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Published on: June 29, 2015
The ins and outs of ferric citrate
1Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA; Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee, USA; Section of Integrative Physiology, Department of Medical Cell Biology, Uppsala University, Uppsala, Sweden; Department of Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, Nashville, Tennessee, USA.
Insights
Ferric citrate effectively treats anemia and high phosphate levels in kidney disease patients. Its iron absorption relies on ferroportin, not passive transport, in genetic models.
Area of Science:
- Nephrology
- Gastroenterology
- Hematology
Background:
- Ferric citrate is clinically used for hyperphosphatemia in chronic kidney disease (CKD) patients.
- It is also approved for iron replacement in iron-deficiency anemia.
- Understanding its absorption mechanism is crucial for optimizing treatment.
Purpose of the Study:
- To investigate the mechanism of enteric iron absorption from ferric citrate.
- To determine the role of ferroportin in ferric citrate iron absorption.
- To assess if paracellular transport contributes to iron absorption from ferric citrate.
Main Methods:
- Utilized genetic models with and without chronic kidney injury.
- Administered ferric citrate to these models.
- Assessed iron absorption in relation to ferroportin expression levels.
Main Results:
- Enteric iron absorption from ferric citrate is dependent on ferroportin expression.
- Paracellular iron transport does not play a significant role in ferric citrate absorption.
- Findings were consistent in models with and without chronic kidney injury.
Conclusions:
- Ferric citrate absorption is primarily mediated by the active transporter ferroportin.
- This study clarifies the molecular mechanism of iron absorption from ferric citrate.
- The findings support the targeted use of ferric citrate in managing iron deficiency and related conditions.
Abstract:
Ferric citrate is used clinically for the treatment of hyperphosphatemia in patients with chronic kidney disease and is approved as an oral iron replacement product for patients with iron-deficiency anemia. In this issue of Kidney International, Hanudel and colleagues take advantage of genetic models with and without chronic kidney injury to demonstrate that the enteric absorption of iron delivered by ferric citrate is dependent on ferroportin expression and does not involve paracellular iron transport.
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