Abstract: SA-PO990

A Case of Hypophosphatemia Due to Ferric Carboxymaltose Induced Renal Phosphate Wasting

Session Information

Category: Nephrology Education

  • 1302 Fellows and Residents Case Reports

Authors

  • Phan, Tramanh, University of Rochester Medical Center, Rochester, New York, United States
  • Liebman, Scott E., University of Rochester Medical Center, Rochester, New York, United States
Background

Hypophosphatemia due to renal phosphate wasting typically results from either hyperparathyroidism or as part of global proximal tubular dysfunction as in Fanconi syndrome. Isolated renal phosphate wasting is rare, but has been described with ferric carboxymaltose (FCM). Here we report a case of transient, but symptomatic hypophosphatemia due to renal phosphate wasting in the setting of FCM infusion.

Methods

A 26-year-old male with a past medical history of ulcerative colitis status post total colectomy and J pouch creation three years prior presented for evaluation of hypophosphatemia. He initially saw his primary care physician complaining of diffuse bone pain. Laboratory studies at that time showed a phosphorus level of 1.5 mg/dL. He did not note any gastrointestinal symptoms, and noted his ostomy output was unchanged from baseline. He did not have any prior history of hypophosphatemia except immediately post-operative following his colectomy. He was not taking any medications known to cause hypophosphatemia, but review of his past medical history showed that he had iron deficiency and had received FCM two days prior to symptom onset. His physical examination was benign and did not show any musculoskeletal abnormalities. Further work up revealed a fractional excretion of phosphate (FEPO4) of 25.5%, normal calcium, parathyroid hormone and 25-OH vitamin D levels, and the absence of glucose in the urine indicating a primary, isolated renal phosphate wasting disorder, suspected due to receipt of FCM. FGF-23 levels were not obtained. He was started on an oral phosphate supplement with subsequent normalization of serum phosphorus and resolution of the bone pain within several days. His phosphorus remained normal and oral phosphate supplements were discontinued six weeks later. Two weeks thereafter, his phosphorus level was maintained off supplementation and his FEPO4 was 9.3%.

Conclusion

FCM is a convenient treatment option for iron deficiency as it only requires a single infusion. Clinicians should be aware of the association between FCM and hypophosphatemia, and consider this diagnosis in patients who present with symptoms consistent with hypophosphatemia after infusion.