Evidence map›Paper›PMID 40085383›Full record

ReviewClinical and experimental nephrology2025

Genetic aspects of pediatric nephrotic syndrome and anti-nephrin antibodies.

Tomoko Horinouchi, Kandai Nozu, Kazumoto Iijima

Abstract readReview
In one paragraph

Review in Clinical and experimental nephrology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. Review
  2. Article
  3. 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

3 authors.

Tomoko HorinouchiDepartment of Pediatrics, Kobe University Graduate School of Medicine, Kobe University, 7-5-1 Kusunoki-cho, Chuo-ku, Kobe, 650-0017, Japan. tohori@med.kobe-u.ac.jp.ORCID http://orcid.org/0000-0003-1655-6030
Kandai NozuDepartment of Pediatrics, Kobe University Graduate School of Medicine, Kobe University, 7-5-1 Kusunoki-cho, Chuo-ku, Kobe, 650-0017, Japan.
Kazumoto IijimaHyogo Prefectural Kobe Children's Hospital, Hyogo, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nephrotic syndrome is the most common glomerular disease in children, and various hypotheses regarding its etiology have been proposed, primarily focusing on immune-related mechanisms. Nephrotic syndrome can manifest as a monogenic disease caused by deleterious variants in genes such as NPHS1, which encodes nephrin. In steroid-sensitive nephrotic syndrome, HLA class II and immune-related genes have been identified as susceptibility genes. Moreover, NPHS1 is a susceptibility gene for steroid-sensitive nephrotic syndrome in patients from East Asian populations. Anti-nephrin antibodies have been identified as a significant factor in the pathogenesis of nephrotic syndrome. These discoveries have substantially advanced our understanding of nephrotic syndrome. However, the mechanisms underlying the production of anti-nephrin antibodies and their association with genetic backgrounds have remained unclear and warrant further investigation.

Indexed as

AutoantibodiesMembrane ProteinsNephrotic SyndromeChildGenetic Predisposition to DiseaseHumansAutoantibodiesMembrane ProteinsnephrinAnti-nephrin antibodiesGenome-wide association studiesNephrotic syndromeNPHS1Steroid-sensitive nephrotic syndrome

Identifiers

PMID40085383
PMCPMC12049277

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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.