Elsevier

Kidney International

Volume 74, Issue 5, 1 September 2008, Pages 566-570
Kidney International

Mini Review
Does Fgf23–klotho activity influence vascular and soft tissue calcification through regulating mineral ion metabolism?

https://doi.org/10.1038/ki.2008.218Get rights and content
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Recent studies describe a novel role of fibroblast growth factor-23 (Fgf23)–klotho activity in the systemic regulation of calcium and phosphate homeostasis. Both Fgf23 and klotho ablated mice develop extensive vascular and soft tissue calcification. Inability to clear the required amount of phosphate by the kidney, due to the absence of Fgf23–klotho activity, leads to increased accumulation of serum phosphate in these genetically modified mice, causing extensive calcification. Serum calcium and 1,25 hydroxyvitamin D levels are also elevated in both Fgf23 and klotho ablated mice. Moreover, increased sodium phosphate co-transporter activity in both Fgf23 and klotho ablated mice increases renal phosphate reabsorption which in turn can facilitate calcification. Collectively, these observations bring new insights into our understanding of the roles of the Fgf23–klotho axis in the development of vascular and soft tissue calcification.

Keywords

Fgf23
klotho
calcification
hyperphosphatemia
NaPi2a

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