Hyperphosphatemia, an elevated level of phosphate in the blood, is a common electrolyte disturbance in critically ill patients. It can result from various underlying conditions such as renal failure, tumor lysis syndrome, or rhabdomyolysis, and may lead to significant complications if not managed appropriately. Phosphate homeostasis is tightly regulated by a complex interplay of hormones, including parathyroid hormone (PTH), fibroblast growth factor 23 (FGF-23), and 1,25-dihydroxyvitamin D (calcitriol). These hormones regulate calcium and phosphate levels through feedback mechanisms involving the kidneys, bones, and intestines. Understanding these physiological mechanisms is essential for effective management of hyperphosphatemia, particularly in patients with chronic kidney disease (CKD), where FGF-23 plays a crucial role in phosphate excretion [1] [Ref: Algorithm 29.1].