Abstract: SA-PO0522
Heavy Is the Iron Crown: Protracted, Symptomatic Hypophosphatemia After a One-Time Iron Sucrose Infusion
Session Information
- Fluid, Electrolyte, and Acid-Base Disorders: Clinical - 3
November 08, 2025 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Fluid, Electrolytes, and Acid-Base Disorders
- 1102 Fluid, Electrolyte, and Acid-Base Disorders: Clinical
Authors
- Brennan, Meghan, Prisma Health Midlands, Columbia, South Carolina, United States
- Pollock, James M, Prisma Health Midlands, Columbia, South Carolina, United States
Introduction
While the recent use of intravenous (IV) iron has been increasing for a number of conditions, relatively little focus has been given toward its potential to cause severe electrolyte derangements. Hypophosphatemia is one such derangement, and it has been commonly associated with ferric carboxymaltose (FCM) solutions. This phenomenon occurs due to increased levels of fibroblast growth factor 23 (FGF23), a hormone which promotes renal phosphorus excretion. However, the process by which other iron infusions, such as iron sucrose, diminish serum phosphorus levels is poorly understood. We present a case of protracted, symptomatic hypophosphatemia following a one-time infusion of iron sucrose.
Case Description
A 61-year-old male with a past medical history of hyperthyroidism status post recent thyroidectomy and iron deficiency anemia presented to the emergency department with complaints of fatigue. Workup on admission revealed hemoglobin and thyroid function tests were within normal limits. However, serum phosphorus was found to be low at 1.4 mg/dL. Urine phosphorus was 49.7 mg/dL on admission, compatible with an elevated fractional excretion of 26.78%. After one day of aggressive IV and oral repletion, repeat check showed a urine phosphorus >186.2 mg/dL and unchanged serum phosphorus. FGF23 was elevated at 248 RU/mL (reference range <180 RU/mL), and intact PTH was elevated at 160.4 pg/mL. Of note, serum calcium, ionized calcium, and 25-hydroxy vitamin D remained within normal limits. Further discussion with the patient revealed that he received IV iron prior to his recent thyroidectomy due to incidental anemia, and review of the medical record revealed this infusion to have been iron sucrose.
Discussion
Diagnosis of hypophosphatemia can be challenging as phosphate levels are not routinely included in standard metabolic panels, and early symptoms, such as muscle weakness and fatigue, are nonspecific. Nonetheless, timely recognition is essential as severe cases can lead to serious complications. Cases like this suggest that physicians should have a high clinical suspicion for hypophosphatemia in patients after any type of IV iron infusion, particularly with their increased use in clinical practice.