CKD disrupts systemic mineral homeostasis, primarily through impaired phosphate excretion and reduced renal synthesis of active vitamin D. Hyperphosphatemia, a hallmark of CKD-MBD, triggers FGF-23 elevation to promote urinary phosphate excretion, but progressive renal failure limits compensatory mechanisms, exacerbating phosphate retention (12). This evidence concerns the gene FGF23 and hyperphosphatemia.