The single most important disturbance in refeeding syndrome is hypophosphatemia. The pathophysiology begins with reintroduced carbohydrate provoking endogenous insulin release. Insulin pushes phosphate, potassium and magnesium into cells and simultaneously ramps up phosphorylation reactions — ATP and 2,3-DPG generation — each of which sequesters inorganic phosphate. Because a starved patient already has depleted total-body phosphate stores, the serum level plunges, sometimes precipitously. Clinically this manifests as muscle weakness, rhabdomyolysis, diaphragmatic failure, cardiac arrhythmia, hemolysis and neurological signs. While potassium and magnesium also drop and require correction, phosphate is the marker that defines the syndrome and guides the cautious 'start low, go slow' refeeding protocol with prophylactic thiamine and electrolyte replacement. Calcium and sodium are not characteristic.\[\boxed{\text{Hypophosphatemia}}\]