Energized or Depleted? A Case of IV Iron-Induced Hypophosphatemia

Introduction: Hypophosphatemia, defined as a serum phosphorus level below 2.5 mg/dL (0.8 mmol/L), can result from decreased intestinal absorption (chronic antiacid use, eating disorders, malabsorption syndromes), intracellular phosphate shifts, renal replacement therapy, or increased urinary phosphate loss. The prevalence in the general population is difficult to estimate because many cases are asymptomatic. This report presents a case of prolonged, symptomatic hypophosphatemia following IV iron administration, which required oral and intravenous phosphate repletion for several months. Case Description: A 27-year-old woman with iron-deficiency anemia treated with two doses of weekly intravenous ferric carboxymaltose presented with fatigue and was found to have severe hypophosphatemia (serum phosphorus 1.3 mg/dL). Calcium, magnesium, vitamin D 25 OH, and parathyroid hormone were within normal range. Her fibroblast growth factor 23 was 77 pg/mL, and 24-hour urine phosphorus was markedly elevated at 1610 mg, indicating renal phosphate wasting. She was treated acutely with intravenous phosphate and started on oral phosphate supplements and calcitriol. Despite the initiation of intravenous phosphate repletion and the addition of oral phosphate and calcitriol, the patient continued to exhibit refractory hypophosphatemia. Over eight months, she required weekly IV phosphate infusions, high-dose oral phosphate, and calcitriol to maintain serum phosphorus levels above 2.5 mg/dL. Discussion: This case highlights prolonged, symptomatic hypophosphatemia associated with intravenous ferric carboxymaltose administration. Intravenous iron-induced hypophosphatemia results from renal wasting caused by sustained elevations in fibroblast growth factor 23 and parathyroid hormone and may persist for weeks to months after discontinuing therapy. In our patient, renal phosphate wasting was confirmed by high 24-hour urinary phosphate and elevated fibroblast growth factor 23 levels. Clinical studies have highlighted this risk, emphasizing the need for routine monitoring of serum phosphate after intravenous iron administration. Although hypophosphatemia has been linked with multiple intravenous iron formulations, intravenous ferric carboxymaltose is thought to be the culprit in the majority of the cases. Patient education is also essential to ensure awareness of this potential adverse effect.