Evidence map›Paper›PMID 19649571›Full record

ReviewJournal of molecular medicine (Berlin, Germany)2009

Genetics of nephrotic syndrome: new insights into molecules acting at the glomerular filtration barrier.

Martin Zenker, Eduardo Machuca, Corinne Antignac

Abstract readReview
PubMed Publisher
In one paragraph

Review in Journal of molecular medicine (Berlin, Germany), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
3.1field-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

34 citing papers in PubMed, 58 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
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  9. Article
  10. Review
  11. 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
  12. Article
  13. Diagnostic and Management Challenges in Congenital Nephrotic Syndrome.Pediatric health, medicine and therapeutics · 2019
    Review
  14. Article
  15. Screening of theFrontiers in genetics · 2018
    Article
  16. Review
  17. Review
  18. Genetic testing in steroid-resistant nephrotic syndrome: when and how?Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2016
    Review
  19. FSGS: Diagnosis and Diagnostic Work-Up.BioMed research international · 2016
    Review
  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 3 institutions in 3 countries.

Martin ZenkerInstitute of Human Genetics, University Hospital Erlangen, University of Erlangen-Nuremberg, Schwabachanlage 10, 91054, Erlangen, Germany, mzenker@humgenet.uni-erlangen.de
Eduardo Machuca
Corinne Antignac
Friedrich-Alexander-Universität Erlangen-Nürnberg · DEInserm · FRPontificia Universidad Católica de Chile · CL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nephrotic syndrome is caused by increased permeability of the glomerular filtration barrier for macromolecules. The identification of mutations of various podocyte-expressed proteins as causes of familial nephrotic syndrome has significantly contributed to shedding light into the molecular pathogenesis of nephrotic proteinuria and into the physiology of the glomerular sieve. More recent findings have changed our conception of the glomerular filtration barrier from a relatively static structure to a highly dynamic one. Both the multiprotein slit diaphragm complex around nephrin and the integrin receptor complex that mediates binding of the podocyte to the glomerular basement membrane, may translate outside-inside signaling and lead to podocyte actin cytoskeleton rearrangement. This may enable the podocyte network to adapt to environmental changes and respond to injury. Disturbance in these processes may not only be involved in the pathogenesis of hereditary nephrotic syndrome but also in that of more common acquired proteinuric diseases. Elucidation of the molecular mechanisms involved will possibly open the way to new therapeutic approaches.

Indexed as

CytoskeletonHumansKidney GlomerulusNephrotic SyndromePermeabilityPodocytes

Identifiers

PMID19649571
OpenAlexW2110895523

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.