Evidence map›Paper›PMID 32867720›Full record

ArticleBMC nephrology2020

Urine concentration ability is reduced to the same degree in adult dominant polycystic kidney disease compared with other chronic kidney diseases in the same CKD-stage and lower THAN in healthy control subjects - a CASE control study.

M H Malmberg, F H Mose, E B Pedersen, J N Bech

Registry-linked trialOpen access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in BMC nephrology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04363554 (The Kidneys Ability to Concentrate and Dilute Urine in Patients With Autosomal Dominant Polycystic Kidney Disease), which is not on this map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.3field-weighted citation impact, top 19% 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.

NCT04363554 nacompletednot on this map

The Kidneys Ability to Concentrate and Dilute Urine in Patients With Autosomal Dominant Polycystic Kidney Disease (ADPKD) or Other Cause of Chronic Renal Disease Compared to Healthy Volunteers

TypeinterventionalSponsorRegional Hospital HolstebroRan2017 to 2020Enrolled51ConditionsPolycystic Kidney, Autosomal Dominant, Chronic Kidney DiseasesArmsFluid intake, Thirsting
3 · Its place in the literature

Who cites it

7 citing papers in PubMed, 11 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

4 authors at 1 institution in 1 country.

M H MalmbergUniversity Clinic in Nephrology and Hypertension, Regional Hospital West Jutland and University of Aarhus, Holsstebro, Denmark. mymalmbe@rm.dk.ORCID 0000-0002-6718-6351
F H MoseUniversity Clinic in Nephrology and Hypertension, Regional Hospital West Jutland and University of Aarhus, Holsstebro, Denmark.
E B PedersenUniversity Clinic in Nephrology and Hypertension, Regional Hospital West Jutland and University of Aarhus, Holsstebro, Denmark.
J N BechUniversity Clinic in Nephrology and Hypertension, Regional Hospital West Jutland and University of Aarhus, Holsstebro, Denmark.
Regional Hospital West Jutland · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundConcentration of the urine is primarily regulated via vasopressin dependent aquaporin-2 water channels in the apical membrane of kidney principal cells. It is unclear whether urine concentration ability in ADPKD differs from other patients with similar degree of impaired renal function (non-ADPKD patients). The purpose of this case control study was to measure urine concentration ability in ADPKD patients compared to non-ADPKD patients and healthy controls.

methodsA seventeen hour long water deprivation test was carried out in 17 ADPKD patients (CKD I-IV), 16 non-ADPKD patients (CKD I-IV), and 18 healthy controls. Urine was collected in 4 consecutive periods during water deprivation (12 h, 1 h, 2 h and 2 h, respectively) and analyzed for osmolality (u-Osm), output (UO), fractional excretion of sodium (FE

resultsU-Osm was significantly lower and FE

conclusionsUrine concentration ability was reduced to the same extent in patients with ADPKD and other chronic kidney diseases with the same level of renal function compared to healthy controls. The lower urine excretion of AQP2 and ENaC suggests that the underlying mechanism may be a reduced tubular response to vasopressin and aldosterone.

trial registrationCurrent Controlled Trial NCT04363554 , date of registration: 20.08.2017.

Indexed as

AdultAgedAldosteroneAquaporin 2Case-Control StudiesEpithelial Sodium ChannelsFemaleHumansKidney Concentrating AbilityMaleMiddle AgedOsmolar ConcentrationPolycystic Kidney, Autosomal DominantRenal EliminationRenal Insufficiency, ChronicSeverity of Illness IndexAldosteroneAquaporin 2Epithelial Sodium ChannelsSodiumVasopressinsAldosteroneAngiotensin IIaquaporin2Blood pressureChronic kidney diseaseEpithelial sodium channelGFROsmolalityPolycystic kidney diseaseReninSodiumVasopressin

Identifiers

PMID32867720
PMCPMC7457520
OpenAlexW3082460485

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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.