Evidence map›Paper›PMID 27812762›Full record

ArticleClinical and experimental nephrology2017

Minimal change nephrotic syndrome and prohibitin-2 gene polymorphism.

Keisuke Sugimoto, Tomoki Miyazawa, Kohei Miyazaki, Hidehiko Yanagida, Takuji Enya, Hitomi Nishi, Norihisa Wada, Mitsuru Okada, Tsukasa Takemura

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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 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.2field-weighted citation impact, top 36% 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

1 citing paper in PubMed, 4 citations in OpenAlex.

  1. Review
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 1 institution in 1 country.

Keisuke SugimotoDepartment of Pediatrics, Faculty of Medicine, Kindai University, 377-2 Ohno-higashi, Osaka-sayama, 589-8511, Japan.
Tomoki MiyazawaDepartment of Pediatrics, Faculty of Medicine, Kindai University, 377-2 Ohno-higashi, Osaka-sayama, 589-8511, Japan.
Kohei MiyazakiDepartment of Pediatrics, Faculty of Medicine, Kindai University, 377-2 Ohno-higashi, Osaka-sayama, 589-8511, Japan.
Hidehiko YanagidaDepartment of Pediatrics, Faculty of Medicine, Kindai University, 377-2 Ohno-higashi, Osaka-sayama, 589-8511, Japan.
Takuji EnyaDepartment of Pediatrics, Faculty of Medicine, Kindai University, 377-2 Ohno-higashi, Osaka-sayama, 589-8511, Japan.
Hitomi NishiDepartment of Pediatrics, Faculty of Medicine, Kindai University, 377-2 Ohno-higashi, Osaka-sayama, 589-8511, Japan.
Norihisa WadaDepartment of Pediatrics, Faculty of Medicine, Kindai University, 377-2 Ohno-higashi, Osaka-sayama, 589-8511, Japan.
Mitsuru OkadaDepartment of Pediatrics, Faculty of Medicine, Kindai University, 377-2 Ohno-higashi, Osaka-sayama, 589-8511, Japan.
Tsukasa TakemuraDepartment of Pediatrics, Faculty of Medicine, Kindai University, 377-2 Ohno-higashi, Osaka-sayama, 589-8511, Japan. tsukasa@med.kindai.ac.jp.
Kindai University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPatients with minimal change nephrotic syndrome (MCNS) often also have allergic diseases. Abnormalities of Th2-derived cytokines and T-cell functions contribute to development of these diseases. On the other hand, imbalances between reactive oxygen species (ROS) and antioxidants have been implicated in MCNS and progression of atopic dermatitis. ROS, produced mainly within mitochondria, subject cells to oxidative stress, while prohibitin 2 protects mitochondria by increasing tolerance to ROS. Additionally, podocin, a member of the slit diaphragm protein complex, contains PHB-like domain that serves as a signaling platform regulating podocyte function through associated transmembrane proteins. PATIENTS AND

methodThen, we performed exome sequencing analysis in five patients with frequently relapsing their MCNS associated with allergic disease and serum IgE concentrations of 2000 IU/L or higher.

resultsWe detected a heterozygous prohibitin 2 polymorphism, c.873-3_873-2 delCA (rs111523336), in 1 patient. This mutation in exon 9 caused frameshifts in regions connected to splicing sites, where they could disrupt transcription of prohibitin 2. Frequency of this polymorphism in exon 9 is 7.3% among Japanese. Increase in peripheral blood ROS even MCNS remission state suggests the heterozygous prohibitin 2 variant may contribute to give more susceptibility towards the recurrence of MCNS as well as atopic skin disease. This increase may have progression of atopic dermatitis, which sometimes heralded.

conclusionThe prohibitin-2 polymorphism may reduce ROS tolerance in glomerular epithelium and led to high local exposure to ROS, increasing permeability of the glomerular basement membrane to result in proteinuria. Imbalance between ROS and antioxidants together with failure of signal transduction in the glomerular slit membrane caused by prohibitin 2 abnormality could have contributed to nephrotic syndrome in our patients. Prohibitin 2 analysis is needed in additional MCNS patients with concomitant allergic disease.

Indexed as

Polymorphism, GeneticAdolescentBiomarkersBiopsyCytokinesDermatitis, AtopicDNA Mutational AnalysisExomeExome SequencingFrameshift MutationGenetic Association StudiesGenetic MarkersGenetic Predisposition to DiseaseHeterozygoteHumansImmunoglobulin EBiomarkersCytokinesGenetic MarkersImmunoglobulin EPHB protein, humanProhibitinsReactive Oxygen SpeciesRepressor ProteinsAntioxidantsAtopic dermatitisMinimal change nephrotic syndromeMutationsProhibitinReactive oxygen species

Identifiers

PMID27812762
OpenAlexW2547574170

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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.