improve the morbidity and mortality associated with this systemic syndrome. CKD-MBD can be assessed through histomorphometry of bone biopsy. Derangements in serum levels of calcium, phosphorus, PTH, and vitamin D, along with their effects on bone turnover, mineralization, and extraskeletal calcifications, are significant aspects of this syndrome. Although most features appear when the glomerular filtration rate (GFR) falls below 40 mL/min, some elements, such as loss of Klotho (a transmembrane protein), increased FGF23 secretion, decreased bone synthesis rates, and vascular calcification, often occur before abnormal biochemical markers manifest. Compelling evidence indicates a causal relationship between these derangements and numerous adverse clinical outcomes, particularly increased fracture risk and cardiovascular mortality. This activity highlights notable discoveries regarding the pathogenesis of CKD-MBD, including insights into the roles of FGF23, Klotho, Wnt inhibitors, and activin A. Management strategies for CKD-MBD primarily focus on preventing adverse effects associated with secondary hyperparathyroidism. Thus, management of secondary hyperparathyroidism is guided by established surrogate markers of deranged mineral bone metabolism, such as serum calcium, phosphate, PTH, and 25-hydroxyvitamin D. Renal osteodystrophy, an aspect of CKD-MBD, represents alterations in bone morphology. Although bone biopsy is the gold standard for diagnosing and classifying it, this invasive procedure is rarely performed. Kidney Disease Improving Global Outcomes (KDIGO) recommends monitoring the serial trend of biochemical markers for ongoing management of renal osteodystrophy. Furthermore, the 2017 update no longer advises performing a bone biopsy before initiating these medications.