| Theme | New Perspectives of Molecular Biomarker in Dialysis Therapy | |
|---|---|---|
| Title | Biomarkers of bone and mineral metabolic disorders | |
| Publish Date | 2011/04 | |
| Author | Fumihiko Koiwa | Division of Nephrology, Department of Internal Medicine, Showa University Fujigaoka Hospital |
| Author | Yuichi Maruta | Division of Nephrology, Department of Internal Medicine, Showa University Fujigaoka Hospital |
| [ Summary ] | Although the standardized diagnostic method for determining bone disease in CKD-MBD patients is bone biopsy, measurement of serum bone metabolic markers can be readily evaluated to determine changes in bone mineral density or bone turnover. It should be kept in mind that there are some bone markers, including serum levels, which are influenced by renal function. Fetuin A is an inhibitor of extraosseous calcification in supersaturated environments which operates through binding excess minerals or the fetuin-mineral complex. Serum fetuin A levels are reduced due to renal failure. However, the relationship between serum fetuin A levels and calcification have not been clarified even for cases of chronic renal failure. Fibroblast growth factor 23 (FGF 23) binds to the FGF receptor klotho complex in the kidneys, induces phosphaturia by decreasing phosphate reabsorption and decreases the synthesis of 1,25-dihydroxyvitamin D. Serum FGF 23 levels increase in early renal failure, leading to the onset and progression of secondary hyperparathyroidism. Moreover, FGF 23 is associated with various clinical outcomes, including phosphate metabolic disorder, progression of renal failure, cardiovascular disease, and mortality. The detectability of these outcomes is higher when using serum phosphate levels as a biomarker. |
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