Evidence map›Paper›PMID 34681722›Full record

ReviewInternational journal of molecular sciences2021

Molecular Basis, Diagnostic Challenges and Therapeutic Approaches of Alport Syndrome: A Primer for Clinicians.

Raquel Martínez-Pulleiro, María García-Murias, Manuel Fidalgo-Díaz, Miguel Ángel García-González

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

14 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
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  5. Expanding theRenal failure · 2025
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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

4 authors at 2 institutions in 1 country.

Raquel Martínez-PulleiroGrupo de Xenética e Bioloxía do Desenvolvemento das Enfermidades Renais, Laboratorio de Nefroloxía (No. 11), Instituto de Investigación Sanitaria de Santiago (IDIS), Complexo Hospitalario de Santiago de Compostela (CHUS), 15706 Santiago de Compostela, Spain.
María García-MuriasGrupo de Xenética e Bioloxía do Desenvolvemento das Enfermidades Renais, Laboratorio de Nefroloxía (No. 11), Instituto de Investigación Sanitaria de Santiago (IDIS), Complexo Hospitalario de Santiago de Compostela (CHUS), 15706 Santiago de Compostela, Spain.ORCID 0000-0001-6416-3480
Manuel Fidalgo-DíazDepartamento de Nefrología, Complexo Hospitalario Universitario de Santiago (CHUS), 15706 Santiago de Compostela, Spain.
Miguel Ángel García-GonzálezGrupo de Xenética e Bioloxía do Desenvolvemento das Enfermidades Renais, Laboratorio de Nefroloxía (No. 11), Instituto de Investigación Sanitaria de Santiago (IDIS), Complexo Hospitalario de Santiago de Compostela (CHUS), 15706 Santiago de Compostela, Spain.
Fundación Pública Galega de Medicina Xenómica · ESComplejo Hospitalario Universitario de Santiago · ES

Funding

Instituto de Salud Carlos III PI15/01467Instituto de Salud Carlos III PI18/00378Xunta de Galicia ED481A-2020/204Xunta de Galicia IN607B-2016/020
6 · The paper itself

Abstract

Alport syndrome is a genetic and hereditary disease, caused by mutations in the type IV collagen genes

Indexed as

Angiotensin-Converting Enzyme InhibitorsAnimalsCollagen Type IVErgocalciferolsHigh-Throughput Nucleotide SequencingHumansIntegrinsLamininNephritis, HereditaryPolymorphism, GeneticAngiotensin-Converting Enzyme InhibitorsCollagen Type IVErgocalciferolsIntegrinsLamininparicalcitolAlport syndromechronic kidney diseaseCOL4Acollagenhereditary kidney disease

Identifiers

PMID34681722
PMCPMC8541626
OpenAlexW3207962085

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.