Evidence map›Paper›PMID 31613925›Full record

ArticlePloS one2019

Urinary Activin A is a novel biomarker reflecting renal inflammation and tubular damage in ANCA-associated vasculitis.

Yoshinori Takei, Shunsuke Takahashi, Masao Nakasatomi, Toru Sakairi, Hidekazu Ikeuchi, Yoriaki Kaneko, Keiju Hiromura, Yoshihisa Nojima, Akito Maeshima

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed, 1 pooled it
0.5field-weighted citation impact, top 35% 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

8 citing papers in PubMed, 1 synthesis or guideline pooled it, 16 citations in OpenAlex.

  1. Pooled it
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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

9 authors at 2 institutions in 1 country.

Yoshinori TakeiDepartment of Nephrology and Rheumatology, Gunma University Graduate School of Medicine, Maebashi, Japan.ORCID 0000-0002-3433-0476
Shunsuke TakahashiDepartment of Nephrology and Rheumatology, Gunma University Graduate School of Medicine, Maebashi, Japan.
Masao NakasatomiDepartment of Nephrology and Rheumatology, Gunma University Graduate School of Medicine, Maebashi, Japan.
Toru SakairiDepartment of Nephrology and Rheumatology, Gunma University Graduate School of Medicine, Maebashi, Japan.
Hidekazu IkeuchiDepartment of Nephrology and Rheumatology, Gunma University Graduate School of Medicine, Maebashi, Japan.ORCID 0000-0002-0768-7090
Yoriaki KanekoDepartment of Nephrology and Rheumatology, Gunma University Graduate School of Medicine, Maebashi, Japan.
Keiju HiromuraDepartment of Nephrology and Rheumatology, Gunma University Graduate School of Medicine, Maebashi, Japan.
Yoshihisa NojimaDepartment of Nephrology and Rheumatology, Japanese Red Cross Hospital, Maebashi, Japan.
Akito MaeshimaDepartment of Nephrology and Rheumatology, Gunma University Graduate School of Medicine, Maebashi, Japan.ORCID 0000-0001-7834-8937
Gunma University · JPMaebashi Red Cross Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Activin A, a member of the transforming growth factor-beta superfamily, is a critical modulator of inflammation and plays a key role in controlling the cytokine cascade that drives the inflammatory response. However, the role of activin A in inflammatory kidney diseases remains unknown. To address this issue, we examined here whether activin A can be detected in the kidney and/or urine from patients with antineutrophil cytoplasmic antibody (ANCA) -associated vasculitis (AAV). Fifty-one patients who had been diagnosed with AAV and were treated in our department between November 2011 to March 2018 were included in this study. Forty-one patients had renal complications (renal AAV). Serum and urinary activin A levels were measured by enzyme-linked immunosorbent assay. Correlation of urinary activin A concentration with clinical parameters was analyzed. Urinary activin A was undetectable in healthy volunteers. In contrast, urinary activin A concentration was significantly increased in patients with renal AAV but not in those with non-renal AAV. Urinary activin A concentration decreased rapidly after immunosuppressive treatment. There was a significant correlation of urinary activin A level with urinary protein, L-FABP, and NAG. Histologic evaluation revealed that urinary activin A levels were significantly higher in patients with cellular crescentic glomeruli than in those lacking this damage. In situ hybridization demonstrated that the mRNA encoding the activin A βA subunit was undetectable in normal kidneys but accumulated in the proximal tubules and crescentic glomeruli of the kidneys of patients with renal AAV. Immunostaining showed that activin A protein also was present in the proximal tubules, crescentic glomeruli, and macrophages infiltrating into the interstitium in the kidneys of patients with renal AAV. These data suggested that urinary activin A concentration reflects renal inflammation and tubular damage in AAV and may be a useful biomarker for monitoring renal AAV.

Indexed as

ActivinsAgedAnti-Neutrophil Cytoplasmic Antibody-Associated VasculitisBiomarkersBiopsyFemaleHumansInflammationInhibin-beta SubunitsKidney TubulesMaleRNA, Messengeractivin AActivinsBiomarkersinhibin beta A subunitInhibin-beta SubunitsRNA, Messenger

Identifiers

PMID31613925
PMCPMC6793943
OpenAlexW2980616956

What OpenQuestion holds

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Registered trials

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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.