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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

The Bone Histology Spectrum in Experimental Renal Failure: Adverse Effects of Phosphate and Parathyroid Hormone Disturbances

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Author(s):
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Batista, Daniella G. [1] ; Neves, Katia R. [1] ; Graciolli, Fabiana G. [1] ; dos Reis, Luciene M. [1] ; Graciolli, Rafael G. [1] ; Dominguez, Wagner V. [1] ; Neves, Carolina L. [1] ; Magalhaes, Andrea O. [1] ; Custodio, Melani R. [1] ; Moyses, Rosa M. [1] ; Jorgetti, Vanda [1, 2]
Total Authors: 11
Affiliation:
[1] Univ Sao Paulo, Sch Med, Div Nephrol, Sao Paulo - Brazil
[2] Lab Fisiopatol Renal LIM16, BR-01246903 Sao Paulo - Brazil
Total Affiliations: 2
Document type: Journal article
Source: CALCIFIED TISSUE INTERNATIONAL; v. 87, n. 1, p. 60-67, JUL 2010.
Web of Science Citations: 5
Abstract

Bone disease is a common disorder of bone remodeling and mineral metabolism, which affects patients with chronic kidney disease. Minor changes in the serum level of a given mineral can trigger compensatory mechanisms, making it difficult to evaluate the role of mineral disturbances in isolation. The objective of this study was to determine the isolated effects that phosphate and parathyroid hormone (PTH) have on bone tissue in rats. Male Wistar rats were subjected to parathyroidectomy and 5/6 nephrectomy or were sham-operated. Rats were fed diets in which the phosphate content was low, normal, or high. Some rats received infusion of PTH at a physiological rate, some received infusion of PTH at a supraphysiological rate, and some received infusion of vehicle only. All nephrectomized rats developed moderate renal failure. High phosphate intake decreased bone volume, and this effect was more pronounced in animals with dietary phosphate overload that received PTH infusion at a physiological rate. Phosphate overload induced hyperphosphatemia, hypocalcemia, and changes in bone microarchitecture. PTH at a supraphysiological rate minimized the phosphate-induced osteopenia. These data indicate that the management of uremia requires proper control of dietary phosphate, together with PTH adjustment, in order to ensure adequate bone remodeling. (AU)