ReviewEuropean journal of pediatrics2011
Clinical practice. Fibroblast growth factor (FGF)23: a new hormone.
Review in European journal of pediatrics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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
16 citing papers in PubMed, 42 citations in OpenAlex.
- Nephrocalcinosis tendency does not worsen under burosumab treatment for X-linked hypophosphatemic rickets: a multicenter pediatric study.Frontiers in pediatrics · 2024Article
- Skeletal and extraskeletal disorders of biomineralization.Nature reviews. Endocrinology · 2022Review
- Rickets, elevated fibroblast growth factor-23 and mild anemia: Answers.Pediatric nephrology (Berlin, Germany) · 2021Article
- Investigation of the serum vitamin D level in infants followed up with the diagnosis of laryngomalacia: a case-control study.European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery · 2021Article
- Congenital Conditions of Hypophosphatemia Expressed in Adults.Calcified tissue international · 2021Review
- Use of calcimimetics in children with normal kidney function.Pediatric nephrology (Berlin, Germany) · 2019Review
- Vitamin DAnimal nutrition (Zhongguo xu mu shou yi xue hui) · 2016Article
- Hypophosphatemic rickets due to perturbations in renal tubular function.Pediatric nephrology (Berlin, Germany) · 2014Review
- FGF23 and Phosphate Wasting Disorders.Bone research · 2013Review
- FGF23 production by osteocytes.Pediatric nephrology (Berlin, Germany) · 2013Review
- Renal phosphate handling in Gitelman syndrome--the results of a case-control study.Pediatric nephrology (Berlin, Germany) · 2013Article
- Phosphate homeostasis and its role in bone health.Pediatric nephrology (Berlin, Germany) · 2012Review
- Genetic disorders of phosphate regulation.Pediatric nephrology (Berlin, Germany) · 2012Review
- Bone disease in pediatric idiopathic hypercalciuria.World journal of nephrology · 2012Review
- Clinical practice: diagnostic approach to the rachitic child.European journal of pediatrics · 2011Review
- Calcitriol, calcidiol, parathyroid hormone, and fibroblast growth factor-23 interactions in chronic kidney disease.Journal of veterinary emergency and critical care (San Antonio, Tex. : 2001)Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Until a decade ago, two main hormones were recognized as directly affecting phosphate homeostasis and, with that, bone metabolism: parathyroid hormone and 1,25(OH)(2) vitamin D (calcitriol). It was only a decade ago that the third major player hormone was found, linking gut, bone, and kidney. The physiologic role of fibrinogen growth factor (FGF)23 is to maintain serum phosphate concentration within a narrow range. Secreted from osteocytes, it modulates kidney handling of phosphate reabsorption and calcitriol production. Genetic and acquired abnormalities in FGF23 structure and metabolism cause conditions of either hyper-FGF23-manifested by hypophosphatemia, low serum calcitriol, and rickets/osteomalacia-or hypo-FGF23, expressed by hyperphosphatemia, high serum calcitriol, and extra-skeletal calcifications. In patients with chronic renal failure, FGF23 levels increase as kidney functions deteriorate and are under investigation to learn if the hormone actually participates in the pathophysiology of the deranged bone and mineral metabolism typical for these patients and, if so, whether it might serve as a therapeutic target. This review addresses the physiology and pathophysiology of FGF23 and its clinical applications.
Indexed as
Identifiers
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.