Abstract

Phosphorus has an essential role in cellular and extracellular metabolism; maintenance of normal phosphorus homeostasis is critical. Phosphorus homeostasis can be affected by diet and certain medications; some intravenous iron formulations can induce renal phosphate excretion and hypophosphatemia, likely through increasing serum concentrations of intact fibroblast growth factor 23. Case studies provide insights into two types of hypophosphatemia: acute symptomatic and chronic hypophosphatemia, while considering the role of pre‐existing conditions and comorbidities, medications, and intravenous iron. This review examines phosphorus homeostasis and hypophosphatemia, with emphasis on effects of iron deficiency and iron replacement using intravenous iron formulations.

Highlights

  • Phosphorus plays a critical biochemical role through its involvement in cellular and extracellular metabolism, as an integral component of nucleic acids, cell membranes, high-energy compounds utilized in metabolism, and through regulating the activity of many enzymes

  • This review focuses on the effects of iron deficiency and parenteral iron replacement on phosphorus homeostasis

  • Chronic hypophosphatemia appears to be associated with inflammatory bowel disease or other causes of chronic gastrointestinal blood loss which may lead to treatment with multiple courses of IV iron without management of the underlying primary cause of the anemia; hypophosphatemia is a distinct possibility through the fibroblast growth factor 23 (FGF23) activation pathway (Table 3).[65,66,67,68,69,70,71,72,73,74,75,76]

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Summary

Introduction

Phosphorus plays a critical biochemical role through its involvement in cellular and extracellular metabolism, as an integral component of nucleic acids, cell membranes, high-energy compounds (eg, adenosine triphosphate [ATP]) utilized in metabolism, and through regulating the activity of many enzymes.

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