Next Article in Journal
Crosstalk between Human Microvascular Endothelial Cells and Tubular Epithelial Cells Modulates Pro-Inflammatory Responses Induced by Shiga Toxin Type 2 and Subtilase Cytotoxin
Next Article in Special Issue
Proteomic Characterization of High-Density Lipoprotein Particles from Non-Diabetic Hemodialysis Patients
Previous Article in Journal
A Novel Niosome-Encapsulated Essential Oil Formulation to Prevent Aspergillus flavus Growth and Aflatoxin Contamination of Maize Grains During Storage
Review

FGF23 and Phosphate–Cardiovascular Toxins in CKD

Department of Pediatric Kidney, Liver and Metabolic Diseases Hannover Medical School, 30625 Hannover, Germany
*
Author to whom correspondence should be addressed.
Toxins 2019, 11(11), 647; https://doi.org/10.3390/toxins11110647
Received: 27 September 2019 / Revised: 30 October 2019 / Accepted: 1 November 2019 / Published: 6 November 2019
(This article belongs to the Special Issue Uremia and Metabolic Complications of Chronic Kidney Disease )
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. View Full-Text
Keywords: FGF23; phosphate; chronic kidney disease; cardiovascular disease; hypertension; vascular calcification; left ventricular hypertrophy FGF23; phosphate; chronic kidney disease; cardiovascular disease; hypertension; vascular calcification; left ventricular hypertrophy
Show Figures

Figure 1

MDPI and ACS Style

Vogt, I.; Haffner, D.; Leifheit-Nestler, M. FGF23 and Phosphate–Cardiovascular Toxins in CKD. Toxins 2019, 11, 647. https://doi.org/10.3390/toxins11110647

AMA Style

Vogt I, Haffner D, Leifheit-Nestler M. FGF23 and Phosphate–Cardiovascular Toxins in CKD. Toxins. 2019; 11(11):647. https://doi.org/10.3390/toxins11110647

Chicago/Turabian Style

Vogt, Isabel, Dieter Haffner, and Maren Leifheit-Nestler. 2019. "FGF23 and Phosphate–Cardiovascular Toxins in CKD" Toxins 11, no. 11: 647. https://doi.org/10.3390/toxins11110647

Find Other Styles
Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Article Access Map by Country/Region

1
Back to TopTop