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Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
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Abstract titles should be brief and reflect the content of the abstract.
Intravenous (i.v.) iron therapy is an effective and widely used treatment for iron deficiency anemia, but may cause hypophosphatemia. This is usually transient and asymptomatic, but with repeated administrations, severe and prolonged hypophosphatemia with serious clinical consequences may develop. The mechanism involves increased fibroblast growth factor 23, which promotes renal phosphate excretion and suppresses calcitriol synthesis, leading to secondary hyperparathyroidism that further enhances phosphate loss. In routineclinical practice, ferric carboxymaltose (FCM) and ferric derisomaltose (FDI) are the most commonly used preparations. This case report highlights hypophosphatemia associated with FMC.
A 55-year-old male patient was referred to the nephrology outpatient clinic at University Medical Center Ljubljana in June 2022 for evaluation of suspected secondary arterial hypertension. Primary hyperaldosteronism and primary hyperparathyroidism were excluded. Iron deficiency anemia was diagnosed in July 2024 and treated with 1000 mg FCM i.v. in July 2024, November 2024, and January 2025. Due to recurrent hypophosphatemia, therapy was switched to 1000 mg FDI in April 2025. Serum phosphate and parathyroid hormone (PTH) were measured before and after each infusion. Oral phosphate replacement was prescribed in case of hypophosphatemia, and clinical symptoms were documented.
After the first FCM infusion, serum phosphate decreased from 1.10 mmol/L to 0.66 mmol/L and the patient reported persistent fatigue despite improved hemoglobin and iron stores. After the second and third FCM doses, phosphate levels fell further from 1.10 mmol/L to 0.65 mmol/L and 0.52 mmol/L, accompanied withsevere fatigue, reduced exercise tolerance, and marked muscle weakness. Oral phosphate supplementation (phosphate powder 625/375 mg, 2 × 1 g daily)
was initiated but hypophosphatemia persisted for several weeks. In contrast, following FDI administration in April 2025, phosphate levels remained within the normal range (0.81 - 0.91 mmol/L), and no symptoms occured. Episodes of hypophosphatemia were associated with increased PTH levels. PTH level increasedafter FCM (peak 116 ng/L) and normalised gradually over several weeks to 78 ng/L, whereas after FDI, PTH peaked at 110 ng/L on day 3 and returned to baseline within 10 days.
This case demonstrates the clinically significant risk of hypophosphatemia associated with ferric carboxymaltose, particularly after repeated dosing, whereas ferric derisomaltose showed a more favourable phosphate safety profile. Routine monitoring of serum phosphate and PTH may be useful in patients receiving high or repeated doses of i.v. iron. In patients at increased risk, FDI may be a safer alternative.
