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Abstract: SA-PO899

Roles for Type III Sodium-Dependent Phosphate Transporter, PiT-2, in Bone Development and Growth in Mice with Normal and Impaired Kidney Function

Session Information

  • Mineral Disease: CKD-Bone
    November 04, 2017 | Location: Hall H, Morial Convention Center
    Abstract Time: 10:00 AM - 10:00 AM

Category: Mineral Disease

  • 1203 Mineral Disease: CKD-Bone


  • Yamada, Shunsuke, University of Washington, Seattle, Washington, United States
  • Wallingford, Mary C., University of Washington, Seattle, Washington, United States
  • Cox, Timothy C, University of Washington, Seattle, Washington, United States
  • Giachelli, Cecilia M., University of Washington, Seattle, Washington, United States

Phosphate (Pi) is an essential component of bone and involved in normal bone development, growth, and homeostasis. The type III sodium-dependent phosphate transporters, PiT-1 and PiT-2, are expressed in bone but their exact functions remain unclear. In this study, the role of PiT-2 in bone homeostasis in normal and chronic kidney disease (CKD) mice was evaluated.


Global PiT-2 knockout (KO) and wild type (WT) male mice with intact kidneys were euthanized at 10 weeks of age and subjected to serum biochemical determination and micro CT analyses, which included measurement of bone length and bone mineral density (BMD) and calculation of static bone parameters. Furthermore, to determine the impact of PiT-2 deficiency on renal Pi handling, 10-week-old WT and PiT-2 heterozygous knockout (HET) female mice were subjected to 24-hour urine collection and serum measurement, followed by kidney collection. WT and PiT-2 HET mice also underwent two-step 5/6th nephrectomy and were subjected to micro CT analyses at 3 weeks after CKD induction.


Bone length in PiT-2 KO mice was significantly shorter in femur, tibia, and vertebral column than the WT mice. BMD in systemic bones including mandibles and both trabecular and cortical bone of femurs were significantly lowered in the PiT-2 KO mice than the WT mice. When femurs were analyzed by micro CT, both cortical and trabecular bone thickness were decreased in the PiT-2 KO mice compared with the WT mice. No significant differences were observed in bone mineral density, serum calcium and Pi levels, kidney function, renal mRNA expression of SLC34A1 and SLC34A3, and fractional excretion of Pi between the WT and PiT-2 HET mice. However, in the setting of CKD and high Pi diet feeding, PiT-2 haploinsufficiency decreased trabecular bone volume and thickness but did not change cortical bone volume and had no effect on serum levels of creatinine, calcium, and Pi.


PiT-2 is required for bone development and growth under both normal kidney function and CKD, and enhancing its activity might provide benefits in CKD patients with bone disorders.


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