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FGF23 and Phosphate–Cardiovascular Toxins in CKD
Elevated levels of fibroblast growth factor 23 (FGF23) and phosphate are highly associated with increased cardiovascular disease and mortality in patients suffering from chronic kidney disease (CKD). As the kidney function declines, serum phosphate levels rise and subsequently induce the secretion o...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6891626/ https://www.ncbi.nlm.nih.gov/pubmed/31698866 http://dx.doi.org/10.3390/toxins11110647 |
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author | Vogt, Isabel Haffner, Dieter Leifheit-Nestler, Maren |
author_facet | Vogt, Isabel Haffner, Dieter Leifheit-Nestler, Maren |
author_sort | Vogt, Isabel |
collection | PubMed |
description | Elevated levels of fibroblast growth factor 23 (FGF23) and phosphate are highly associated with increased cardiovascular disease and mortality in patients suffering from chronic kidney disease (CKD). As the kidney function declines, serum phosphate levels rise and subsequently induce the secretion of the phosphaturic hormone FGF23. In early stages of CKD, FGF23 prevents the increase of serum phosphate levels and thereby attenuates phosphate-induced vascular calcification, whereas in end-stage kidney disease, FGF23 fails to maintain phosphate homeostasis. Both hyperphosphatemia and elevated FGF23 levels promote the development of hypertension, vascular calcification, and left ventricular hypertrophy by distinct mechanisms. Therefore, FGF23 and phosphate are considered promising therapeutic targets to improve the cardiovascular outcome in CKD patients. Previous therapeutic strategies are based on dietary and pharmacological reduction of serum phosphate, and consequently FGF23 levels. However, clinical trials proving the effects on the cardiovascular outcome are lacking. Recent publications provide evidence for new promising therapeutic interventions, such as magnesium supplementation and direct targeting of phosphate and FGF receptors to prevent toxicity of FGF23 and hyperphosphatemia in CKD patients. |
format | Online Article Text |
id | pubmed-6891626 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-68916262019-12-12 FGF23 and Phosphate–Cardiovascular Toxins in CKD Vogt, Isabel Haffner, Dieter Leifheit-Nestler, Maren Toxins (Basel) Review Elevated levels of fibroblast growth factor 23 (FGF23) and phosphate are highly associated with increased cardiovascular disease and mortality in patients suffering from chronic kidney disease (CKD). As the kidney function declines, serum phosphate levels rise and subsequently induce the secretion of the phosphaturic hormone FGF23. In early stages of CKD, FGF23 prevents the increase of serum phosphate levels and thereby attenuates phosphate-induced vascular calcification, whereas in end-stage kidney disease, FGF23 fails to maintain phosphate homeostasis. Both hyperphosphatemia and elevated FGF23 levels promote the development of hypertension, vascular calcification, and left ventricular hypertrophy by distinct mechanisms. Therefore, FGF23 and phosphate are considered promising therapeutic targets to improve the cardiovascular outcome in CKD patients. Previous therapeutic strategies are based on dietary and pharmacological reduction of serum phosphate, and consequently FGF23 levels. However, clinical trials proving the effects on the cardiovascular outcome are lacking. Recent publications provide evidence for new promising therapeutic interventions, such as magnesium supplementation and direct targeting of phosphate and FGF receptors to prevent toxicity of FGF23 and hyperphosphatemia in CKD patients. MDPI 2019-11-06 /pmc/articles/PMC6891626/ /pubmed/31698866 http://dx.doi.org/10.3390/toxins11110647 Text en © 2019 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Review Vogt, Isabel Haffner, Dieter Leifheit-Nestler, Maren FGF23 and Phosphate–Cardiovascular Toxins in CKD |
title | FGF23 and Phosphate–Cardiovascular Toxins in CKD |
title_full | FGF23 and Phosphate–Cardiovascular Toxins in CKD |
title_fullStr | FGF23 and Phosphate–Cardiovascular Toxins in CKD |
title_full_unstemmed | FGF23 and Phosphate–Cardiovascular Toxins in CKD |
title_short | FGF23 and Phosphate–Cardiovascular Toxins in CKD |
title_sort | fgf23 and phosphate–cardiovascular toxins in ckd |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6891626/ https://www.ncbi.nlm.nih.gov/pubmed/31698866 http://dx.doi.org/10.3390/toxins11110647 |
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