Evidence map›Paper›PMID 26846784›Full record

ArticleClinical and experimental nephrology2017

Association of apoptosis inhibitor of macrophage (AIM) expression with urinary protein and kidney dysfunction.

Megumi Oshima, Yasunori Iwata, Kengo Furuichi, Norihiko Sakai, Miho Shimizu, Akinori Hara, Shinji Kitajima, Tadashi Toyama, Yasuyuki Shinozaki, Akihiro Sagara and 5 more

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In one paragraph

Article in Clinical and experimental nephrology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.2field-weighted citation impact, top 40% 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

6 citing papers in PubMed, 9 citations in OpenAlex.

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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

15 authors at 3 institutions in 1 country.

Megumi OshimaDivision of Nephrology, Kanazawa University Hospital, Kanazawa, Ishikawa, Japan.
Yasunori IwataDivision of Nephrology, Kanazawa University Hospital, Kanazawa, Ishikawa, Japan. iwata-knz@umin.ac.jp.
Kengo FuruichiDivision of Nephrology, Kanazawa University Hospital, Kanazawa, Ishikawa, Japan.
Norihiko SakaiDivision of Nephrology, Kanazawa University Hospital, Kanazawa, Ishikawa, Japan.
Miho ShimizuDivision of Nephrology, Kanazawa University Hospital, Kanazawa, Ishikawa, Japan.
Akinori HaraDivision of Nephrology, Kanazawa University Hospital, Kanazawa, Ishikawa, Japan.
Shinji KitajimaDivision of Nephrology, Kanazawa University Hospital, Kanazawa, Ishikawa, Japan.
Tadashi ToyamaDivision of Nephrology, Kanazawa University Hospital, Kanazawa, Ishikawa, Japan.
Yasuyuki ShinozakiDivision of Nephrology, Kanazawa University Hospital, Kanazawa, Ishikawa, Japan.
Akihiro SagaraDivision of Nephrology, Kanazawa University Hospital, Kanazawa, Ishikawa, Japan.
Eri UmedaDivision of Nephrology, Kanazawa University Hospital, Kanazawa, Ishikawa, Japan.
Shuichi KanekoDepartment of Disease Control and Homeostasis, Faculty of Medicine, Institute of Medical, Pharmaceutical and Health Sciences, Kanazawa University, Kanazawa, Ishikawa, Japan.
Satoko AraiLaboratory of Molecular Biomedicine for Pathogenesis, Faculty of Medicine, Center for Disease Biology and Integrative Medicine, The University of Tokyo, Tokyo, Japan.
Toru MiyazakiLaboratory of Molecular Biomedicine for Pathogenesis, Faculty of Medicine, Center for Disease Biology and Integrative Medicine, The University of Tokyo, Tokyo, Japan.
Takashi WadaDivision of Nephrology, Kanazawa University Hospital, Kanazawa, Ishikawa, Japan.
Kanazawa University · JPKanazawa University Hospital · JPThe University of Tokyo · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundApoptosis inhibitor of macrophage (AIM) expressed on macrophages prolongs inflammation by protecting macrophages from apoptosis. Most circulating AIM co-exists with immunoglobulin M (IgM). AIM's pathophysiological role in relation to IgM remains unclear. Here we evaluated the glomerular expression/deposition of AIM and IgM in the kidney using immunohistochemistry and its associations with clinical manifestations in 43 patients with biopsy-confirmed kidney diseases.

methodsKidney biopsy tissue from all patients was immunostained for AIM and IgM. Staining patterns and percent stained areas within the glomeruli were determined. Cells expressing AIM were identified by co-staining with macrophage and endothelial cell surface markers. Correlations between staining results and clinical parameters were evaluated using univariate and multivariate analyses.

resultsAIM was deposited in various areas, such as mesangial and capillary area. A part of AIM expression was localized to CD68-positive macrophages in the glomerulus. Amount of glomerular expression was positively correlated with urinary protein in patients with severe proteinuria (urinary protein ≥0.5 g/day) and kidney dysfunction [estimated glomerular filtration ratio (eGFR) <60 ml/min/1.73 m

conclusionAIM expression in the kidney was associated with urinary protein and decline in kidney function. Co-expression with IgM appeared to exacerbate AIM's deleterious effects on kidney function. Combined glomerular AIM and IgM expression is a candidate prognostic index for kidney disease.

Indexed as

AdultAgedAged, 80 and overApoptosis Regulatory ProteinsBiopsyEndothelial CellsFemaleGlomerular Filtration RateHumansImmunoglobulin MImmunohistochemistryKidney DiseasesKidney GlomerulusMacrophagesMaleMiddle AgedApoptosis Regulatory ProteinsCD5L protein, humanImmunoglobulin MReceptors, ScavengerApoptosis inhibitor of macrophage (AIM)IgMKidney disease

Identifiers

PMID26846784
OpenAlexW2253041125

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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.