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NDT Advance Access originally published online on November 7, 2008
Nephrology Dialysis Transplantation 2009 24(1):4-7; doi:10.1093/ndt/gfn620
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© The Author [2008]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org



Does FGF23 toxicity influence the outcome of chronic kidney disease?

Mohammed Shawkat Razzaque

Department of Developmental Biology, Harvard School of Dental Medicine, Boston, MA, USA

M. Shawkat Razzaque, Department of Developmental Biology, Harvard School of Dental Medicine, Research and Education Building, Room # 304, 190 Longwood Avenue, Boston, MA 02115, USA. Tel: +1-617-432-5768; Fax: +617-432-5767; E-mail: mrazzaque@hms.harvard.edu; razzaquems@yahoo.com

Keywords: CKD; FGF23; phosphate homeostasis; vitamin D

The first 150 words of the full text of this article appear below.



   Fibroblast growth factor-23 (FGF23)
 
Maintenance of physiologic phosphate balance is important for essential cellular functions [1]. Dysregulation of the phosphate balance in the form of hypophosphataemia can lead to the development of myopathy, cardiac dysfunction, haematological abnormalities and bone mineralization defects [1]. In contrast, hyperphosphataemia can cause vascular and soft tissue calcification [2,3]. Studies have convincingly demonstrated that FGF23 is a master regulator of systemic phosphate homeostasis [4–9].

FGF23 is a 30 kDa protein that is proteolytically processed to generate smaller N-terminal (~18 kDa) and C-terminal (~12 kDa) fragments. The N-terminal fragment of FGF23 contains the FGF receptor-binding domain, while the C-terminal fragment is proposed to be necessary for interaction with Klotho (a type 1 membrane protein with homology to ß-glucosidase), which is believed to be a cofactor in FGF23–FGF receptor interactions [10]. FGF23 is a circulating phosphaturic factor that controls systemic . . . [Full Text of this Article]



   FGF23 and CKD
 


   Elevated serum FGF23 and mortality
 


   Concluding remarks
 

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FASEB J.Home page
T. Nakatani, M. Ohnishi, and M. S. Razzaque
Inactivation of klotho function induces hyperphosphatemia even in presence of high serum fibroblast growth factor 23 levels in a genetically engineered hypophosphatemic (Hyp) mouse model
FASEB J, November 1, 2009; 23(11): 3702 - 3711.
[Abstract] [Full Text] [PDF]


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Am. J. Physiol. Renal Physiol.Home page
M. S. Razzaque
FGF23-mediated regulation of systemic phosphate homeostasis: is Klotho an essential player?
Am J Physiol Renal Physiol, March 1, 2009; 296(3): F470 - F476.
[Abstract] [Full Text] [PDF]