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Updated: Jun 11, 2026
Murine Hind Limb Long Bone Dissection and Bone Marrow Isolation
Published on: April 14, 2016
The bone and the kidney
Sandro Mazzaferro1, Marzia Pasquali, Giuliana Pirrò
1Department of Clinical Science, Sapienza University of Rome, Italy. sandro.mazzaferro@uniroma1.it
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.
Insights
Bone and kidney diseases are linked through a newly identified bone-kidney axis. This axis involves fibroblast growth factor 23 (FGF23) and Klotho, crucial for mineral homeostasis and bone health.
Area of Science:
- Nephrology
- Endocrinology
- Bone Biology
Background:
- Renal tubular diseases can cause bone disorders like osteopenia and osteoporosis due to electrolyte imbalances.
- Renal failure can lead to renal osteodystrophy from insufficient calcitriol synthesis.
- Emerging evidence suggests fibroblast growth factor 23 (FGF23) and Klotho play roles in bone-kidney communication.
Purpose of the Study:
- To explore the reciprocal communication between bone and kidney.
- To highlight the significance of the newly discovered bone-kidney axis.
- To understand the roles of FGF23 and Klotho in mineral homeostasis.
Main Methods:
- Review of existing literature on renal osteodystrophy and mineral metabolism.
- Analysis of the roles of FGF23 and Klotho in bone and kidney function.
- Examination of feedback mechanisms between FGF23, calcitriol, and Klotho.
Main Results:
- Osteocytes produce FGF23, a hormone that influences renal calcitriol synthesis, indicating bone impacts kidney function.
- A feedback loop exists between FGF23 and calcitriol, with kidney-derived Klotho regulating FGF23 activity.
- Human diseases linked to FGF23 and Klotho dysfunction underscore the importance of this bone-kidney axis.
Conclusions:
- The bone-kidney axis, mediated by FGF23 and Klotho, is critical for regulating divalent ion homeostasis.
- This axis is essential for proper osseous and extraosseous mineralization processes.
- Understanding this communication pathway is vital for managing bone and kidney diseases.
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