Background:Fibroblast growth factors are polypeptide growth factors essential for developmental processes like differentiation, cell proliferation, and migration. They are secreted into circulation through paracrine or autocrine mechanisms. Fibroblast growth factor-23 (FGF23), a circulating phosphaturic factor, regulates inorganic phosphate homeostasis. It binds to FGF receptors, likely requiring klotho for cell surface interaction. FGF23's most significant effects are on the kidney and parathyroid gland. In patients with chronic kidney disease (CKD), circulating FGF-23 levels are progressively elevated to compensate for persistent phosphate retention. In End-stage renal disease (ESRD), FGF-23 cannot reduce serum phosphate levels, and abnormally high FGF-23 concentration may exert unwarranted effects, including left ventricular hypertrophy, faster CKD progression, and premature mortality. Few data are available on FGF-23 metabolism in CKD children. ESRD is a leading cause of death for up to 40-50% of patients, primarily due to cardiovascular disease. Altered calcium, phosphorus, parathyroid hormone (PTH), and vitamin D levels in ESRD cause bone-like metabolism and mineralization in the vascular tunica media. FGF-23 levels also start rising early in patients with chronic kidney disease, which is implicated in cardiovascular and overall mortality of hemodialysis patients