Evidence map›Paper›PMID 25822700›Full record

ReviewWorld journal of pediatrics : WJP2015

Pathogenesis of childhood idiopathic nephrotic syndrome: a paradigm shift from T-cells to podocytes.

Kazunari Kaneko, Shoji Tsuji, Takahisa Kimata, Tetsuya Kitao, Sohsaku Yamanouchi, Shogo Kato

Abstract readReview
PubMed Publisher
In one paragraph

Review in World journal of pediatrics : WJP, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

21 citing papers in PubMed, 59 citations in OpenAlex.

  1. Trial
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  6. Observational
  7. Article
  8. Article
  9. Article
  10. Article
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  12. Review
  13. Trends in pediatric nephrotic syndrome.World journal of nephrology · 2021
    Review
  14. Review
  15. Review
  16. A review of nephrotic syndrome and atopic diseases in children.Translational andrology and urology · 2021
    Review
  17. Review
  18. Article
  19. Article
  20. 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

6 authors at 1 institution in 1 country.

Kazunari KanekoDepartment of Pediatrics, Kansai Medical University, 2-5-1 Shin-machi, Hirakata, Osaka, 573-1010, Japan, kanekok@hirakata.kmu.ac.jp.
Shoji Tsuji
Takahisa Kimata
Tetsuya Kitao
Sohsaku Yamanouchi
Shogo Kato
Kansai Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundNephrotic syndrome is the most common cause of kidney disease in children, but its pathogenesis remains unclear. This article reviews the novel aspects of the mechanisms underlying massive proteinuria in minimal-change disease, which is the most common form of childhood nephrotic syndrome. DATA SOURCES: This article integrates the findings of a PubMed database search for English language articles published in the past 40 years (from September 1974 to February 2014) using the key words "pathogenesis", "minimal change nephrotic syndrome" or "idiopathic nephrotic syndrome".

resultsUnknown humoral factors associated with T-cell dysfunction have been thought to play an important role in the pathogenesis of minimal-change disease. However, recent findings are changing this paradigm, i.e., visceral glomerular epithelial cells (podocytes) may be involved via expression of molecules such as CD80 and angiopoietin-like 4.

conclusionsRecent evidence suggests that minimal-change disease results from interactions between humoral factors and dysfunctional podocytes. In addition to immunosuppressant drugs that target lymphocytes, a biological agent such as an antibody against the abnormal molecule(s) expressed by podocytes may provide novel drug treatment for minimal-change disease.

Indexed as

Angiopoietin-Like Protein 4AngiopoietinsB7-1 AntigenChildCytokinesHumansNephrosis, LipoidPodocytesProteinuriaT-LymphocytesAngiopoietin-Like Protein 4AngiopoietinsANGPTL4 protein, humanB7-1 AntigenCytokines

Identifiers

PMID25822700
OpenAlexW2144493296

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.