Evidence map›Paper›PMID 27732656›Full record

Observational studyPloS one2016

Soluble CD73 in Critically Ill Septic Patients - Data from the Prospective FINNAKI Study.

Suvi T Vaara, Maija Hollmén, Anna-Maija Korhonen, Mikael Maksimow, Tero Ala-Kokko, Marko Salmi, Sirpa Jalkanen, Ville Pettilä, FINNAKI Study Group

Open access · goldAbstract readMulticenter StudyObservational Study
PubMed Full text at PMC Publisher
In one paragraph

Observational study in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.6field-weighted citation impact, top 25% 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

8 citing papers in PubMed, 9 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

9 authors at 5 institutions in 2 countries.

Suvi T VaaraDivision of Intensive Care Medicine, Department of Anaesthesiology, Intensive Care and Pain Medicine, University of Helsinki and Helsinki University Hospital, Helsinki, Finland.
Maija HollménMedicity Research Laboratory and Department of Medical Microbiology and Immunology, University of Turku, Turku, Finland.
Anna-Maija KorhonenDivision of Intensive Care Medicine, Department of Anaesthesiology, Intensive Care and Pain Medicine, University of Helsinki and Helsinki University Hospital, Helsinki, Finland.
Mikael MaksimowMedicity Research Laboratory and Department of Medical Microbiology and Immunology, University of Turku, Turku, Finland.
Tero Ala-KokkoDepartment of Anaesthesiology, University of Oulu and Division of Intensive Care Medicine, Oulu University Hospital, Medical Research Centre Oulu, Oulu, Finland.
Marko SalmiMedicity Research Laboratory and Department of Medical Microbiology and Immunology, University of Turku, Turku, Finland.
Sirpa JalkanenMedicity Research Laboratory and Department of Medical Microbiology and Immunology, University of Turku, Turku, Finland.
Ville PettiläDivision of Intensive Care Medicine, Department of Anaesthesiology, Intensive Care and Pain Medicine, University of Helsinki and Helsinki University Hospital, Helsinki, Finland.
FINNAKI Study Group
University of Turku · FIHelsinki University Hospital · FIOulu University Hospital · FIUniversity Hospital of Bern · CHUniversity of Helsinki · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCD73 dephosphorylates adenosine monophosphate to adenosine that is an anti-inflammatory molecule inhibiting immune activation and vascular leakage. Therefore, CD73 could be an interesting mediator both in sepsis and acute kidney injury (AKI). We aimed to explore the soluble CD73 (sCD73) levels and their evolution in critically ill patients with severe sepsis and, second, to scrutinize the potential association of sCD73 levels with AKI and 90-day mortality.

methodsThis was a post-hoc laboratory analysis of the prospective, observational FINNAKI study conducted in 17 Finnish ICU during 5 months in 2011-2012. Plasma samples of 588 patients admitted with severe sepsis/shock or with developing severe sepsis were analyzed at 0h (ICU admission) and 24h, and additionally, on day 3 or day 5 from a subset of the patients.

resultsThe median [IQR] sCD73 levels at 0h were 5.11 [3.29-8.28] ng/mL and they decreased significantly from 0h to 4.14 [2.88-7.11] ng/mL at 24h, P<0.001. From 24h to Day 3 (n = 132) the sCD73 levels rose to 5.18 [2.98-8.83] ng/mL (P = 0.373) and from 24h to Day 5 (n = 224) to 5.52 [3.57-8.90] ng/mL (P<0.001). Patients with AKI had higher sCD73 values at 0h and at 24h compared to those without AKI. Non-survivors with severe sepsis, but not with septic shock, had higher CD73 levels at each time-point compared to survivors. After multivariable adjustments, sCD73 levels at 0h associated independently neither with the development of AKI nor 90-day mortality.

conclusionsCompared to normal population, the sCD73 levels were generally low at 0h, showed a decrease to 24h, and later an increase by day 5. The sCD73 levels do not seem useful in predicting the development of AKI or 90-day mortality among patients with severe sepsis or shock.

Indexed as

5'-NucleotidaseAcute Kidney InjuryAgedCritical IllnessFemaleFinlandGPI-Linked ProteinsHumansIntensive Care UnitsMaleMiddle AgedProspective StudiesSepsisShock, Septic5'-NucleotidaseGPI-Linked ProteinsNT5E protein, human

Identifiers

PMID27732656
PMCPMC5061395
OpenAlexW2531284357

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LicenceCC BY
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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.