Chronic kidney disease–mineral and bone disorder (CKD-MBD) is a systemic complication affecting 5–10% of the global population with CKD. It involves abnormalities in calcium, phosphate, parathyroid hormone (PTH), and vitamin D metabolism, as well as disruptions in bone turnover, mineralization, and vascular or soft tissue calcification.1,2 CKD-MBD is often asymptomatic in its early stages, with later manifestations including joint pain, tendon rupture, fractures, and proximal muscle weakness. Both low- and high-turnover bone abnormalities may present with similar clinical features. Diagnosis typically relies on measuring calcium, phosphorus, and PTH levels, with bone biopsy considered the gold standard—though its use is limited due to its invasive nature.3 Management primarily aims to prevent secondary hyperparathyroidism. KDIGO guidelines emphasize monitoring serial biochemical markers and highlight the importance of preventing hyperphosphatemia rather than focusing solely on normalization of phosphate levels.1