Next Article in Journal
Venom Gland Transcriptomic and Proteomic Analyses of the Enigmatic Scorpion Superstitionia donensis (Scorpiones: Superstitioniidae), with Insights on the Evolution of Its Venom Components
Next Article in Special Issue
Modified Lipids and Lipoproteins in Chronic Kidney Disease: A New Class of Uremic Toxins
Previous Article in Journal
Evolution of the Cytolytic Pore-Forming Proteins (Actinoporins) in Sea Anemones
Previous Article in Special Issue
Indoxyl Sulfate—Review of Toxicity and Therapeutic Strategies
Article Menu
Issue 12 (December) cover image

Export Article

Open AccessReview
Toxins 2016, 8(12), 369; doi:10.3390/toxins8120369

Fibroblast Growth Factor-23—A Potential Uremic Toxin

Department of Nephrology, Transplantation and Internal Medicine, Medical University of Silesia, Katowice 40-027, Poland
*
Author to whom correspondence should be addressed.
Academic Editor: R. Vanholder
Received: 28 September 2016 / Revised: 30 November 2016 / Accepted: 1 December 2016 / Published: 8 December 2016
(This article belongs to the Special Issue Novel Issues in Uremic Toxicity)
View Full-Text   |   Download PDF [432 KB, uploaded 8 December 2016]   |  

Abstract

Fibroblast growth factor-23 (FGF23) is a circulating member of the FGF family produced mainly by the osteocytes and osteoblasts that can act as a hormone. The main action of FGF23 is to lower phosphatemia via the reduction of urinary phosphate reabsorption and the decrease of 1,25(OH)2-D generation in the kidney. In the course of chronic kidney disease (CKD), plasma FGF23 concentration rises early, most probably to compensate the inability of the deteriorating kidneys to excrete an adequate amount of phosphate. However, this comes at the cost of FGF23-related target organ toxicity. Results of clinical studies suggest that elevated plasma FGF23 concentration is independently associated with the increased risk of CKD progression, occurrence of cardio-vascular complications, and mortality in different stages of CKD. FGF23 also contributes to cardiomyocyte hypertrophy, vascular calcification, and endothelial dysfunction. The impact of FGF23 on heart muscle is not dependent on Klotho, but rather on the PLCγ–calcineurin–NFAT (nuclear factor of activated T-cells) pathway. Among the factors increasing plasma FGF23 concentration, active vitamin D analogues play a significant role. Additionally, inflammation and iron deficiency can contribute to the increase of plasma FGF23. Among the factors decreasing plasma FGF23, dietary phosphate restriction, some intestinal phosphate binders, cinacalcet (and other calcimimetics), and nicotinamide can be enumerated. Anti-FGF23 antibodies have also recently been developed to inhibit the action of FGF23 in target organs. Still, the best way to normalize plasma FGF23 in maintenance hemodialysis patients is restoring kidney function by successful kidney transplantation. View Full-Text
Keywords: fibroblast growth factor 23; renal replacement therapy; uremia fibroblast growth factor 23; renal replacement therapy; uremia
Figures

Figure 1

This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

Scifeed alert for new publications

Never miss any articles matching your research from any publisher
  • Get alerts for new papers matching your research
  • Find out the new papers from selected authors
  • Updated daily for 49'000+ journals and 6000+ publishers
  • Define your Scifeed now

SciFeed Share & Cite This Article

MDPI and ACS Style

Kuczera, P.; Adamczak, M.; Wiecek, A. Fibroblast Growth Factor-23—A Potential Uremic Toxin. Toxins 2016, 8, 369.

Show more citation formats Show less citations formats

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

Related Articles

Article Metrics

Article Access Statistics

1

Comments

[Return to top]
Toxins EISSN 2072-6651 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top