| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 3883369 | Kidney International | 2010 | 4 Pages |
Abstract
Secondary hyperparathyroidism in chronic kidney disease (CKD) develops in response to disturbances in calcium and phosphate metabolism associated with CKD, including FGF23 and klotho. FGF23 activates its receptor FGFR1, splice variant IIIC, in the parathyroid gland via a klotho-dependent mechanism and suppresses parathyroid hormone (PTH) secretion. Klotho also may regulate PTH secretion in an FGF23-independent mode, by modulating parathyroid Na+/K+-ATPase activity. The persistence of hyperparathyroidism with progressing CKD despite high serum FGF23 is indicative of FGF23 resistance.
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Authors
Tilman B. Drüeke,