Evidence map›Paper›PMID 41398421›Full record

ArticleScientific reports2025

Clinical features of hearing loss and genotype-phenotype correlations in Alport syndrome caused by COL4A4 or COL4A5 variants.

Saeko Matsuzaki, Kiyomitsu Nara, Hideki Mutai, Sayaka Katsunuma, Hirokazu Sakamoto, Mizuki Hirose, Naohiro Wakisaka, Nodoka Adachi, Satoshi Asanuma, Masato Fujioka and 1 more

Abstract read
In one paragraph

Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. 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

11 authors.

Saeko MatsuzakiDivision of Hearing and Balance Research, National Institute of Sensory Organs, NHO Tokyo Medical Center, Tokyo, Japan.
Kiyomitsu NaraDivision of Hearing and Balance Research, National Institute of Sensory Organs, NHO Tokyo Medical Center, Tokyo, Japan.
Hideki MutaiDivision of Hearing and Balance Research, National Institute of Sensory Organs, NHO Tokyo Medical Center, Tokyo, Japan.
Sayaka KatsunumaDepartment of Otolaryngology, Hyogo Prefectural Kobe Children's Hospital, Kobe, Japan.
Hirokazu SakamotoDepartment of Otolaryngology, Hyogo Prefectural Kobe Children's Hospital, Kobe, Japan.
Mizuki HiroseDepartment of Otolaryngology, NHO Kanazawa Medical Center, Kanazawa, Japan.
Naohiro WakisakaDepartment of Otolaryngology, NHO Kanazawa Medical Center, Kanazawa, Japan.
Nodoka AdachiDepartment of Otolaryngology, Saitama Prefectural Children's Medical Center, Saitama, Japan.
Satoshi AsanumaDepartment of Otolaryngology, Saitama Prefectural Children's Medical Center, Saitama, Japan.
Masato FujiokaDepartment of Molecular Genetics, Kitasato University School of Medicine, Kanagawa, Japan.
Tatsuo MatsunagaDivision of Hearing and Balance Research, National Institute of Sensory Organs, NHO Tokyo Medical Center, Tokyo, Japan. tatsuo.matsunaga@kankakuki.jp.

Funding

Japan Agency for Medical Research and Development (AMED) 23gn010063h0002Japan Society for the Promotion of Science (KAKENHI) 21K09660Japan Society for the Promotion of Science (KAKENHI) 24H00648National Hospital Organization of Japan R3-NHO (kankakuki)-02
6 · The paper itself

Abstract

Alport syndrome (AS) is a genetic disorder characterized by progressive nephritis, hearing loss, and visual impairment. Quantitative analyses of hearing in AS are rare. We conducted a retrospective chart review of clinical features and longitudinal follow-up of patients with AS, including multiple evaluations of pure-tone audiograms in each individual and examination of the relationships between hearing loss and genetic variants. Twelve AS cases from eight Japanese families were studied: one family had an autosomal dominant COL4A4 variant and seven carried X-linked variants in COL4A5; all cases presented with moderate hearing loss. Progression of hearing loss was 0.25, 0.29, 0.57, and 2.60 dB HL/year at 500, 1000, 4000, and 8000 Hz, respectively. During follow-up (1-10 years), all families exhibited mid-frequency hearing loss. Hearing loss onset occurred later than renal symptoms in all patients with COL4A5 variants, and the COL4A4 variant did not cause renal symptoms. Hearing loss severity and age of onset appeared to vary depending on the characteristics of the genetic variants, indicating genotype-phenotype correlations; however, hearing decline was predominantly at high frequencies, regardless of genetic variation. These findings provide valuable insights into genotype-phenotype correlations in AS, particularly regarding hearing loss progression and characteristics.

Indexed as

Collagen Type IVHearing LossNephritis, HereditaryAdolescentAdultAge of OnsetChildFemaleGenetic Association StudiesGenotypeHumansMaleMiddle AgedMutationPedigreePhenotypeCOL4A4 protein, humanCOL4A5 protein, humanCollagen Type IV

Identifiers

PMID41398421
PMCPMC12705733

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.