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Abstract: FR-PO500

Effects of Ferric Citrate on Phosphate Metabolism in Alport Mice with CKD

Session Information

Category: Bone and Mineral Metabolism

  • 401 Bone and Mineral Metabolism: Basic


  • Myakala, Komuraiah, Georgetown University, Washington, District of Columbia, United States
  • Wang, Xiaoxin, Georgetown University, Washington, District of Columbia, United States
  • Levi, Moshe, Georgetown University, Washington, District of Columbia, United States

The maintenance of phosphate (Pi) homeostasis depends on the absorption of Pi across the intestine, reabsorption by the kidney and resorption by the bone. The mechanisms however still remain unknown and the role of intestinal Pi transport is subject of ongoing debate. Hyperphosphatemia is a common occurrence and plays important roles in cardiovascular and metabolic bone disease. Normalizing the serum Pi by reducing the dietary Pi intake can resolve the biochemical changes which may improve the clinical outcomes in CKD. To investigate the role of intestinal Pi absorption, we studied the effects of the Pi-binder Ferric Citrate (FC) on reducing intestinal absorption of Pi in a mouse model of progressive CKD


4-week old wild type (WT) and Col4a3 knockout (Alport, CKD) mice (n=6 to 8 per group) were fed with control diet (0.9% Pi, 0.6% Ca2+) or control diet supplemented with 2% or 3% ferric citrate (FC) for 5 to 6 weeks. Tissues were harvested and serum biochemistry was measured at 9-10 weeks old mice. To determine the intestinal Pi transport mechanism in CKD, we isolated apical brush border membrane vesicles (BBMVs) from the ileum and studied sodium gradient dependent Pi (Na+/Pi) transport and NaPi-2b protein abundance.


Serum BUN and Pi were increased significantly in Alport CKD mice compared to WT. In parallel to Pi, serum FGF23 levels were markedly increased in CKD mice. Dietary FC administration in CKD mice significantly reduces the serum Pi levels along with a significant decrease in intact FGF23. In addition, serum calcium (Ca2+) was reduced significantly in CKD mice compared to WT. FC diet improved Ca2+ levels in CKD mice. The excretion of Pi in the urine was increased in CKD mice compared to WT mice and in contrast, urinary Pi was reduced in both wild type and CKD mice fed with FC. BBMV Na+/Pi cotransport activity was comparable between WT and CKD mice fed with control diet. However, BBMV Na+/Pi transport activity was increased in both WT and CKD mice fed with FC diet. This was associated with a 2-fold increase in BBMV NaPi-2b protein abundance.


Our data indicates that, the administration of FC improved the dysregulated Pi metabolism in CKD. However, the resultant increase in NaPi-2b protein abundance suggest that FC or any other Pi binder needs to be administered at all times with the diet.


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