ReviewToxins2019
FGF23 and Phosphate-Cardiovascular Toxins in CKD.
Review in Toxins, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 4 of them syntheses that pooled 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.
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.
Who cites it
57 citing papers in PubMed, 4 syntheses or guidelines pooled it, 90 citations in OpenAlex.
- Association between fibroblast growth factor 23 and coronary artery calcification in patients with chronic kidney disease: a meta-analysis.Frontiers in endocrinology · 2026Pooled it
- Phosphate binders for preventing and treating chronic kidney disease-mineral and bone disorder (CKD-MBD).The Cochrane database of systematic reviews · 2025Pooled it
- FGF-23 as a Biomarker for Carotid Plaque Vulnerability: A Systematic Review.Medical sciences (Basel, Switzerland) · 2025Pooled it
- Role of klotho and fibroblast growth factor 23 in arterial calcification, thickness, and stiffness: a meta-analysis of observational studies.Scientific reports · 2024Pooled it
- High cut-off dialysis mitigates pro-calcific effects of plasma on vascular progenitor cells.Scientific reports · 2021Trial
- Phosphate: An Anion Controlling Metabolic Functions.Nutrients · 2026Review
- Gestational diabetes as an inter-generational cardiometabolic risk factor: spotlight on emerging exerkines.Cardiovascular diabetology · 2026Review
- DNA hypermethylation of FGFR2 drives fibrosis in the aging kidney.Scientific reports · 2026Article
- Band keratopathy and conjunctival calcification in end-stage kidney disease: epidemiology, pathophysiology and clinical management.Clinical kidney journal · 2026Review
- High-Phosphate-Induced Hypertension: The Pathogenic Role of Fibroblast Growth Factor 23 (FGF23) Signaling in Sympathetic Nervous System Activation.International journal of molecular sciences · 2026Review
- Heterogeneous regulation of fibroblast growth factor 23 in acute kidney injury, chronic kidney disease, and polycystic kidney disease: mechanisms, diagnostic utility, and clinical implications.Frontiers in molecular biosciences · 2026Review
- Chronic kidney disease as an active driver of digestive tract tumors: mechanistic insights and emerging management strategies.Frontiers in cell and developmental biology · 2026Review
- Combined concentrations and genetic variability of fibroblast growth factors predict cardiovascular risk in renal patients.iScience · 2025Article
- Pathophysiological changes in patients during hemodialysis and blood reinfusion predict potential development of hemodialysis reactions.Renal failure · 2025Article
- Effects of Fibroblast Growth Factor 23 (FGF23) on the Cardiovascular System: A Review of Literature.Cureus · 2025Review
- New and Emerging Biomarkers in Chronic Kidney Disease.Biomedicines · 2025Review
- Hyperphosphatemia in Kidney Failure: Pathophysiology, Challenges, and Critical Role of Phosphorus Management.Nutrients · 2025Review
- A machine learning-based nomogram for predicting graft survival in allograft kidney transplant recipients: a 20-year follow-up study.Frontiers in medicine · 2025Article
- Emerging concepts on the FGF23 regulation and activity.Molecular and cellular biochemistry · 2025Review
- Tight Phosphate Control in ESKD Patients Is Warranted: PRO.Kidney360 · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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What OpenQuestion holds
Registered trials
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.