Dietary potassium restriction causes hypercalciuria, hypocalcemia and bone loss in male mice

Sathish K. Murali; Mariavittoria D'Acierno; Xiang Zheng; Lena K. Rosenbaek; Louise N. Odgaard; Paul Richard Grimm; Alice Ramesova; Robert Little; Judith Radloff; Paul A. Welling; Qi Wu; Reinhold G. Erben; Robert A. Fenton

doi:10.1172/jci.insight.196339

¹Department of Biomedical Sciences, University of Veterinary Medicine, Vienna, Austria

²Department of Biomedicine, Aarhus University, Aarhus, Denmark

³Division of Nephrology, Johns Hopkins University and School of Medicine, Baltimore, United States of America

⁴Ludwig Boltzmann Institute of Osteology, Vienna, Austria

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¹Department of Biomedical Sciences, University of Veterinary Medicine, Vienna, Austria

²Department of Biomedicine, Aarhus University, Aarhus, Denmark

³Division of Nephrology, Johns Hopkins University and School of Medicine, Baltimore, United States of America

⁴Ludwig Boltzmann Institute of Osteology, Vienna, Austria

Find articles by D'Acierno, M. in: PubMed | Google Scholar

¹Department of Biomedical Sciences, University of Veterinary Medicine, Vienna, Austria

²Department of Biomedicine, Aarhus University, Aarhus, Denmark

³Division of Nephrology, Johns Hopkins University and School of Medicine, Baltimore, United States of America

⁴Ludwig Boltzmann Institute of Osteology, Vienna, Austria

Find articles by Zheng, X. in: PubMed | Google Scholar

¹Department of Biomedical Sciences, University of Veterinary Medicine, Vienna, Austria

²Department of Biomedicine, Aarhus University, Aarhus, Denmark

³Division of Nephrology, Johns Hopkins University and School of Medicine, Baltimore, United States of America

⁴Ludwig Boltzmann Institute of Osteology, Vienna, Austria

Find articles by Rosenbaek, L. in: PubMed | Google Scholar

¹Department of Biomedical Sciences, University of Veterinary Medicine, Vienna, Austria

²Department of Biomedicine, Aarhus University, Aarhus, Denmark

³Division of Nephrology, Johns Hopkins University and School of Medicine, Baltimore, United States of America

⁴Ludwig Boltzmann Institute of Osteology, Vienna, Austria

Find articles by Odgaard, L. in: PubMed | Google Scholar

¹Department of Biomedical Sciences, University of Veterinary Medicine, Vienna, Austria

²Department of Biomedicine, Aarhus University, Aarhus, Denmark

³Division of Nephrology, Johns Hopkins University and School of Medicine, Baltimore, United States of America

⁴Ludwig Boltzmann Institute of Osteology, Vienna, Austria

Find articles by Grimm, P. in: PubMed | Google Scholar |

¹Department of Biomedical Sciences, University of Veterinary Medicine, Vienna, Austria

²Department of Biomedicine, Aarhus University, Aarhus, Denmark

³Division of Nephrology, Johns Hopkins University and School of Medicine, Baltimore, United States of America

⁴Ludwig Boltzmann Institute of Osteology, Vienna, Austria

Find articles by Ramesova, A. in: PubMed | Google Scholar

¹Department of Biomedical Sciences, University of Veterinary Medicine, Vienna, Austria

²Department of Biomedicine, Aarhus University, Aarhus, Denmark

³Division of Nephrology, Johns Hopkins University and School of Medicine, Baltimore, United States of America

⁴Ludwig Boltzmann Institute of Osteology, Vienna, Austria

Find articles by Little, R. in: PubMed | Google Scholar

¹Department of Biomedical Sciences, University of Veterinary Medicine, Vienna, Austria

²Department of Biomedicine, Aarhus University, Aarhus, Denmark

³Division of Nephrology, Johns Hopkins University and School of Medicine, Baltimore, United States of America

⁴Ludwig Boltzmann Institute of Osteology, Vienna, Austria

Find articles by Radloff, J. in: PubMed | Google Scholar

¹Department of Biomedical Sciences, University of Veterinary Medicine, Vienna, Austria

²Department of Biomedicine, Aarhus University, Aarhus, Denmark

³Division of Nephrology, Johns Hopkins University and School of Medicine, Baltimore, United States of America

