Research
Print page Print page
Switch language
Rigshospitalet - a part of Copenhagen University Hospital
Published

Kidney fibroblast growth factor 23 does not contribute to elevation of its circulating levels in uremia

Research output: Contribution to journalJournal articleResearchpeer-review

  1. Cost-effectiveness of lipid lowering with statins and ezetimibe in chronic kidney disease

    Research output: Contribution to journalJournal articleResearchpeer-review

  2. Challenges and opportunities for nephrology in Western Europe

    Research output: Contribution to journalJournal articleResearchpeer-review

  3. Arterial oxygen content regulates plasma erythropoietin independent of arterial oxygen tension: a blinded crossover study

    Research output: Contribution to journalJournal articleResearchpeer-review

  4. U-shaped dietary sodium-associated incidence of chronic kidney disease cautions against salt overrestriction in hypertension

    Research output: Contribution to journalJournal articleResearchpeer-review

  1. New Aspects of the Kidney in the Regulation of Fibroblast Growth Factor 23 (FGF23) and Mineral Homeostasis

    Research output: Contribution to journalReviewResearchpeer-review

  2. Circadian rhythms of mineral metabolism in chronic kidney disease-mineral bone disorder

    Research output: Contribution to journalJournal articleResearchpeer-review

  3. Kidney-Bone-Vascular Axis: Early Signals and Disturbed Circadian Rhythmicity in Uremia

    Research output: Book/ReportPh.D. thesisResearch

  4. Circadian rhythm of activin A and related parameters of mineral metabolism in normal and uremic rats

    Research output: Contribution to journalJournal articleResearchpeer-review

View graph of relations

Fibroblast growth factor 23 (FGF23) secreted by osteocytes is a circulating factor essential for phosphate homeostasis. High plasma FGF23 levels are associated with cardiovascular complications and mortality. Increases of plasma FGF23 in uremia antedate high levels of phosphate, suggesting a disrupted feedback regulatory loop or an extra-skeletal source of this phosphatonin. Since induction of FGF23 expression in injured organs has been reported we decided to examine the regulation of FGF23 gene and protein expressions in the kidney and whether kidney-derived FGF23 contributes to the high plasma levels of FGF23 in uremia. FGF23 mRNA was not detected in normal kidneys, but was clearly demonstrated in injured kidneys, already after four hours in obstructive nephropathy and at 8 weeks in the remnant kidney of 5/6 nephrectomized rats. No renal extraction was found in uremic rats in contrast to normal rats. Removal of the remnant kidney had no effect on plasma FGF23 levels. Well-known regulators of FGF23 expression in bone, such as parathyroid hormone, calcitriol, and inhibition of the FGF receptor by PD173074, had no impact on kidney expression of FGF23. Thus, the only direct contribution of the injured kidney to circulating FGF23 levels in uremia appears to be reduced renal extraction of bone-derived FGF23. Kidney-derived FGF23 does not generate high plasma FGF23 levels in uremia and is regulated differently than the corresponding regulation of FGF23 gene expression in bone.

Original languageEnglish
JournalKidney International
Volume92
Issue number1
Pages (from-to)165-178
Number of pages14
ISSN0085-2538
DOIs
Publication statusPublished - 2017

    Research areas

  • Journal Article

ID: 52424576