The bone and the kidney.

Abstract

Renal tubular diseases may present with osteopenia, osteoporosis or osteomalacia, as a result of significant derangements in body electrolytes. In case of insufficient synthesis of calcitriol, as in renal failure, the more complex picture of renal osteodystrophy may develop. Hypothetically, also disturbed renal production of BMP-7 and Klotho could cause bone disease. However, the acknowledgment that osteocytes are capable of producing FGF23, a phosphaturic hormone at the same time modulating renal synthesis of calcitriol, indicates that it is also bone that can influence renal function. Importantly, a feed-back mechanism exists between FGF23 and calcitriol synthesis, while Klotho, produced by the kidney, determines activity and selectivity of FGF23. Identification of human diseases linked to disturbed production of FGF23 and Klotho underlines the importance of this new bone-kidney axis. Kidney and bone communicate reciprocally to regulate the sophisticated machinery responsible for divalent ions homeostasis and for osseous or extraosseous mineralisation processes.

• Authors: Sandro Mazzaferro, Marzia Pasquali, Giuliana Pirrò, Silverio Rotondi, Lida Tartaglione
• Journal: Archives of biochemistry and biophysics (Arch Biochem Biophys) Vol. 503 Issue 1 Pg. 95-102 (Nov 01 2010) ISSN: 1096-0384 [Electronic] United States
• PMID: 20599669 (Publication Type: Journal Article, Review)
• Copyright: Copyright © 2010 Elsevier Inc. All rights reserved.

Chemical References

• Bone Morphogenetic Protein 7
• FGF23 protein, human
• Fibroblast Growth Factors
• Fibroblast Growth Factor-23
• Glucuronidase
• Klotho Proteins

Topics

• Animals
• Bone Diseases (complications, metabolism, physiopathology)
• Bone Morphogenetic Protein 7 (biosynthesis, metabolism)
• Fibroblast Growth Factor-23
• Fibroblast Growth Factors (metabolism)
• Glucuronidase (biosynthesis, metabolism)
• Humans
• Kidney Diseases (complications, metabolism, physiopathology)
• Klotho Proteins