⁴Ludwig Boltzmann Institute of Osteology, Vienna, Austria

Find articles by Welling, P. in: PubMed | Google Scholar |

¹Department of Biomedical Sciences, University of Veterinary Medicine, Vienna, Austria

²Department of Biomedicine, Aarhus University, Aarhus, Denmark

³Division of Nephrology, Johns Hopkins University and School of Medicine, Baltimore, United States of America

⁴Ludwig Boltzmann Institute of Osteology, Vienna, Austria

Find articles by Wu, Q. in: PubMed | Google Scholar |

¹Department of Biomedical Sciences, University of Veterinary Medicine, Vienna, Austria

²Department of Biomedicine, Aarhus University, Aarhus, Denmark

³Division of Nephrology, Johns Hopkins University and School of Medicine, Baltimore, United States of America

⁴Ludwig Boltzmann Institute of Osteology, Vienna, Austria

Find articles by Erben, R. in: PubMed | Google Scholar

¹Department of Biomedical Sciences, University of Veterinary Medicine, Vienna, Austria

²Department of Biomedicine, Aarhus University, Aarhus, Denmark

³Division of Nephrology, Johns Hopkins University and School of Medicine, Baltimore, United States of America

⁴Ludwig Boltzmann Institute of Osteology, Vienna, Austria

Find articles by Fenton, R. in: PubMed | Google Scholar |

JCI Insight. https://doi.org/10.1172/jci.insight.196339.
Copyright © 2026, Murali et al. This work is licensed under the Creative Commons Attribution 4.0 International License. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

Published January 22, 2026 - Version history

Loss of bone mass has a devastating effect on quality of life. Higher potassium (K⁺) intake is positively correlated with bone health. Here, we investigated whether kidney calcium (Ca²⁺) and phosphate (Pi) handling mechanisms mediate dietary K⁺ effects. Kidney Ca²⁺ and Pi handling proteins were altered in abundance in mice fed a 0% K⁺ diet for 2 weeks. In mice fed a 0.1% K⁺ diet for 4 or 8 weeks, urinary Ca²⁺ excretion increased, plasma Ca²⁺ levels were lower and plasma parathyroid hormone (PTH) levels were higher relative to control 1% K⁺ fed mice. The 0.1% K⁺ fed mice had greater excretion of the bone resorption marker deoxypyridinoline, increased osteoclast number, and decreased total femoral bone mineral density. During chronic low K⁺ intake, major changes in renal Ca²⁺ and Pi transport pathways were absent, except higher abundances of the sodium-potassium-chloride co-transporter (NKCC2) and the sodium-chloride co-transporter (NCC), in line with their role in kidney Ca²⁺ handling. Low dietary K⁺ induced hypocalcemia and changes in PTH were absent in mice with constitutively active NCC, supporting its role in mediating low K⁺ effects on Ca²⁺ homeostasis. Our study provides insights into the management of bone disorders in conditions of chronic electrolyte imbalance.

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Dietary potassium restriction causes hypercalciuria, hypocalcemia and bone loss in male mice

Sathish K. Murali,¹ Mariavittoria D'Acierno,² Xiang Zheng,² Lena K. Rosenbaek,² Louise N. Odgaard,² Paul Richard Grimm,³ Alice Ramesova,¹ Robert Little,² Judith Radloff,¹ Paul A. Welling,³ Qi Wu,² Reinhold G. Erben,⁴ and Robert A. Fenton²

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Dietary potassium restriction causes hypercalciuria, hypocalcemia and bone loss in male mice

Sathish K. Murali,1 Mariavittoria D'Acierno,2 Xiang Zheng,2 Lena K. Rosenbaek,2 Louise N. Odgaard,2 Paul Richard Grimm,3 Alice Ramesova,1 Robert Little,2 Judith Radloff,1 Paul A. Welling,3 Qi Wu,2 Reinhold G. Erben,4 and Robert A. Fenton2

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Sathish K. Murali,¹ Mariavittoria D'Acierno,² Xiang Zheng,² Lena K. Rosenbaek,² Louise N. Odgaard,² Paul Richard Grimm,³ Alice Ramesova,¹ Robert Little,² Judith Radloff,¹ Paul A. Welling,³ Qi Wu,² Reinhold G. Erben,⁴ and Robert A. Fenton²