Evidence map›Paper›PMID 22688744›Full record

ReviewNature reviews. Nephrology2012

Childhood nephrotic syndrome--current and future therapies.

Larry A Greenbaum, Rainer Benndorf, William E Smoyer

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Nephrology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed, 1 pooled it
3.8field-weighted citation impact, top 6% 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

59 citing papers in PubMed, 1 synthesis or guideline pooled it, 108 citations in OpenAlex.

  1. Corticosteroid therapy for nephrotic syndrome in children.The Cochrane database of systematic reviews · 2015
    Pooled it
  2. Trial
  3. Review
  4. Hyperlipidemia in membranous nephropathy.Clinical kidney journal · 2026
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Metabolomics Profiling of Nephrotic Syndrome towards Biomarker Discovery.International journal of molecular sciences · 2022
    Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. The potential mechanism ofTranslational pediatrics · 2021
    Article
  17. Article
  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

3 authors at 2 institutions in 1 country.

Larry A GreenbaumEmory University, Atlanta, GA 30322, USA.
Rainer Benndorf
William E Smoyer
Nationwide Children's Hospital · USEmory University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The introduction of corticosteroids more than 50 years ago dramatically improved the prognosis of children with nephrotic syndrome. Corticosteroids remain the standard initial treatment for children with this disease, but a considerable proportion of patients do not respond and are therefore at risk of progressing to end-stage renal disease. Because of this risk, new therapeutic strategies are needed for steroid-resistant nephrotic syndrome. These strategies have historically focused on identifying effective alternative immunosuppressive agents, such as ciclosporin and tacrolimus, yet evidence now indicates that nephrotic syndrome results from podocyte dysfunction. Even conventional immunosuppressive agents, such as glucocorticoids and ciclosporin, directly affect podocyte structure and function, challenging the 'immune theory' of the pathogenesis of childhood nephrotic syndrome in which disease is caused by T cells. This Review summarizes the currently available treatments for childhood nephrotic syndrome, and discusses selected novel pathways in podocytes that could be targeted for the development of next-generation treatments for children with this syndrome.

Indexed as

AdalimumabAntibodies, MonoclonalAntibodies, Monoclonal, HumanizedAntibodies, Monoclonal, Murine-DerivedAnti-Inflammatory AgentsAntineoplastic Agents, AlkylatingChildCyclophosphamideCyclosporineEnzyme InhibitorsGalactoseGlucocorticoidsHomeostasisHumansImmunologic FactorsImmunosuppressive AgentsAdalimumabAntibodies, MonoclonalAntibodies, Monoclonal, HumanizedAntibodies, Monoclonal, Murine-DerivedAnti-Inflammatory AgentsAntineoplastic Agents, AlkylatingCyclophosphamideCyclosporineEnzyme InhibitorsGalactoseGlucocorticoidsImmunologic FactorsImmunosuppressive AgentsInterleukin-13Intracellular Signaling Peptides and ProteinslebrikizumabMAP-Kinase-Activated Kinase 2mizoribineMycophenolic Acidp38 Mitogen-Activated Protein KinasesProtein Serine-Threonine KinasesReceptors, NotchRibonucleosidesRituximabTacrolimusThiazolidinediones

Identifiers

PMID22688744
OpenAlexW2088616569

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.