Evidence map›Paper›PMID 24970686›Full record

Trial reportBMC nephrology2014

Abnormal urinary excretion of NKCC2 and AQP2 in response to hypertonic saline in chronic kidney disease: an intervention study in patients with chronic kidney disease and healthy controls.

Janni M Jensen, Frank H Mose, Anna-Ewa O Kulik, Jesper N Bech, Robert A Fenton, Erling B Pedersen

Registry-linked trialOpen access · goldAbstract readClinical TrialComparative Study
In one paragraph

Trial report in BMC nephrology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT01623661 (Effect of Intravenous Sodium Chloride on Urinary Biomarkers for Measurement of Sodium- and Water Channel Activity in the Nephron in Healthy Subject an Patients With Chronic Kidney Disease. A Case Control Study), which is not on this map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.3field-weighted citation impact, top 20% 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.

NCT01623661 nacompletednot on this map

Effect of Intravenous Sodium Chloride on Urinary Biomarkers for Measurement of Sodium- and Water Channel Activity in the Nephron in Healthy Subject an Patients With Chronic Kidney Disease. A Case Control Study

TypeinterventionalSponsorRegional Hospital HolstebroRan2011 to 2013Enrolled47ConditionsNephropathyArmshypertonic saline
3 · Its place in the literature

Who cites it

15 citing papers in PubMed, 21 citations in OpenAlex.

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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

6 authors at 3 institutions in 1 country.

Janni M JensenDepartment of Medical Research, Holstebro Hospital, University Clinic in Nephrology and Hypertension, Laegaardvej 12, 7500 Holstebro, Denmark. jannimaj@gmail.com.
Frank H Mose
Anna-Ewa O Kulik
Jesper N Bech
Robert A Fenton
Erling B Pedersen
Aarhus University · DKRegional Hospital Holstebro · DKRegional Hospital West Jutland · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundRenal handling of sodium and water is abnormal in chronic kidney disease (CKD). The aim of this study was to test the hypothesis that abnormal activity of the aquaporin-2 water channels (AQP2), the sodium-potassium-2chloride transporter (NKCC2) and/or the epithelial sodium channels (ENaC) contribute to this phenomenon.

methods23 patients with CKD and 24 healthy controls at baseline and after 3% saline infusion were compared. The following measurements were performed: urinary concentrations of AQP2 (u-AQP2), NKCC2 (u-NKCC2), ENaC (u-ENaCγ), glomerular filtration rate (GFR) estimated by 51Cr-EDTA clearance, free water clearance (CH2O), urinary output (UO), fractional excretion of sodium (FENa), plasma concentrations of AVP, renin (PRC), Angiotensin II (ANG II), Aldosterone (Aldo) and body fluid volumes.

resultsAt baseline, GFR was 34 ml/min in CKD patients and 89 ml/ml in controls. There were no significant differences in u-AQP2, u-NKCC2 or u-ENaCγ, but FENa, p-Aldo and p-AVP were higher in CKD patients than controls. In response to hypertonic saline, patients with CKD had an attenuated decrease in CH2O and UO. A greater increase in U-AQP2 was observed in CKD patients compared to controls. Furthermore, u-NKCC2 increased in CKD patients, whereas u-NKCC2 decreased in controls. Body fluid volumes did not significantly differ.

conclusionsIn response to hypertonic saline, u-NKCC2 increased, suggesting an increased sodium reabsorption via NKCC2 in patients with CKD. U-AQP2 increased more in CKD patients, despite an attenuated decrease in CH2O. Thus, though high levels of p-AVP and p-Aldo, the kidneys can only partly compensate and counteract acute volume expansion due to a defective tubular response.

trial registrationClinical trial no: NCT01623661. Date of trial registration: 18.06.2012.

Indexed as

AdolescentAdultAgedAquaporin 2Case-Control StudiesFemaleHumansMaleMiddle AgedRenal Insufficiency, ChronicSaline Solution, HypertonicSolute Carrier Family 12, Member 1UrinationYoung AdultAQP2 protein, humanAquaporin 2Saline Solution, HypertonicSLC12A1 protein, humanSolute Carrier Family 12, Member 1

Identifiers

PMID24970686
PMCPMC4094915
OpenAlexW2136367817

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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.