The Authors Reply

Abstract

We agree with Ohkido et al.1.Ohkido I. Yokoyama K. Kagami S. et al.The hypothesis that bone turnover influences FGF23 secretion.Kidney Int. 2010; 77: 743Abstract Full Text Full Text PDF PubMed Scopus (6) Google Scholar that osteocytes likely have a critical role in fibroblast growth factor (FGF)23 regulation in chronic kidney disease (CKD). In addition to the supportive findings from their animal studies outlined in ‘The hypothesis that bone turnover influences FGF23 secretion,’ recent human studies have shown that FGF23 expression in bone is already elevated in the early stages of CKD.2.Pereira R.C. Juppner H. Azucena-Serrano C.E. et al.Patterns of FGF-23, DMP1, and MEPE expression in patients with chronic kidney disease.Bone. 2009; 45: 1161-1168Abstract Full Text Full Text PDF PubMed Scopus (209) Google Scholar Moreover, emerging data on the structure and function of osteocytes, their dendritic processes, and surrounding capillary networks have provided further support for the existence of a bone–kidney axis.3.Bonewald L.F. Osteocytes as dynamic multifunctional cells.Ann NY Acad Sci. 2007; 1116: 281-290Crossref PubMed Scopus (289) Google Scholar Future explorations of this hypothesis are likely to yield significant new insights into bone physiology and regulation of phosphorus metabolism and, ideally, the discovery of novel therapeutic targets for various bone and mineral illnesses. However, assessments of bone disease with bone biopsies in the large-scale randomized trials we propose would increase the complexity of trial design and diminish feasibility, and therefore these measurements were not included in the blueprint.4.Isakova T. Gutierrez O.M. Wolf M. A blueprint for randomized trials targeting phosphorus metabolism in chronic kidney disease.Kidney Int. 2009; 76: 705-716Abstract Full Text Full Text PDF PubMed Scopus (94) Google Scholar