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Kidney Week

Abstract: FR-PO602

IV Iron Therapy Induced Acute Hypophosphatemia in CKD Patients

Session Information

  • Trainee Case Reports - III
    October 26, 2018 | Location: Exhibit Hall, San Diego Convention Center
    Abstract Time: 10:00 AM - 12:00 PM

Category: Trainee Case Reports

  • 402 Bone and Mineral Metabolism: Clinical


  • Chung, Annise, Medstar Georgetown University Hospital, Washington, District of Columbia, United States
  • Li, Ping, DC VA Medical Center, Washington, District of Columbia, United States

Intravenous (IV) iron-induced hypophosphatemia is a well-documented side effect in iron deficient patients. Single dosing studies suggest that decreases in serum phosphate are asymptomatic and fully reversible with phosphate repletion. Long term complications such as arrhythmias, muscular weakness, osteomalacia and bone fractures have also been documented. We report a case of hypophosphatemia with a newer formulation of IV iron: ferric carboxymaltose (FCM) induced severe acute hypophosphatemia.

Case Description

A 97 year old male with past medical history of atrial fibrillation, iron deficient anemia, hypothyroidism, chronic kidney disease III, and hypertension was referred to renal clinic for acute hypophosphatemia. The patient had been on oral iron supplementation for iron deficient anemia and it was not effective. He received IV FCM for iron deficient anemia twice in the previous month. The patient was sent to the emergency department after he was found to have a phosphate level of 0.8 mg/dL by routine lab work. Patient initially received both oral and intravenous phosphate repletion in the emergency department and subsequently received oral phosphate supplementation. However, the hypophosphatemia persisted in the presence of oral phosphate supplementation.
Laboratory data showed calcium was 7.9 mg/dl, phosphate 1.5mg/dl, magnesium 2.1 mg/ml, intact parathyroid hormone 295pg/ml and 25-OH, vitamin D 30.8 ng/ml. His serum creatinine was at his baseline of 1.5-1.8 mg/dL. In addition, intact FGF23 level was found to be 1424 RU/ml (reference range < 180). Parathyroid scan showed no adenoma in parathyroid glands.
Based on the above temporal association, patient was suspected of FCM induced, FGF23 mediated renal phosphate wasting. IV FCM was stopped and patient received oral active vitamin D, calcium and phosphate supplementation. The acute hypophosphatemia improved.


This case highlights the association between FCM and low serum phosphate levels. Although there has been a growing body of literature on the association, many nephrologists may not be aware of the hypophosphatemic side effects of FCM. In the recently published phase 3 study of IV ferumoxytol versus FCM, hypophosphatemia was seen in 38.7% of the FCM group 2 weeks after treatment. In patients who receive IV FCM for iron deficient anemia, serum phosphate levels should be monitored.