Evidence map›Paper›PMID 25117488›Full record

ArticleClinical and experimental nephrology2015

Podocyte proteins in congenital and minimal change nephrotic syndrome.

Maija Suvanto, Timo Jahnukainen, Marjo Kestilä, Hannu Jalanko

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Article in Clinical and experimental nephrology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing 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

9 citing papers in PubMed, 12 citations in OpenAlex.

  1. Congenital nephrotic syndrome.Journal of perinatology : official journal of the California Perinatal Association · 2021
    Review
  2. Article
  3. Identification of a NovelBioMed research international · 2019
    Article
  4. Diagnostic and Management Challenges in Congenital Nephrotic Syndrome.Pediatric health, medicine and therapeutics · 2019
    Review
  5. Article
  6. Article
  7. Inverted formins: A subfamily of atypical formins.Cytoskeleton (Hoboken, N.J.) · 2017
    Review
  8. Article
  9. 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

4 authors at 2 institutions in 1 country.

Maija SuvantoChildren's Hospital, University of Helsinki and Helsinki University Central Hospital, Tukholmankatu 8, 00290, Helsinki, Finland. maija.suvanto@helsinki.fi.
Timo JahnukainenChildren's Hospital, University of Helsinki and Helsinki University Central Hospital, Tukholmankatu 8, 00290, Helsinki, Finland.
Marjo KestiläDepartment of Chronic Disease Prevention, National Institute for Health and Welfare, Helsinki, Finland.
Hannu JalankoChildren's Hospital, University of Helsinki and Helsinki University Central Hospital, Tukholmankatu 8, 00290, Helsinki, Finland.
Helsinki University Hospital · FIFinnish Institute for Health and Welfare · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPodocyte foot process effacement is a uniform finding in kidneys with heavy proteinuria. Its molecular mechanisms, however, are unsolved. We analyzed the expression of podocyte proteins in two kidney disorders: Congenital nephrotic syndrome of the Finnish type (CNF) and minimal change nephrotic syndrome (MCNS).

methodsImmunoperoxidase and immunofluorescence stainings were used to semiquantitatively analyze the expression of 13 and 4 podocyte proteins from different cellular compartments in CNF and MCNS, respectively.

resultsThe expression of a major slit diaphragm (SD) protein, Neph 1, showed a 46-fold decrease (p < 0.0001) in CNF kidneys as compared to controls. The three cytosolic adaptor proteins, podocin, NCK1/2, CD2AP, connecting SD proteins to the actin cytoskeleton were slightly upregulated (1.1-fold, 1.4-fold, and 3.3-fold, respectively). Also, the staining of the two actin-regulator proteins, ACTN4 and INF2, was modestly increased (2.2-fold and 1.7-fold, respectively, p < 0.0001). Staining for α3-integrin showed 1.9-fold increase (p < 0.0001) indicating that the major podocyte anchoring complex, α3β1, was well preserved in CNF glomeruli. In contrast to CNF kidneys, Neph1 FAT1, ACTN4, and CD2AP were quite normally expressed in proteinuric and non-proteinuric MCNS kidneys.

conclusionCNF kidneys lacking nephrin show decreased expression of other SD proteins but not cytosolic podocyte proteins involved in the foot process architecture or function. In MCNS kidneys, these changes in expression were not observed.

Indexed as

ActininAdaptor Proteins, Signal TransducingAdultCadherinsCytoskeletal ProteinsForminsHumansImmunohistochemistryInfantIntegrin alpha3Integrin alpha3beta1Intracellular Signaling Peptides and ProteinsMembrane ProteinsMicrofilament ProteinsNephrosis, LipoidNephrotic SyndromeActininACTN4 protein, humanAdaptor Proteins, Signal TransducingCadherinsCD2-associated proteinCytoskeletal ProteinsFAT1 protein, humanForminsINF2 protein, humanIntegrin alpha3Integrin alpha3beta1Intracellular Signaling Peptides and ProteinsKIRREL1 protein, humanMembrane ProteinsMicrofilament ProteinsNPHS2 proteinActin cytoskeletonCNFMCNSNeph1NephrinPodocyte

Identifiers

PMID25117488
OpenAlexW2006489461

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Registered trials

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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.