Evidence map›Paper›PMID 31343478›Full record

ArticleCritical care medicine2019

Use of Cell Cycle Arrest Biomarkers in Conjunction With Classical Markers of Acute Kidney Injury.

Michael Joannidis, Lui G Forni, Michael Haase, Jay Koyner, Jing Shi, Kianoush Kashani, Lakhmir S Chawla, John A Kellum, Sapphire Investigators

Open access · hybridAbstract read
In one paragraph

Article in Critical care medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 2 pooled it
6.1field-weighted citation impact, top 3% 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

35 citing papers in PubMed, 2 syntheses or guidelines pooled it, 66 citations in OpenAlex.

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  16. Subphenotypes in acute kidney injury: a narrative review.Critical care (London, England) · 2022
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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 4 institutions in 3 countries.

Michael JoannidisDivision of Intensive Care and Emergency Medicine, Department of Internal Medicine, Medical University Innsbruck, Innsbruck, Austria.
Lui G ForniDepartment of Clinical and Experimental Medicine, Faculty of Health Sciences, University of Surrey and Intensive Care Unit, Royal Surrey County Hospital NHS Foundation Trust, Guildford, United Kingdom.
Michael HaaseDepartment of Nephrology, Otto-von-Guericke-Universitat Magdeburg, Magdeburg, Germany.
Jay KoynerSection of Nephrology, Department of Medicine, University of Chicago, Chicago, IL.
Jing ShiDepartment of Statistics, Walker Bioscience, Carlsbad, CA.
Kianoush KashaniDivision of Nephrology & Hypertension, Department of Medicine, Mayo Clinic, Rochester, MN.
Lakhmir S ChawlaVeterans Affairs Medical Center, Medicine, Department of Medicine, San Diego, CA.
John A KellumCenter for Critical Care Nephrology, Department of Critical Care Medicine, University of, Pittsburgh, Pittsburgh PA.
Sapphire Investigators
Mayo Clinic in Arizona · USInnsbruck Medical University · ATRoyal Surrey NHS Foundation Trust · GBUniversity of Chicago · US

Funding

Integrating data, algorithms and clinical reasoning for surgical risk assessmentR01GM110240 · NIGMS · UNIVERSITY OF FLORIDA · PI BIHORAC, AZRA, RASHIDI, PARISA · 2016 to 2025
$5.1M
NIGMS NIH HHS R01 GM110240
6 · The paper itself

Abstract

objectivesDecreased urine output and/or increased serum creatinine may herald the development of acute kidney injury or reflect normal physiology. In this secondary analysis of the Sapphire study, we examined biomarkers of cell cycle arrest in the settings of oliguria and/or azotemia to improve risk assessment when used with conventional indices in predicting severe acute kidney injury (Kidney Disease: Improving Global Outcomes 3 defined by the need for renal replacement therapy or changes in urine output, serum creatinine or both) or death.

designProspective, international, Sapphire study.

settingAcademic Medical Center. PATIENTS: Patients without acute kidney injury Kidney Disease: Improving Global Outcomes stage 2 or 3.

interventionsNone. MEASUREMENTS AND MAIN

resultsThe primary endpoint being development of severe acute kidney injury or death within 1 week. Secondary analysis examined the relationship between tissue inhibitor of metalloproteinases-2 ([TIMP-2]) and insulin growth factor binding protein 7 ([IGFBP7]) and 9-month death or dialysis conditioned on progression to stage 2-3 acute kidney injury within 1 week. Seventy-nine patients reached the primary endpoint and were more likely to be surgical, with higher nonrenal Acute Physiology and Chronic Health Evaluation III scores and more chronic kidney disease. Stage 1 urine output, serum creatinine, and urinary [TIMP-2]•[IGFBP7] greater than 2.0 were all predictive of progression to the primary endpoint independent from nonrenal Acute Physiology and Chronic Health Evaluation III score. Combinations of predictors increased the hazard ratios considerably (from 2.17 to 4.14 to 10.05, respectively). In the presence of acute kidney injury (stage 1), [TIMP-2]•[IGFBP7] greater than 2.0 leads to an increased risk of death or dialysis at 9 months even in the absence of progression of acute kidney injury (stage 2-3) within 7 days.

conclusionsCell cycle arrest biomarkers, TIMP-2 and IGFBP7, improve risk stratification for severe outcomes in patients with stage 1 acute kidney injury by urine output, serum creatinine or both, with risk increasing with each acute kidney injury indicator. Longer term outcomes demonstrate that the associated risks of a [TIMP-2]•[IGFBP7] greater than 2.0 is equivalent to acute kidney injury progression even where no progression from stage 1 acute kidney injury is observed.

Indexed as

Cell Cycle CheckpointsAcute Kidney InjuryBiomarkersCreatinineHumansInsulin-Like Growth Factor Binding ProteinsProspective StudiesTissue Inhibitor of Metalloproteinase-2BiomarkersCreatinineinsulin-like growth factor binding protein-related protein 1Insulin-Like Growth Factor Binding ProteinsTIMP2 protein, humanTissue Inhibitor of Metalloproteinase-2

Identifiers

PMID31343478
PMCPMC6750148
OpenAlexW2963730652

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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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.