Evidence map›Paper›PMID 24402710›Full record

ReviewSeminars in immunopathology2014

Immunopathogenesis of idiopathic nephrotic syndrome with relapse.

Djillali Sahali, Kelhia Sendeyo, Melanie Mangier, Vincent Audard, Shao Yu Zhang, Philippe Lang, Mario Ollero, Andre Pawlak

Open access · greenAbstract readReview
In one paragraph

Review in Seminars in immunopathology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.1field-weighted citation impact, top 14% 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

28 citing papers in PubMed, 47 citations in OpenAlex.

  1. Article
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  4. Review
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  7. Review
  8. Review
  9. Article
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  13. CMaf-Inducing Protein Promotes LUAD Proliferation and Metastasis by Activating the MAPK/ERK Pathway.Evidence-based complementary and alternative medicine : eCAM · 2022
    Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Gangliosides in Podocyte Biology and Disease.International journal of molecular sciences · 2020
    Review
  19. CMIP is a negative regulator of T cell signaling.Cellular & molecular immunology · 2020
    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

8 authors at 3 institutions in 1 country.

Djillali SahaliService de Néphrologie et Transplantation, AP-HP, CHU Henri Mondor, Creteil, 94010, France, dil.sahali@inserm.fr.
Kelhia Sendeyo
Melanie Mangier
Vincent Audard
Shao Yu Zhang
Philippe Lang
Mario Ollero
Andre Pawlak
Université Paris-Est Créteil · FRInserm · FRCentre Hospitalier Universitaire Henri-Mondor · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Idiopathic change nephrotic syndrome (INS), the most frequent glomerular disease in children and young adults, is characterized by heavy proteinuria and a relapsing remitting course. Although the mechanisms underlying the pathophysiology of proteinuria remain unclear, clinical and experimental observations suggest that lymphocyte and podocyte disturbances are two sides of the disease. The current hypothesis suggests that immune cells release a putative factor, which alters podocyte function resulting in nephrotic proteinuria. Besides T-cell abnormalities, recent evidence of B-cell depletion efficacy in sustained remissions added a new challenge in understanding the immunological mechanisms of INS. In this review, we discuss recent insights related to podocyte disorders occurring in INS and their relevance in human diseases.

Indexed as

B-LymphocytesKidney DiseasesPodocytesProteinuriaT-LymphocytesAdultChildChild, PreschoolHumansSyndrome

Identifiers

PMID24402710
PMCPMC5385209
OpenAlexW2025522570

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.