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Abstract: FR-PO264

Effects of Repeated Ferric Carboxymaltose on Phosphate and FGF23 Levels

Session Information

Category: Mineral Disease

  • 1202 Mineral Disease: Vitamin D, PTH, FGF-23


  • Mehta, Rupal, Northwestern Univesrsity, Feinberg School of Medicine, Chicago, Illinois, United States
  • Hodakowski, Alex, Northwestern University, Chicago, Illinois, United States
  • Cai, Xuan, Northwestern University, Chicago, Illinois, United States
  • Wolf, Myles S., Duke University, Durham, North Carolina, United States
  • Isakova, Tamara, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, United States

Treatment of iron deficiency anemia (IDA) with a single dose of ferric carboxymaltose (FCM) reduces c-terminal FGF23 (cFGF23) levels, but paradoxically increases levels of biologically intact FGF23 (iFGF23), which results in hypophosphatemia. Although clinical trials of single doses of FCM reported high rates of reversible hypophosphatemia of unknown clinical significance, numerous reports have emerged of prolonged hypophosphatemia with severe skeletal complications in those who received repeated doses of FCM. No studies reported on the effects of repeated FCM dosing on phosphate and FGF23 levels.


We are conducting a longitudinal observational study of individuals who are receiving two doses of FCM for treatment of their IDA. We aim to test the following hypotheses: 1) repeated FCM dosing will be associated with prolonged increases in iFGF23 levels and hypophosphatemia; 2) repeated FCM dosing will be associated with increased levels of markers of inflammation.


We present data from 7 enrolled participants. Laboratory measurements (Table 1) were taken prior to each dose of FCM, 1 week after completion of therapy, and monthly until hypophosphatemia resolved. After a single FCM dose, ferritin markedly increased, cFGF23 decreased, but iFGF23 increased resulting in hypophosphatemia. After a second dose of FCM, iFGF23 further increased and hypophosphatemia persisted (Figure 1). During FCM treatment, serum phosphate decreased to ≤ 1.9 mg/dl in all 7 participants and ≤ 1.4 mg/dl n 5 of 7 participants, and criticlly low < 1.0 mg/dl in 2 patients (Figure 2). Two patients had persistent hypophosphatemia < 2.5 mg/dl at 90 days. Analyses of inflammatory marker are pending.


Administration of repeated doses of FCM treats ID and can lower cFGF23, but results in elevation of iFGF23 and prolonged hypophosphatemia. Given the increased utilization of FCM, the mechanisms and consequences of prolonged hypophosphatemia and elevated iFGF23 on bone and mineral metabolism markers necessitate further study.


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