Evidence map›Paper›PMID 29482511›Full record

Observational studyBMC nephrology2018

Increased urinary excretion of kynurenic acid is associated with non-recovery from acute kidney injury in critically ill patients.

Fabienne Aregger, Dominik E Uehlinger, Gerhard Fusch, Aldin Bahonjic, Rene Pschowski, Michael Walter, Joerg C Schefold

Open access · goldAbstract readObservational Study
In one paragraph

Observational study in BMC nephrology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
0.6field-weighted citation impact, top 39% 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

22 citing papers in PubMed, 30 citations in OpenAlex.

  1. Observational
  2. Integrative Pharmacokinetic and Metabolomic Profiling ofInternational journal of molecular sciences · 2026
    Article
  3. Article
  4. Observational
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Observational
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Kynurenine pathway in kidney diseases.Pharmacological reports : PR · 2022
    Review
  17. Article
  18. Article
  19. Article
  20. Article
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 4 institutions in 3 countries.

Fabienne AreggerDepartment of Nephrology and Intensive Care Medicine, Charité Universitätsmedizin Berlin, Campus Virchow Klinikum, Berlin, Germany.
Dominik E UehlingerDepartment of Nephrology and Hypertension, Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland.
Gerhard FuschDepartment of Pediatrics, McMaster University, Hamilton, ON, Canada.
Aldin BahonjicDepartment of Pediatrics, McMaster University, Hamilton, ON, Canada.
Rene PschowskiDepartment of Nephrology and Intensive Care Medicine, Charité Universitätsmedizin Berlin, Campus Virchow Klinikum, Berlin, Germany.
Michael WalterInstitute of Laboratory Medicine, Clinical Chemistry and Pathobiochemistry, Charité University Medicine, Berlin, Germany.
Joerg C SchefoldDepartment of Intensive Care Medicine, Inselspital, Bern University Hospital, University of Bern, 3010, Bern, Switzerland. joerg.schefold@insel.ch.ORCID http://orcid.org/0000-0001-9162-5724
University of Bern · CHMcMaster University · CACharité - Universitätsmedizin Berlin · DEVivantes Klinikum · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAcute kidney injury (AKI) is often observed in critically ill patients and is associated with high morbidity and mortality. Non-recovery from AKI has a negative impact on the prognosis of affected patients and early risk stratification seems key to improve clinical outcomes. We analyzed metabolites of a conserved key inflammatory pathway (i.e. tryptophan degradation pathway) in serial urine samples of patients with AKI.

methodsOne hundred twelve ICU patients with AKI were included in a prospective observational analysis. After exclusion criteria, 92 patients were eligible for analysis. Serial urine samples were collected and tryptophan levels including key tryptophan metabolites were measured using tandem mass spectrometry.

resultsSixty-seven patients recovered in the first 7 days of AKI (early recovery, ER) whereas n = 25 had late-/non-recovery (LNR). Urinary concentrations of tryptophan, kynurenine, 3-OH anthranillic acid, serotonine, and kynurenine/tryptophan were significantly lower in LNR patients. In contrast, creatinine normalized excretion of kynurenic acid (KynA) was substantially increased in LNR patients (7.59 ± 6.81 vs. 3.19 ± 3.44 (ER) μmol/mmol, p <  0.005). High urinary KynA excretion was associated with higher RIFLE class, longer AKI duration, increased need for RRT, and 30-day mortality. Logistic regression revealed KynA as the single most important predictor of renal recovery on days 1 and 2 of AKI.

conclusionsIncreased urinary levels of kynurenic acid, a key inflammatory metabolite of the tryprophan degradation pathway, are associated with adverse renal and clinical outcomes in critically ill patients with AKI. Urinary KynA may serve as an early risk stratificator in respective patients with AKI.

Indexed as

Recovery of FunctionAcute Kidney InjuryAgedAged, 80 and overBiomarkersCritical IllnessFemaleHumansKynurenic AcidMaleMiddle AgedProspective StudiesRetrospective StudiesBiomarkersKynurenic AcidIDOInflammationIntensive care unitKynureninesRenal failureRenal recoveryTryptophan metablism

Identifiers

PMID29482511
PMCPMC5828079
OpenAlexW2796846300

What OpenQuestion holds

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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.