Evidence map›Paper›PMID 27941640›Full record

ReviewToxins2016

Fibroblast Growth Factor-23-A Potential Uremic Toxin.

Piotr Kuczera, Marcin Adamczak, Andrzej Wiecek

Open access · goldAbstract readReview
In one paragraph

Review in Toxins, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
3.4field-weighted citation impact, top 8% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

24 citing papers in PubMed, 41 citations in OpenAlex.

  1. Trial
  2. A guide to uraemic toxicity.Nature reviews. Nephrology · 2026
    Review
  3. Article
  4. Review
  5. Vitamin D-Parathyroid Hormone-Fibroblast Growth Factor 23 Axis and Cardiac Remodeling.American journal of cardiovascular drugs : drugs, devices, and other interventions · 2025
    Review
  6. Review
  7. Article
  8. The direct effect of fibroblast growth factor 23 on vascular smooth muscle cell phenotype and function.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2023
    Article
  9. Article
  10. Article
  11. Classification of Uremic Toxins and Their Role in Kidney Failure.Clinical journal of the American Society of Nephrology : CJASN · 2021
    Review
  12. Review
  13. Article
  14. Review
  15. Review
  16. Review
  17. Review
  18. Review
  19. Survival of patients treated with extended-hours haemodialysis in Europe: an analysis of the ERA-EDTA Registry.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2020
    Article
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Piotr KuczeraDepartment of Nephrology, Transplantation and Internal Medicine, Medical University of Silesia, Katowice 40-027, Poland. pkuczera@sum.edu.pl.
Marcin AdamczakDepartment of Nephrology, Transplantation and Internal Medicine, Medical University of Silesia, Katowice 40-027, Poland. madamczak1@op.pl.
Andrzej WiecekDepartment of Nephrology, Transplantation and Internal Medicine, Medical University of Silesia, Katowice 40-027, Poland. awiecek@sum.edu.pl.
Medical University of Silesia · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

Fibroblast Growth FactorsAnimalsFibroblast Growth Factor-23HumansRenal Insufficiency, ChronicUremiaFGF23 protein, humanFibroblast Growth Factor-23Fibroblast Growth Factorsfibroblast growth factor 23renal replacement therapyuremia

Identifiers

PMID27941640
PMCPMC5198563
OpenAlexW2560177215

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.