"Phosphatonins" and the regulation of phosphorus homeostasis

Division of Nephrology and Hypertension, Department of Medicine, Mayo Clinic Rochester, Mayo College of Medicine, MN 55905, USA.
American journal of physiology. Renal physiology (Impact Factor: 3.3). 01/2006; 289(6):F1170-82. DOI: 10.1152/ajprenal.00072.2005
Source: PubMed

ABSTRACT Phosphate ions are critical for normal bone mineralization, and phosphate plays a vital role in a number of other biological processes such as signal transduction, nucleotide metabolism, and enzyme regulation. The study of rare disorders associated with renal phosphate wasting has resulted in the discovery of a number of proteins [fibroblast growth factor 23 (FGF-23), secreted frizzled related protein 4 (sFRP-4), matrix extracellular phosphoglycoprotein, and FGF 7 (FGF-7)] that decrease renal sodium-dependent phosphate transport in vivo and in vitro. The "phosphatonins," FGF-23 and sFRP-4, also inhibit the synthesis of 1alpha,25-dihydroxyvitamin D, leading to decreased intestinal phosphate absorption and further reduction in phosphate retention by the organism. In this review, we discuss the biological properties of these proteins, alterations in their concentrations in various clinical disorders, and their possible physiological role.

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    ABSTRACT: Hyperphosphatemia in chronic kidney disease (CKD) patients is a potentially life altering condition that can lead to cardiovascular calcification, metabolic bone disease (renal osteodystrophy) and the development of secondary hyperparathyroidism (SHPT). It is also associated with increased prevalence of cardiovascular diseases and mortality rates. To effectively manage hyperphosphatemia in CKD patients it is important to not only consider pharmacological and nonpharmacological treatment options but also to understand the underlying physiologic pathways involved in phosphorus homeostasis. This review will therefore provide both a background into phosphorus homeostasis and the management of hyperphosphatemia in CKD patients. In addition, it will cover some of the most important reasons for failure to control hyperphosphatemia with emphasis on the effect of the gastric pH on phosphate binders efficiency.
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    ABSTRACT: RESUMEN Uno de los problemas más importantes a los que se enfren-tan los nefrólogos es el alto grado de mortalidad cardiovas-cular de los pacientes en diálisis. Este aumento de la enfer-medad cardiovascular se ha asociado a varios factores, pero entre ellos, la hiperfosfatemia brilla con luz propia. Los ni-veles plasmáticos de fósforo considerados normales en estos pacientes se han ido bajando paulatinamente en los últimos años. Por tanto, el control del fósforo en el paciente con enfermedad renal crónica se ha convertido en un reto que ha incentivado la investigación básica en los últimos años. La siguiente revisión pretende reunir los resultados más novedosos presentados en el último año, haciendo énfasis en los métodos de control de la absorción de fósfo-ro, de su eliminación renal y en las calcificaciones vascula-res, que son una de las consecuencias directas más graves de la hiperfosfatemia. Palabras clave: Fósforo. Enfermedad renal crónica. Quelantes del fósforo. Fosfotoninas. FGF23. Ezrina. Calcificaciones vasculares. SUMMARY One of the most important problems faced by nephrologists is the high degree of cardiovascular mortality in patients on dialy-sis. This increase in cardiovascular disease has been associated with various factors, but, among them, hyperphosphatemia stands out particularly. The serum phosphate levels considered normal in these patients have gradually decreased in recent years. Therefore, phosphate control in the chronic kidney disea-se patient has become a challenge that has stimulated basic re-search in recent years. The aim of the following review is to bring together the most novel results presented in the last year, with emphasis on the methods for control of phosphate absorp-tion, its elimination by the kidneys and vascular calcifications, which are one of the most serious direct consequences of hy-perphosphatemia. Key words: Phosphorus. Chronic kidney disease. Phosphate bin-ders. Phosphotonins. FGF-23. Ezrin. Vascular calcifications.