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...
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| Format: | Article |
| Language: | English |
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MDPI AG
2019-11-01
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| Series: | Toxins |
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| Online Access: | https://www.mdpi.com/2072-6651/11/11/647 |
| _version_ | 1828115914522886144 |
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| author | Isabel Vogt Maren Leifheit-Nestler |
| author_facet | Isabel Vogt Maren Leifheit-Nestler |
| author_sort | Isabel Vogt |
| collection | DOAJ |
| 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. |
| first_indexed | 2024-04-11T12:48:52Z |
| format | Article |
| id | doaj.art-ac71eecbf311477795053a0f1e5fbac1 |
| institution | Directory Open Access Journal |
| issn | 2072-6651 |
| language | English |
| last_indexed | 2024-04-11T12:48:52Z |
| publishDate | 2019-11-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Toxins |
| spelling | doaj.art-ac71eecbf311477795053a0f1e5fbac12022-12-22T04:23:16ZengMDPI AGToxins2072-66512019-11-01111164710.3390/toxins11110647toxins11110647FGF23 and Phosphate–Cardiovascular Toxins in CKDIsabel Vogt0Maren Leifheit-Nestler1Department of Pediatric Kidney, Liver and Metabolic Diseases Hannover Medical School, 30625 Hannover, GermanyDepartment of Pediatric Kidney, Liver and Metabolic Diseases Hannover Medical School, 30625 Hannover, GermanyElevated 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.https://www.mdpi.com/2072-6651/11/11/647fgf23phosphatechronic kidney diseasecardiovascular diseasehypertensionvascular calcificationleft ventricular hypertrophy |
| spellingShingle | Isabel Vogt Maren Leifheit-Nestler FGF23 and Phosphate–Cardiovascular Toxins in CKD Toxins fgf23 phosphate chronic kidney disease cardiovascular disease hypertension vascular calcification left ventricular hypertrophy |
| 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 | fgf23 phosphate chronic kidney disease cardiovascular disease hypertension vascular calcification left ventricular hypertrophy |
| url | https://www.mdpi.com/2072-6651/11/11/647 |
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