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Iron-induced hypophosphatemia: an emerging complication
Heinz Zoller1, Benedikt Schaefer, Bernhard Glodny
1aDepartment of Medicine I, Gastroenterology, Hepatology, Endocrinology and Metabolism bDepartment of Radiology, Medical University of Innsbruck, Innsbruck, Austria.
Current Opinion in Nephrology and Hypertension
|April 12, 2017
Summary
Iron-induced hypophosphatemia can cause severe complications like bone fractures, especially with high-dose iron. Prompt diagnosis and phosphate substitution are crucial for managing this condition.
Area of Science:
- Nephrology
- Endocrinology
- Bone Metabolism
Background:
- Iron-induced hypophosphatemia is a known side effect, often considered transient and asymptomatic.
- However, severe symptomatic cases and long-term complications like osteomalacia and fractures are increasingly reported, particularly with repeated high-dose intravenous iron.
- These complications are often overlooked due to the focus on transient phosphate level decreases.
Purpose of the Study:
- To review the current understanding of iron-induced hypophosphatemia.
- To highlight the associated severe and long-term complications.
- To discuss diagnostic and therapeutic strategies.
Main Methods:
- Review of clinical trials and case reports on iron-induced hypophosphatemia.
- Analysis of mechanisms, including renal phosphate wasting mediated by fibroblast growth factor 23 (FGF23).
- Evaluation of risk factors and patient populations affected.
Main Results:
- Ferric carboxymaltose, iron polymaltose, and saccharated iron oxide are associated with the highest risk.
- Increased FGF23 leads to renal phosphate wasting, causing hypophosphatemia.
- Impaired renal function may be protective, while uncorrectable iron deficiency increases risk and severity.
Conclusions:
- Diagnosis requires clinical suspicion.
- Treatment involves phosphate substitution (oral or IV) based on severity.
- Future therapies may include anti-FGF23 antibodies; vitamin D correction is supportive.