2013Current Opinion in Endocrinology Diabetes and ObesityRequires access

Phosphate wasting and fibroblast growth factor-23

Mark S. Nanes

Open publisher page 10 citations

Abstract

PURPOSE OF REVIEW: The purpose of this study is to review the regulation of phosphate and recent progress in fibroblast growth factor-23 (FGF-23), a key phosphate regulatory hormone. RECENT FINDINGS: Phosphate is required for mineralization of bone, muscle strength and a host of biologic functions. Phosphate is sensed by bone that responds with secretion of FGF-23. The major action of FGF-23 is to stimulate phosphaturia. Feedback loops between FGF-23, 1,25-dihydroxyvitamin D3 and parathyroid hormone maintain phosphate homeostasis. Information about FGF-23 has accumulated from studies in patients with oncogenic osteomalacia and inherited disorders of phosphate wasting rickets that explains the pathophysiology. Exciting new discoveries have highlighted FGF-23 as an independent risk factor for cardiovascular disease in patients with chronic kidney disease. The phosphate sensor triggering FGF-23 production remains to be identified. SUMMARY: Derangements in FGF-23 production, half-life or downstream response are responsible for several disorders of phosphate wasting, rickets and oncogenic osteomalacia. Very high levels of FGF-23 in renal failure are an independent risk for cardiovascular disease.

About this research paper

What this paper is about

PURPOSE OF REVIEW: The purpose of this study is to review the regulation of phosphate and recent progress in fibroblast growth factor-23 (FGF-23), a key phosphate regulatory hormone. RECENT FINDINGS: Phosphate is required for mineralization of bone, muscle strength and a host of biologic functions. Phosphate is sensed by bone that responds with secretion of FGF-23. The major action of FGF-23 is to stimulate phosphaturia. Feedback loops between FGF-23, 1,25-dihydroxyvitamin D3 and parathyroid hormone maintain phosphate homeostasis. Information about FGF-23 has accumulated from studies in patients with oncogenic osteomalacia and inherited disorders of phosphate wasting rickets that explains the pathophysiology. Exciting new discoveries have highlighted FGF-23 as an independent risk factor for cardiovascular disease in patients with chronic kidney disease. The phosphate sensor triggering FGF-23 production remains to be identified. SUMMARY: Derangements in FGF-23 production, half-life or downstream response are responsible for several disorders of phosphate wasting, rickets and oncogenic osteomalacia. Very high levels of FGF-23 in renal failure are an independent risk for cardiovascular disease.

Why it matters

OpenAlex reports 10 citations for this work. Citation counts describe recorded attention and do not establish research quality.

Key contribution

A contribution statement is not available in the OpenAlex record.

Method / approach

Method details are not available in the OpenAlex metadata.

Main findings

Findings are not separately available in the OpenAlex metadata.

Limitations

Limitations are not available in the OpenAlex metadata.

Applications

Application details are not available in the OpenAlex metadata.

Available abstract

PURPOSE OF REVIEW: The purpose of this study is to review the regulation of phosphate and recent progress in fibroblast growth factor-23 (FGF-23), a key phosphate regulatory hormone. RECENT FINDINGS: Phosphate is required for mineralization of bone, muscle strength and a host of biologic functions. Phosphate is sensed by bone that responds with secretion of FGF-23. The major action of FGF-23 is to stimulate phosphaturia. Feedback loops between FGF-23, 1,25-dihydroxyvitamin D3 and parathyroid hormone maintain phosphate homeostasis. Information about FGF-23 has accumulated from studies in patients with oncogenic osteomalacia and inherited disorders of phosphate wasting rickets that explains the pathophysiology. Exciting new discoveries have highlighted FGF-23 as an independent risk factor for cardiovascular disease in patients with chronic kidney disease. The phosphate sensor triggering FGF-23 production remains to be identified. SUMMARY: Derangements in FGF-23 production, half-life or downstream response are responsible for several disorders of phosphate wasting, rickets and oncogenic osteomalacia. Very high levels of FGF-23 in renal failure are an independent risk for cardiovascular disease.

Key concepts: Fibroblast growth factor 23, Osteomalacia, Rickets, Wasting, Parathyroid hormone, Endocrinology, Fibroblast growth factor, Internal medicine

Related papers

Back to paper searchBrowse research topicsOriginal source
Phosphate wasting and fibroblast growth factor-23 — Research Paper | ScholarLens