Case Presentation: A 33-year-old Caucasian woman presented with increasing fatigue, palpitations and shortness of breath for the previous three weeks. She had a history of iron deficiency anemia, gluten sensitivity, and compensated anorexia. One month prior to admission, she received two doses of intravenous ferric carboxymaltose (FCM) supplementation. Upon evaluation, vitals were BP: 134/69 mmHg, HR: 74 bpm, RR: 18 rpm (SaO2: 98%), T: 37 C. Physical examination revealed mild muscle tenderness in the thighs, but otherwise unremarkable.

Discussion: Laboratory findings were relevant for severe hypophosphatemia (serum phosphorus: 1.2mg/dL), sCa: 8.8 mg/dL and alkaline phosphatase: 88 IU/L. Additional studies revealed PTH: 38.7 pg/mL, 25(OH) vitD: 22.0 ng/mL, c-terminal FGF-23: 116 RU/mL (ref: 44 – 215 RU/mL) and TSH: 1.8 uIU/mL. CBC, basic chemistry, hepatic function panel and iron studies were all within normal limits. She was found to have hyperphosphaturia (fractional excretion of PO4-3: 99.76%). Despite intensive replacement with both intravenous phosphorus (90 mmol/L/day) and oral phosphorus (32 mmol/L/day), her serum levels remained critical, dropping as low as 0.7 mg/dL and associated with increased respiratory symptoms. Due to concerns of FCM-induced Na/PO4-3 co-transporter dysfunction, we attempted to replete her calcitriol deposits by prescribing intravenous calcitriol (1 mcg/day) with slow titration up to 3 mcg/day. After two weeks of treatment with high dose calcitriol, her serum phosphorus levels were noted to rise back within normal limits. During follow-up, the patient was noticed to be in good health with a phosphorus level at 4 mg/dL.

Conclusions: Ferric carboxymaltose is an emerging cause of transient severe hypophosphatemia in hospital medicine, which can result in death if not appropriately addressed. Our case highlights the importance of a physiology-driven approach to treating hypophosphatemia including the use of innovative therapies such as calcitriol repletion.