Evidence map›Paper›PMID 28975359›Full record

ArticleJournal of molecular medicine (Berlin, Germany)2017

Urine metabolomics insight into acute kidney injury point to oxidative stress disruptions in energy generation and H

Marta Martin-Lorenzo, Laura Gonzalez-Calero, Angeles Ramos-Barron, Maria D Sanchez-Niño, Carlos Gomez-Alamillo, Juan Manuel García-Segura, Alberto Ortiz, Manuel Arias, Fernando Vivanco, Gloria Alvarez-Llamas

Abstract read
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In one paragraph

Article in Journal of molecular medicine (Berlin, Germany), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

24 citing papers in PubMed, 39 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

10 authors at 5 institutions in 1 country.

Marta Martin-LorenzoDepartment of Immunology, IIS-Fundacion Jimenez Diaz-UAM, REDinREN, Madrid, Spain.
Laura Gonzalez-CaleroDepartment of Immunology, IIS-Fundacion Jimenez Diaz-UAM, REDinREN, Madrid, Spain.
Angeles Ramos-BarronNephrology Department, Hospital Valdecilla, Universidad de Cantabria, Instituto de Investigación Marqués de Valdecilla, IDIVAL, Santander, Cantabria, Spain.
Maria D Sanchez-NiñoDepartment of Nephrology/IRSIN, IIS-Fundación Jiménez Díaz-UAM, REDinREN, Madrid, Spain.
Carlos Gomez-AlamilloNephrology Department, Hospital Valdecilla, Universidad de Cantabria, Instituto de Investigación Marqués de Valdecilla, IDIVAL, Santander, Cantabria, Spain.
Juan Manuel García-SeguraCAI-RMN, Universidad Complutense, Madrid, Spain.
Alberto OrtizDepartment of Nephrology/IRSIN, IIS-Fundación Jiménez Díaz-UAM, REDinREN, Madrid, Spain.
Manuel AriasNephrology Department, Hospital Valdecilla, Universidad de Cantabria, Instituto de Investigación Marqués de Valdecilla, IDIVAL, Santander, Cantabria, Spain.
Fernando VivancoDepartment of Immunology, IIS-Fundacion Jimenez Diaz-UAM, REDinREN, Madrid, Spain.
Gloria Alvarez-LlamasDepartment of Immunology, IIS-Fundacion Jimenez Diaz-UAM, REDinREN, Madrid, Spain. galvarez@fjd.es.
Hospital Universitario Fundación Jiménez Díaz · ESInstituto de Investigación Marqués de Valdecilla · ESUniversidad Complutense de Madrid · ESUniversidad Autónoma de Madrid · ESUniversidad de Cantabria · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute kidney injury (AKI) is one of the main complications in acute care medicine and a risk factor for chronic kidney disease (CKD). AKI incidence has increased; however, its diagnosis has limitations and physiopathological mechanisms are underexplored. We investigated urine samples, aiming to identify major metabolite changes during human AKI evolution. Metabolic signatures found were further explored for a potential link to severity of injury. Twenty-four control subjects and 38 hospitalized patients with AKI were recruited and urine samples were collected at the time of diagnosis, during follow-up and at discharge. Nuclear magnetic resonance (NMR) was used in a first discovery phase for identifying potential metabolic differences. Target metabolites of interest were confirmed by liquid chromatography-mass spectrometry (LC-MS/MS) in an independent group. Underlying metabolic defects were further explored by kidney transcriptomics of murine toxic AKI. Urinary 2-hydroxybutyric acid, pantothenic acid, and hippuric acid were significantly downregulated and urinary N-acetylneuraminic acid, phosphoethanolamine, and serine were upregulated during AKI. Hippuric acid, phosphoethanolamine, and serine showed further downregulation/upregulation depending on the metabolite in acute tubular necrosis (ATN) AKI compared to prerenal AKI. Kidney transcriptomics disclosed decreased expression of cystathionase, cystathionine-β-synthase, and ethanolamine-phosphate cytidylyltransferase, and increased N-acetylneuraminate synthase as the potentially underlying cause of changes in urinary metabolites. A urinary metabolite panel identified AKI patients and provided insight into intrarenal events. A urine fingerprint made up of six metabolites may be related to pathophysiological changes in oxidative stress, energy generation, and H KEY MESSAGES: The urinary metabolome reflects AKI evolution and severity of injury. Kidney transcriptomics revealed enzymatic expression changes. Enzymatic expression changes may be the potentially underlying cause of changes in urine metabolites. Identified metabolite changes link oxidative stress, energy generation, and H

Indexed as

Energy MetabolismMetabolomicsOxidative StressAcute Kidney InjuryAdultAgedAged, 80 and overFemaleGene Expression RegulationHumansHydrogen SulfideLinear ModelsMaleMiddle AgedROC CurveSeverity of Illness IndexHydrogen SulfideAcute kidney injuryH2SMetabolomicsOxidative stressUrine

Identifiers

PMID28975359
OpenAlexW2763615699

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.