Evidence map›Paper›PMID 15599641›Full record

ArticleJournal of human genetics2005

Association of a single-nucleotide polymorphism in the immunoglobulin mu-binding protein 2 gene with immunoglobulin A nephropathy.

Shigeru Ohtsubo, Aritoshi Iida, Kosaku Nitta, Toshihiro Tanaka, Ryo Yamada, Yozo Ohnishi, Shiro Maeda, Tatsuhiko Tsunoda, Takashi Takei, Wataru Obara and 15 more

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Journal of human genetics, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.8field-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

7 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. Review
  3. Development of a model of early-onset IgA nephropathy.Journal of the American Society of Nephrology : JASN · 2012
    Article
  4. Article
  5. Genetics and immunopathogenesis of IgA nephropathy.Clinical reviews in allergy & immunology · 2011
    Review
  6. Genetic studies of IgA nephropathy: past, present, and future.Pediatric nephrology (Berlin, Germany) · 2010
    Review
  7. 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

25 authors at 7 institutions in 1 country.

Shigeru OhtsuboHuman Genome Center, The Institute of Medical Science, University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo, 108-8639, Japan.
Aritoshi IidaLaboratory for Genotyping, SNP Research Center, The Institute of Physical and Chemical Research (RIKEN), Tokyo, Japan.
Kosaku NittaDepartment of Medicine, Kidney Center, Tokyo Women's Medical University, Tokyo, Japan.
Toshihiro TanakaLaboratory for Cardiovascular Diseases, SNP Research Center, The Institute of Physical and Chemical Research (RIKEN), Tokyo, Japan.
Ryo YamadaLaboratory for Rheumatic Diseases, SNP Research Center, The Institute of Physical and Chemical Research (RIKEN), Tokyo, Japan.
Yozo OhnishiLaboratory for Cardiovascular Diseases, SNP Research Center, The Institute of Physical and Chemical Research (RIKEN), Tokyo, Japan.
Shiro MaedaLaboratory for Diabetic Nephropathy, SNP Research Center, The Institute of Physical and Chemical Research (RIKEN), Tokyo, Japan.
Tatsuhiko TsunodaLaboratory for Medical Informatics, SNP Research Center, The Institute of Physical and Chemical Research (RIKEN), Tokyo, Japan.
Takashi TakeiDepartment of Medicine, Kidney Center, Tokyo Women's Medical University, Tokyo, Japan.
Wataru ObaraDepartment of Urology, Iwate Medical University, Iwate, Japan.
Fumihiro AkiyamaDivision of Clinical Nephrology and Rheumatology, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan.
Kyoko ItoDepartment of Medicine, Kidney Center, Tokyo Women's Medical University, Tokyo, Japan.
Kazuho HondaDepartment of Medicine, Kidney Center, Tokyo Women's Medical University, Tokyo, Japan.
Keiko UchidaDepartment of Medicine, Kidney Center, Tokyo Women's Medical University, Tokyo, Japan.
Ken TsuchiyaDepartment of Medicine, Kidney Center, Tokyo Women's Medical University, Tokyo, Japan.
Wako YumuraDepartment of Medicine, Kidney Center, Tokyo Women's Medical University, Tokyo, Japan.
Takashi UjiieDepartment of Urology, Iwate Prefectural Ofunato Hospital, Iwate, Japan.
Yutaka NaganeDepartment of Urology, Sanai Hospital, Iwate, Japan.
Satoru MiyanoHuman Genome Center, The Institute of Medical Science, University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo, 108-8639, Japan.
Yasushi SuzukiDepartment of Urology, Iwate Medical University, Iwate, Japan.
Ichiei NaritaDivision of Clinical Nephrology and Rheumatology, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan.
Fumitake GejyoDivision of Clinical Nephrology and Rheumatology, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan.
Tomoaki FujiokaDepartment of Urology, Iwate Medical University, Iwate, Japan.
Hiroshi NiheiDepartment of Medicine, Kidney Center, Tokyo Women's Medical University, Tokyo, Japan.
Yusuke NakamuraHuman Genome Center, The Institute of Medical Science, University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo, 108-8639, Japan. yusuke@ims.u-tokyo.ac.jp.
Tokyo Women's Medical University · JPRIKEN · JPIwate Medical University · JPNiigata University · JPThe University of Tokyo · JPIwate Prefectural Central Hospital · JPTokyo University of Science · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Immunoglobulin A (IgA) nephropathy is the most common form of primary glomerulonephritis worldwide. The pathogenesis of IgA nephropathy is unknown, but it is certain that some genetic factors are involved in susceptibility to the disease. Employing a large-scale, case-control association study using gene-based single-nucleotide polymorphism (SNP) markers, we previously reported four candidate genes. We report here an additional significant association between IgA nephropathy and an SNP located in the gene encoding immunoglobulin micro-binding protein 2 (IGHMBP2) at chromosome 11q13.2-q13.4. The association (chi2 =17.1, p = 0.00003; odds ratio of 1.85 with 95% confidence interval of 1.39-2.50 in a dominant association model) was found using DNA from 465 affected individuals and 634 controls. The SNP (G34448A) caused an amino acid substitution from glutamine to lysine (E928K). As the gene product is involved in immunoglobulin-class switching and patients with the A allele revealed higher serum levels of IgA (p = 0.048), the amino acid change might influence a class switch to increase serum IgA levels, resulting in a higher risk of IgA nephropathy.

Indexed as

AdultAmino Acid SubstitutionCase-Control StudiesChromosomes, Human, Pair 11DNA-Binding ProteinsFemaleGlomerulonephritis, IGAHumansImmunoglobulin Class SwitchingLinkage DisequilibriumMaleMiddle AgedPolymorphism, Single NucleotideTranscription FactorsDNA-Binding ProteinsIGHMBP2 protein, humanTranscription Factors

Identifiers

PMID15599641
OpenAlexW2081433238

What OpenQuestion holds

Textmetadata
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.