Evidence map›Paper›PMID 29740447›Full record

ArticleFrontiers in immunology2018

High Complement Factor H-Related (FHR)-3 Levels Are Associated With the Atypical Hemolytic-Uremic Syndrome-Risk Allele

Richard B Pouw, Irene Gómez Delgado, Alberto López Lera, Santiago Rodríguez de Córdoba, Diana Wouters, Taco W Kuijpers, Pilar Sánchez-Corral

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.5field-weighted citation impact, top 19% 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, 30 citations in OpenAlex.

  1. Article
  2. Role of factor H-related protein 3 inFrontiers in immunology · 2024
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  14. A genome-wide association study identifies key modulators of complement factor H binding to malondialdehyde-epitopes.Proceedings of the National Academy of Sciences of the United States of America · 2020
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  15. Article
  16. Journal of the American Society of Nephrology : JASN · 2020
    Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 5 institutions in 2 countries.

Richard B PouwDepartment of Immunopathology, Sanquin Research and Landsteiner Laboratory of the Academic Medical Center, University of Amsterdam, Amsterdam, Netherlands.
Irene Gómez DelgadoComplement Research Group, Hospital La Paz Institute for Health Research (IdiPAZ), La Paz University Hospital, Center for Biomedical Network Research on Rare Diseases (CIBERER), Madrid, Spain.
Alberto López LeraImmunology Unit, Hospital La Paz Institute for Health Research (IdiPAZ), La Paz University Hospital, Center for Biomedical Network Research on Rare Diseases (CIBERER), Madrid, Spain.
Santiago Rodríguez de CórdobaBiological Research Center (CIB)-CSIC, Center for Biomedical Network Research on Rare Diseases (CIBERER), Madrid, Spain.
Diana WoutersDepartment of Immunopathology, Sanquin Research and Landsteiner Laboratory of the Academic Medical Center, University of Amsterdam, Amsterdam, Netherlands.
Taco W KuijpersDepartment of Pediatric Hematology, Immunology and Infectious Diseases, Emma Children's Hospital, Academic Medical Center, Amsterdam, Netherlands.
Pilar Sánchez-CorralComplement Research Group, Hospital La Paz Institute for Health Research (IdiPAZ), La Paz University Hospital, Center for Biomedical Network Research on Rare Diseases (CIBERER), Madrid, Spain.
Centre for Biomedical Network Research on Rare Diseases · ESHospital La Paz Institute for Health Research · ESAcademic Medical Center · NLEmma Kinderziekenhuis · NLUniversity of Amsterdam · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dysregulation of the complement alternative pathway (AP) is a major pathogenic mechanism in atypical hemolytic-uremic syndrome (aHUS). Genetic or acquired defects in factor H (FH), the main AP regulator, are major aHUS drivers that associate with a poor prognosis. FH activity has been suggested to be downregulated by homologous FH-related (FHR) proteins, including FHR-3 and FHR-1. Hence, their relative levels in plasma could be disease-relevant. The genes coding for FH, FHR-3, and FHR-1 (

Indexed as

Genetic Predisposition to DiseaseAdolescentAdultAllelesAtypical Hemolytic Uremic SyndromeBlood ProteinsChildChild, PreschoolComplement Factor HComplement Pathway, AlternativeEnzyme-Linked Immunosorbent AssayHaplotypesHumansInfantInfant, NewbornYoung AdultBlood ProteinsCFH protein, humanCFHR3 protein, humanComplement Factor Hatypical hemolytic-uremic syndromeCFHR3 genecomplementfactor Hfactor H-related protein 3

Identifiers

PMID29740447
PMCPMC5928496
OpenAlexW2800747112

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.