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Two Techniques to Create Hypoparathyroid Mice: Parathyroidectomy Using GFP Glands and Diphtheria-Toxin-Mediated Parathyroid Ablation
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FGF23 neutralization improves chronic kidney disease-associated hyperparathyroidism yet increases mortality
Victoria Shalhoub1, Edward M Shatzen, Sabrina C Ward
1Department of Metabolic Disorders, Amgen Inc., Thousand Oaks, CA, USA.
The Journal of Clinical Investigation
|June 26, 2012
Summary
Neutralizing FGF23 in chronic kidney disease-mineral and bone disorder (CKD-MBD) reduced secondary hyperparathyroidism but worsened mineral imbalances and mortality in rats.
Area of Science:
- Nephrology
- Endocrinology
- Bone Biology
Background:
- Chronic kidney disease-mineral and bone disorder (CKD-MBD) involves secondary hyperparathyroidism (HPT) and elevated FGF23.
- High FGF23 levels in CKD-MBD may contribute to poor outcomes.
Purpose of the Study:
- To investigate the role of FGF23 in CKD-MBD pathogenesis.
- To assess the effects of FGF23 neutralization on secondary HPT and related complications in a rat model.
Main Methods:
- Developed a monoclonal FGF23 antibody (FGF23-Ab).
- Treated CKD-MBD rats with high-phosphate diet using FGF23-Ab or control antibody.
- Evaluated changes in parathyroid hormone, vitamin D, calcium, bone markers, phosphate, and aortic calcification.
Main Results:
- FGF23 neutralization significantly reduced secondary HPT markers (parathyroid hormone, increased vitamin D and calcium).
- Bone metabolism markers improved with FGF23 neutralization.
- However, FGF23-Ab treatment led to dose-dependent increases in serum phosphate and aortic calcification, increasing mortality risk.
Conclusions:
- While FGF23 neutralization ameliorates secondary HPT and improves bone markers in CKD-MBD rats, it causes detrimental mineral disturbances.
- These mineral imbalances, including hyperphosphatemia and calcification, limit therapeutic efficacy and increase mortality, highlighting FGF23's complex role.
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