Evidence for a bone-kidney axis regulating phosphate homeostasis

• Published in: The Journal of clinical investigation Vol. 112; no. 5; pp. 642 - 646
• Main Author: Quarles, L Darryl
• Format: Journal Article
• Language: English
• Published: Ann Arbor American Society for Clinical Investigation 01.09.2003
• Subjects: Biomedical research
• ISSN: 0021-9738; 1558-8238
• DOI: 10.1172/JCI200319687

The control of systemic phosphate homeostasis is not completely understood. Increased circulating levels of the calcemic parathyroid hormone (PTH) results in phosphaturia due to inhibition of sodium-dependent phosphate transport in the renal proximal tubule (1). Reductions in serum phosphate concentrations stimulate renal proximal tubule production of 1,25(OH) sub(2)D sub(3), which in turn increases the gastrointestinal absorption of calcium and phosphorus (2). The resulting increase in calcium leads to the secondary suppression of parathyroid hormone (PTH) and increases in sodium-dependent phosphate transport in the renal proximal tubule. The PTH-vitamin D axis, however, is not sufficient to explain the physiological complexity of systemic phosphate homeostasis. Indeed, phosphate loading has a marked effect to reduce the net rate of proximal tubule phosphate reabsorption that is independent of PTH and vitamin D. In addition, a novel circulating phosphaturic factor, called phosphatonin, is postulated to be primarily responsible for modulating urinary phosphate excretion in a variety of hypophosphatemic disorders.