Evidence map›Paper›PMID 34536161›Full record

ReviewMolecular and cellular pediatrics2021

How FGF23 shapes multiple organs in chronic kidney disease.

Maren Leifheit-Nestler, Dieter Haffner

Open access · goldAbstract readReview
In one paragraph

Review in Molecular and cellular pediatrics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

19 citing papers in PubMed, 26 citations in OpenAlex.

  1. Review
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  7. Emerging concepts on the FGF23 regulation and activity.Molecular and cellular biochemistry · 2025
    Review
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  9. Article
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  16. Biological Activity of Different Forms of Oxidized Parathyroid Hormone.International journal of molecular sciences · 2022
    Review
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  19. Article
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

2 authors at 1 institution in 1 country.

Maren Leifheit-NestlerDepartment of Pediatric Kidney, Liver and Metabolic Diseases, Pediatric Research Center, Hannover Medical School Children's Hospital, Carl-Neuberg-Str. 1, 30625, Hannover, Germany. leifheit-nestler.maren@mh-hannover.de.ORCID http://orcid.org/0000-0002-9203-7622
Dieter HaffnerDepartment of Pediatric Kidney, Liver and Metabolic Diseases, Pediatric Research Center, Hannover Medical School Children's Hospital, Carl-Neuberg-Str. 1, 30625, Hannover, Germany.
Medizinische Hochschule Hannover · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic kidney disease (CKD) is associated with distinct alterations in mineral metabolism in children and adults resulting in multiple organ dysfunctions. Children with advanced CKD often suffer from impaired bone mineralization, bone deformities and fractures, growth failure, muscle weakness, and vascular and soft tissue calcification, a complex which was recently termed CKD-mineral and bone disorder (CKD-MBD). The latter is a major contributor to the enhanced cardiovascular disease comorbidity and mortality in these patients. Elevated circulating levels of the endocrine-acting phosphaturic hormone fibroblast growth factor (FGF) 23 are the first detectable alteration of mineral metabolism and thus CKD-MBD. FGF23 is expressed and secreted from osteocytes and osteoblasts and rises, most likely due to increased phosphate load, progressively as kidney function declines in order to maintain phosphate homeostasis. Although not measured in clinical routine yet, CKD-mediated increased circulating levels of FGF23 in children are associated with pathological cardiac remodeling, vascular alterations, and increased cognitive risk. Clinical and experimental studies addressing other FGF23-mediated complications of kidney failure, such as hypertension and impaired bone mineralization, show partly conflicting results, and the causal relationships are not always entirely clear. This short review summarizes regulators of FGF23 synthesis altered in CKD and the main CKD-mediated organ dysfunctions related to high FGF23 levels.

Indexed as

BoneCardiovascular diseasesChronic kidney diseaseCognitionFibroblast growth factor 23Left ventricular hypertrophy

Identifiers

PMID34536161
PMCPMC8449753
OpenAlexW3199545040

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.