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Emerging role of a phosphatonin in mineral homeostasis and its derangements.
Eur J Clin Invest. 2006 Aug; 36 Suppl 2:34-42.EJ

Abstract

BACKGROUND

The study of a distinct group of renal phosphate wasting disorders with bone disease which comprise X-linked hypophosphatemic rickets (XLH), autosomal dominant hypophosphatemic rickets (ADHR) and tumour-induced osteomalacia (TIO) gave rise to the identification of different hormone-like peptides, also known as phosphatonins. These factors are responsible for the major disease features that characterize XLH, ADHR and TIO. Recent reports on one of these phosphatonins, fibroblast growth factor-23 (FGF-23), point to a general role of this factor in mineral ion metabolism.

OBJECTIVES

The main focus regards recent evidence implicating FGF-23 in normal and disordered mineral homeostasis with special emphasis on chronic kidney disease. The interactions of FGF-23 with phosphate, parathyroid hormone and vitamin D are discussed in detail.

SUMMARY

The FGF-23 has been shown to increase urinary phosphate excretion, inhibit bone mineralization and suppress 1,25-dihydroxy vitamin D(3)[1,25(OH)(2)D(3)], the main characteristics that XLH, ADHR and TIO have in common. Apart from its role in these phosphate wasting disorders serum FGF-23 is elevated in hypoparathyroidism and humoral hypercalcaemia of malignancy and responds to altered dietary phosphate and calcium supply in healthy subjects. The FGF-23 is also variably elevated in chronic kidney disease and associated secondary hyperparathyroidism where it correlates positively with serum phosphate and parathyroid hormone and negatively with 1,25(OH)(2)D(3). Such relationships, along with data from experimental studies, raise the question of whether FGF-23 contributes to the pathophysiology of chronic kidney disease.

Authors+Show Affiliations

Institute of Physiology, Zurich, Switzerland. bernd.bielesz@gmx.net

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Review

Language

eng

PubMed ID

16884396

Citation

Bielesz, B. "Emerging Role of a Phosphatonin in Mineral Homeostasis and Its Derangements." European Journal of Clinical Investigation, vol. 36 Suppl 2, 2006, pp. 34-42.
Bielesz B. Emerging role of a phosphatonin in mineral homeostasis and its derangements. Eur J Clin Invest. 2006;36 Suppl 2:34-42.
Bielesz, B. (2006). Emerging role of a phosphatonin in mineral homeostasis and its derangements. European Journal of Clinical Investigation, 36 Suppl 2, 34-42.
Bielesz B. Emerging Role of a Phosphatonin in Mineral Homeostasis and Its Derangements. Eur J Clin Invest. 2006;36 Suppl 2:34-42. PubMed PMID: 16884396.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Emerging role of a phosphatonin in mineral homeostasis and its derangements. A1 - Bielesz,B, PY - 2006/8/4/pubmed PY - 2007/2/23/medline PY - 2006/8/4/entrez SP - 34 EP - 42 JF - European journal of clinical investigation JO - Eur J Clin Invest VL - 36 Suppl 2 N2 - BACKGROUND: The study of a distinct group of renal phosphate wasting disorders with bone disease which comprise X-linked hypophosphatemic rickets (XLH), autosomal dominant hypophosphatemic rickets (ADHR) and tumour-induced osteomalacia (TIO) gave rise to the identification of different hormone-like peptides, also known as phosphatonins. These factors are responsible for the major disease features that characterize XLH, ADHR and TIO. Recent reports on one of these phosphatonins, fibroblast growth factor-23 (FGF-23), point to a general role of this factor in mineral ion metabolism. OBJECTIVES: The main focus regards recent evidence implicating FGF-23 in normal and disordered mineral homeostasis with special emphasis on chronic kidney disease. The interactions of FGF-23 with phosphate, parathyroid hormone and vitamin D are discussed in detail. SUMMARY: The FGF-23 has been shown to increase urinary phosphate excretion, inhibit bone mineralization and suppress 1,25-dihydroxy vitamin D(3)[1,25(OH)(2)D(3)], the main characteristics that XLH, ADHR and TIO have in common. Apart from its role in these phosphate wasting disorders serum FGF-23 is elevated in hypoparathyroidism and humoral hypercalcaemia of malignancy and responds to altered dietary phosphate and calcium supply in healthy subjects. The FGF-23 is also variably elevated in chronic kidney disease and associated secondary hyperparathyroidism where it correlates positively with serum phosphate and parathyroid hormone and negatively with 1,25(OH)(2)D(3). Such relationships, along with data from experimental studies, raise the question of whether FGF-23 contributes to the pathophysiology of chronic kidney disease. SN - 0014-2972 UR - https://www.unboundmedicine.com/medline/citation/16884396/Emerging_role_of_a_phosphatonin_in_mineral_homeostasis_and_its_derangements_ L2 - https://doi.org/10.1111/j.1365-2362.2006.01659.x DB - PRIME DP - Unbound Medicine ER -