Evidence map›Paper›PMID 26113616›Full record

ArticleJournal of the American Society of Nephrology : JASN2016

Activation of the Endogenous Renin-Angiotensin-Aldosterone System or Aldosterone Administration Increases Urinary Exosomal Sodium Channel Excretion.

Ying Qi, Xiaojing Wang, Kristie L Rose, W Hayes MacDonald, Bing Zhang, Kevin L Schey, James M Luther

Open access · bronzeAbstract read
In one paragraph

Article in Journal of the American Society of Nephrology : JASN, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed, 1 pooled it
2.3field-weighted citation impact, top 12% 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

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

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  13. Urinary extracellular vesicles and tubular transport.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2023
    Review
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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

7 authors at 2 institutions in 2 countries.

Ying QiDepartments of Biochemistry.
Xiaojing WangBioinformatics.
Kristie L RoseDepartments of Biochemistry.
W Hayes MacDonaldDepartments of Biochemistry.
Bing ZhangBioinformatics.
Kevin L ScheyDepartments of Biochemistry.
James M LutherDivision of Clinical Pharmacology, Department of Medicine, Division of Nephrology, Department of Medicine, and Department of Pharmacology, Vanderbilt University School of Medicine, Nashville, Tennessee James.Luther@Vanderbilt.edu.
Institute of Bioinformatics · INVanderbilt University Medical Center · US

Funding

VANDERBILT UNIVERSITY CTSA FOR PEDIATRIC RESEARCHUL1RR024975 · NCRR · VANDERBILT UNIVERSITY · PI BERNARD, GORDON RAPHAEL · 2007 to 2011
$45.7M
The Vanderbilt Institute for Clinical and Translational Research (VICTR)UL1TR000445 · NCATS · VANDERBILT UNIVERSITY MEDICAL CENTER · PI BERNARD, GORDON RAPHAEL · 2012 to 2016
$41.4M
Vanderbilt Diabetes Research CenterP30DK020593 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI OWEN P MCGUINNESS · 2012 to 2026
$29.3M
TRANSGENIC MOUSE/ ES CELL SHARES RESOURCESP60DK020593 · NIDDK · VANDERBILT UNIVERSITY · PI MCGUINNESS, OWEN P · 1986 to 2011
$28.1M
TRANSPORT EFFECTS OF ARACHIDONATE METABOLITES IN PERFUSED TUBULEP01DK038226 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI BROWN, NANCY J. · 1986 to 2015
$22.1M
Endogenous Aldosterone and Glucose HomeostasisR01DK096994 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI LUTHER, JAMES MATTHEW · 2013 to 2017
$2.1M
Proteome and Transcriptome Markers of Hypertension in Urine and Plasma ExosomesRC1HL100016 · NHLBI · VANDERBILT UNIVERSITY · PI SCHEY, KEVIN L · 2009 to 2010
$950k
Aldosterone and Glucose MetabolismK23DK081662 · NIDDK · VANDERBILT UNIVERSITY · PI LUTHER, JAMES MATTHEW · 2008 to 2012
$863k
GPU-Accelerated Parallel Computer for Drug Discovery ApplicationsS10OD020154 · OD · VANDERBILT UNIVERSITY · PI SMITH, JARROD ANSON · 2015 to 2015
$225k
NCATS NIH HHS UL1 TR000445NCATS NIH HHS UL1-TR000445NCRR NIH HHS UL1 RR024975NCRR NIH HHS UL1-RR024975NHLBI NIH HHS HL100016NHLBI NIH HHS RC1 HL100016NIDDK NIH HHS DK081662NIDDK NIH HHS DK20593NIDDK NIH HHS DK38226NIDDK NIH HHS K23 DK081662NIDDK NIH HHS P01 DK038226NIDDK NIH HHS P30 DK020593NIDDK NIH HHS R01 DK096994
6 · The paper itself

Abstract

Urinary exosomes secreted by multiple cell types in the kidney may participate in intercellular signaling and provide an enriched source of kidney-specific proteins for biomarker discovery. Factors that alter the exosomal protein content remain unknown. To determine whether endogenous and exogenous hormones modify urinary exosomal protein content, we analyzed samples from 14 mildly hypertensive patients in a crossover study during a high-sodium (HS, 160 mmol/d) diet and low-sodium (LS, 20 mmol/d) diet to activate the endogenous renin-angiotensin-aldosterone system. We further analyzed selected exosomal protein content in a separate cohort of healthy persons receiving intravenous aldosterone (0.7 μg/kg per hour for 10 hours) versus vehicle infusion. The LS diet increased plasma renin activity and aldosterone concentration, whereas aldosterone infusion increased only aldosterone concentration. Protein analysis of paired urine exosome samples by liquid chromatography-tandem mass spectrometry-based multidimensional protein identification technology detected 2775 unique proteins, of which 316 exhibited significantly altered abundance during LS diet. Sodium chloride cotransporter (NCC) and α- and γ-epithelial sodium channel (ENaC) subunits from the discovery set were verified using targeted multiple reaction monitoring mass spectrometry quantified with isotope-labeled peptide standards. Dietary sodium restriction or acute aldosterone infusion similarly increased urine exosomal γENaC[112-122] peptide concentrations nearly 20-fold, which correlated with plasma aldosterone concentration and urinary Na/K ratio. Urine exosomal NCC and αENaC concentrations were relatively unchanged during these interventions. We conclude that urinary exosome content is altered by renin-angiotensin-aldosterone system activation. Urinary measurement of exosomal γENaC[112-122] concentration may provide a useful biomarker of ENaC activation in future clinical studies.

Indexed as

AdultAldosteroneCross-Over StudiesEpithelial Sodium ChannelsExosomesFemaleHumansMaleRenin-Angiotensin SystemSodium, DietaryAldosteroneEpithelial Sodium ChannelsSodium, Dietaryaldosteroneclinical nephrologyepithelial sodium channelexosomehypertensionrenin angiotensin system

Identifiers

PMID26113616
PMCPMC4731116
OpenAlexW2216243113

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.