Evidence map›Paper›PMID 28232870›Full record

ReviewF1000Research2017

Recent advances in understanding and treating nephrotic syndrome.

Agnieszka Bierzynska, Moin Saleem

Open access · goldAbstract readReview
In one paragraph

Review in F1000Research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

23 citing papers in PubMed, 45 citations in OpenAlex.

  1. Trial
  2. New therapeutic hope for rare podocytopathies.Pediatric nephrology (Berlin, Germany) · 2026
    Review
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Assessment of the Link ofJournal of advanced research · 2021
    Article
  14. Review
  15. MicroRNAs as Biomarkers for Nephrotic Syndrome.International journal of molecular sciences · 2020
    Review
  16. Article
  17. Proteome Analysis of Isolated Podocytes Reveals Stress Responses in Glomerular Sclerosis.Journal of the American Society of Nephrology : JASN · 2020
    Article
  18. Article
  19. Genetic variants in the LAMA5 gene in pediatric nephrotic syndrome.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2019
    Article
  20. 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

2 authors at 1 institution in 1 country.

Agnieszka BierzynskaUniversity of Bristol, Bristol Royal Hospital for Children, Bristol, UK.
Moin SaleemUniversity of Bristol, Bristol Royal Hospital for Children, Bristol, UK.ORCID 0000-0002-9808-4518
Bristol Royal Hospital for Children · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Idiopathic nephrotic syndrome (INS) is one of the most common glomerular diseases in children and adults, and the central event is podocyte injury. INS is a heterogeneous disease, and treatment is largely empirical and in many cases unsuccessful, and steroids are the initial mainstay of therapy. Close to 70% of children with INS have some response to steroids and are labelled as steroid-'sensitive', and the rest as steroid-'resistant' (also termed focal segmental glomerulosclerosis), and single-gene mutations underlie a large proportion of the latter group. The burden of morbidity is enormous, both to patients with lifelong chronic disease and to health services, particularly in managing dialysis and transplantation. The target cell of nephrotic syndrome is the glomerular podocyte, and podocyte biology research has exploded over the last 15 years. Major advances in genetic and biological understanding now put clinicians and researchers at the threshold of a major reclassification of the disease and testing of targeted therapies both identified and novel. That potential is based on complete genetic analysis, deep clinical phenotyping, and the introduction of mechanism-derived biomarkers into clinical practice. INS can now be split off into those with a single-gene defect, of which currently at least 53 genes are known to be causative, and the others. Of the others, the majority are likely to be immune-mediated and caused by the presence of a still-unknown circulating factor or factors, and whether there is a third (or more) mechanistic group or groups remains to be discovered. Treatment is therefore now being refined towards separating out the monogenic cases to minimise immunosuppression and further understanding how best to stratify and appropriately direct immunosuppressive treatments within the immune group. Therapies directed specifically towards the target cell, the podocyte, are in their infancy but hold considerable promise for the near future.

Indexed as

focal segmental glomerulosclerosisFSGSidiopathic nephrotic syndromeMCNSminimal change nephrotic syndromeSRNS

Identifiers

PMID28232870
PMCPMC5302149
OpenAlexW2586137293

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.