Evidence map›Paper›PMID 26847765›Full record

ArticleScientific reports2016

Polyhydramnios in Lrp4 knockout mice with bilateral kidney agenesis: Defects in the pathways of amniotic fluid clearance.

Hiroshi Tanahashi, Qing-Bao Tian, Yoshinobu Hara, Hiroyuki Sakagami, Shogo Endo, Tatsuo Suzuki

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. 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
2.2field-weighted citation impact, top 13% 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, 17 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

6 authors at 3 institutions in 1 country.

Hiroshi TanahashiDepartment of Neuroplasticity, Institute of Pathogenesis and Disease Prevention, Graduate School of Medicine, Shinshu University, 3-1-1 Asahi, Matsumoto 390-8621, Japan.
Qing-Bao TianDepartment of Neuroplasticity, Institute of Pathogenesis and Disease Prevention, Graduate School of Medicine, Shinshu University, 3-1-1 Asahi, Matsumoto 390-8621, Japan.
Yoshinobu HaraDepartment of Anatomy, Kitasato University School of Medicine, 1-15-1, Kitasato, Sagamihara, Kanagawa 252-0374, Japan.
Hiroyuki SakagamiDepartment of Anatomy, Kitasato University School of Medicine, 1-15-1, Kitasato, Sagamihara, Kanagawa 252-0374, Japan.
Shogo EndoResearch Team for Aging Neuroscience, Tokyo Metropolitan Geriatric Hospital and Institute of Gerontology, Sakae-cho, Itabashi, Tokyo 173-0015, Japan.
Tatsuo SuzukiDepartment of Neuroplasticity, Institute of Pathogenesis and Disease Prevention, Graduate School of Medicine, Shinshu University, 3-1-1 Asahi, Matsumoto 390-8621, Japan.
Shinshu University · JPKitasato University · JPTokyo Metropolitan Geriatric Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Amniotic fluid volume during mid-to-late gestation depends mainly on the urine excretion from the foetal kidneys and partly on the fluid secretion from the foetal lungs during foetal breathing-like movements. Urine is necessary for foetal breathing-like movements, which is critical for foetal lung development. Bilateral renal agenesis and/or obstruction of the urinary tract lead to oligohydramnios, which causes infant death within a short period after birth due to pulmonary hypoplasia. Lrp4, which functions as an agrin receptor, is essential for the formation of neuromuscular junctions. Herein, we report novel phenotypes of Lrp4 knockout (Lrp4(-/-)) mice. Most Lrp4(-/-) foetuses showed unilateral or bilateral kidney agenesis, and Lrp4 knockout resulted in polyhydramnios. The loss of Lrp4 compromised foetal swallowing and breathing-like movements and downregulated the expression of aquaporin-9 in the foetal membrane and aquaporin-1 in the placenta, which possibly affected the amniotic fluid clearance. These results suggest that amniotic fluid removal was compromised in Lrp4(-/-) foetuses, resulting in polyhydramnios despite the impairment of urine production. Our findings indicate that amniotic fluid removal plays an essential role in regulating the amniotic fluid volume.

Indexed as

AmnionAmniotic FluidAnimalsAquaporin 1AquaporinsElectrolytesFemaleKidneyLDL-Receptor Related ProteinsLungMaleMiceMice, Inbred C57BLMice, KnockoutMyometriumOsmolar ConcentrationAqp1 protein, mouseAqp9 protein, mouseAquaporin 1AquaporinsElectrolytesLDL-Receptor Related ProteinsLrp4 protein, mousePulmonary Surfactant-Associated Protein AReceptors, LDL

Identifiers

PMID26847765
PMCPMC4742865
OpenAlexW2286905102

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LicenceCC BY
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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.