Evidence map›Paper›PMID 34166227›Full record

ArticleJCI insight2021

A variant of ASIC2 mediates sodium retention in nephrotic syndrome.

Marc Fila, Ali Sassi, Gaëlle Brideau, Lydie Cheval, Luciana Morla, Pascal Houillier, Christine Walter, Michel Gennaoui, Laure Collignon, Mathilde Keck and 9 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in JCI insight, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.7field-weighted citation impact, top 31% 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

6 citing papers in PubMed, 11 citations in OpenAlex.

  1. Nephrotic syndrome and adrenoleukodystrophy in a 5-year-old boy.Pediatric nephrology (Berlin, Germany) · 2024
    Article
  2. Review
  3. Article
  4. Review
  5. Role of ion channels in the mechanism of proteinuria (Review).Experimental and therapeutic medicine · 2023
    Review
  6. 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

19 authors at 5 institutions in 3 countries.

Marc FilaCordeliers Research Center, Sorbonne University, INSERM, University of Paris, Laboratory of Renal Metabolism and Physiology, Paris, France.
Ali SassiCordeliers Research Center, Sorbonne University, INSERM, University of Paris, Laboratory of Renal Metabolism and Physiology, Paris, France.
Gaëlle BrideauCordeliers Research Center, Sorbonne University, INSERM, University of Paris, Laboratory of Renal Metabolism and Physiology, Paris, France.
Lydie ChevalCordeliers Research Center, Sorbonne University, INSERM, University of Paris, Laboratory of Renal Metabolism and Physiology, Paris, France.
Luciana MorlaCordeliers Research Center, Sorbonne University, INSERM, University of Paris, Laboratory of Renal Metabolism and Physiology, Paris, France.
Pascal HouillierCordeliers Research Center, Sorbonne University, INSERM, University of Paris, Laboratory of Renal Metabolism and Physiology, Paris, France.
Christine WalterCordeliers Research Center, Sorbonne University, INSERM, University of Paris, Laboratory of Renal Metabolism and Physiology, Paris, France.
Michel GennaouiCordeliers Research Center, Sorbonne University, INSERM, University of Paris, Laboratory of Renal Metabolism and Physiology, Paris, France.
Laure CollignonCordeliers Research Center, Sorbonne University, INSERM, University of Paris, Laboratory of Renal Metabolism and Physiology, Paris, France.
Mathilde KeckCordeliers Research Center, Sorbonne University, INSERM, University of Paris, Laboratory of Renal Metabolism and Physiology, Paris, France.
Gabrielle PlanellesCordeliers Research Center, Sorbonne University, INSERM, University of Paris, Laboratory of Renal Metabolism and Physiology, Paris, France.
Naziha BakouhCordeliers Research Center, Sorbonne University, INSERM, University of Paris, Laboratory of Renal Metabolism and Physiology, Paris, France.
Michel PeuchmaurCytology and Pathology Department and.
Georges DeschênesPediatric Nephrology Department, Robert Debré Hospital, Paris, France.
Ignacio AnegonINSERM UMR 1064, Center for Research in Transplantation and Immunology Transgenic Rats ImmunoPhenomic Facility, Nantes, France.
Séverine RemyINSERM UMR 1064, Center for Research in Transplantation and Immunology Transgenic Rats ImmunoPhenomic Facility, Nantes, France.
Bruno VogtDepartment of Nephrology and Hypertension, Inselspital, Bern University Hospital, Bern, Switzerland.
Gilles CrambertCordeliers Research Center, Sorbonne University, INSERM, University of Paris, Laboratory of Renal Metabolism and Physiology, Paris, France.
Alain DoucetCordeliers Research Center, Sorbonne University, INSERM, University of Paris, Laboratory of Renal Metabolism and Physiology, Paris, France.
Centre National de la Recherche Scientifique · FRTransgene (France) · FRHôpital Robert-Debré · FRInstitute of Cytology · RUUniversity Hospital of Bern · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Idiopathic nephrotic syndrome (INS) is characterized by proteinuria and renal sodium retention leading to edema. This sodium retention is usually attributed to epithelial sodium channel (ENaC) activation after plasma aldosterone increase. However, most nephrotic patients show normal aldosterone levels. Using a corticosteroid-clamped (CC) rat model of INS (CC-PAN), we showed that the observed electrogenic and amiloride-sensitive Na retention could not be attributed to ENaC. We then identified a truncated variant of acid-sensing ion channel 2b (ASIC2b) that induced sustained acid-stimulated sodium currents when coexpressed with ASIC2a. Interestingly, CC-PAN nephrotic ASIC2b-null rats did not develop sodium retention. We finally showed that the expression of the truncated ASIC2b in the kidney was dependent on the presence of albumin in the tubule lumen and activation of ERK in renal cells. Finally, the presence of ASIC2 mRNA was also detected in kidney biopsies from patients with INS but not in any of the patients with other renal diseases. We have therefore identified a variant of ASIC2b responsible for the renal Na retention in the pathological context of INS.

Indexed as

KidneyMAP Kinase Signaling SystemNephrotic SyndromeSodiumAcid Sensing Ion ChannelsAlbuminsAnimalsDisease Models, AnimalGene Expression ProfilingHomeostasisProteinuriaRatsSodium ChannelsAcid Sensing Ion ChannelsAlbuminsAsic2 protein, ratSodiumSodium ChannelsHomeostasisIon channelsNephrologySodium channels

Identifiers

PMID34166227
PMCPMC8410034
OpenAlexW3173215621

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.