Evidence map›Paper›PMID 28814331›Full record

ArticleCritical care (London, England)2017

Circulating levels of soluble Fas (sCD95) are associated with risk for development of a nonresolving acute kidney injury subphenotype.

Pavan K Bhatraju, Cassianne Robinson-Cohen, Carmen Mikacenic, Susanna Harju-Baker, Victoria Dmyterko, Natalie S J Slivinski, W Conrad Liles, Jonathan Himmelfarb, Susan R Heckbert, Mark M Wurfel

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Critical care (London, England), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

11 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Molecular Phenotyping of Sepsis and Differential Response to Fluid Resuscitation.American journal of respiratory and critical care medicine · 2025
    Trial
  3. Identification of prognostic biomarkers for antibiotic associated nephrotoxicity in cystic fibrosis.Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society · 2024
    Article
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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.

Pavan K BhatrajuPulmonary and Critical Care Medicine, University of Washington, Harborview Medical Center, 325 9th Avenue, Seattle, WA, 98104, USA. bhatraju@uw.edu.
Cassianne Robinson-CohenKidney Research Institute, Division of Nephrology, University of Washington, Seattle, WA, USA.
Carmen MikacenicPulmonary and Critical Care Medicine, University of Washington, Harborview Medical Center, 325 9th Avenue, Seattle, WA, 98104, USA.
Susanna Harju-BakerPulmonary and Critical Care Medicine, University of Washington, Harborview Medical Center, 325 9th Avenue, Seattle, WA, 98104, USA.
Victoria DmyterkoPulmonary and Critical Care Medicine, University of Washington, Harborview Medical Center, 325 9th Avenue, Seattle, WA, 98104, USA.
Natalie S J SlivinskiUniversity of Leeds, Leeds, UK.
W Conrad LilesDepartment of Medicine, University of Washington, Harborview Medical Center, Seattle, WA, USA.
Jonathan HimmelfarbKidney Research Institute, Division of Nephrology, University of Washington, Seattle, WA, USA.
Susan R HeckbertDepartment of Epidemiology, University of Washington, Seattle, WA, USA.
Mark M WurfelPulmonary and Critical Care Medicine, University of Washington, Harborview Medical Center, 325 9th Avenue, Seattle, WA, 98104, USA.

Funding

MOLECULAR EPIDEMIOLOGY OF ARDSR01HL060710 · NHLBI · HARVARD UNIVERSITY (SCH OF PUBLIC HLTH) · PI CHRISTIANI, DAVID C · 2000 to 2015
$8.4M
Identification of Sub-phenotypes of Acute Kidney Injury in the Intensive Care UnitF32DK112532 · NIDDK · UNIVERSITY OF WASHINGTON · PI BHATRAJU, PAVAN KUMAR · 2016 to 2017
$139k
NHLBI NIH HHS R01 HL060710NIDDK NIH HHS F32 DK112532
6 · The paper itself

Abstract

backgroundCritically ill patients with acute kidney injury (AKI) can be divided into two subphenotypes, resolving or nonresolving, on the basis of the trajectory of serum creatinine. It is unknown if the biology underlying these two AKI recovery patterns is different.

methodsWe measured eight circulating biomarkers in plasma obtained from a cohort of patients admitted to an intensive care unit (ICU) (n = 1241) with systemic inflammatory response syndrome. The biomarkers were representative of several biologic processes: apoptosis (soluble Fas), inflammation (soluble tumor necrosis factor receptor 1, interleukin 6, interleukin 8) and endothelial dysfunction, (angiopoietin 1, angiopoietin 2, and soluble vascular cell adhesion molecule 1). We tested for associations between biomarker levels and AKI subphenotypes using relative risk regression accounting for multiple hypotheses with the Bonferroni correction.

resultsDuring the first 3 days of ICU admission, 868 (70%) subjects developed AKI; 502 (40%) had a resolving subphenotype, and 366 (29%) had a nonresolving subphenotype. Hospital mortality was 12% in the resolving subphenotype and 21% in the nonresolving subphenotype. Soluble Fas was the only biomarker associated with a nonresolving subphenotype after adjustment for age, body mass index, diabetes, and Acute Physiology and Chronic Health Evaluation III score (p = 0.005).

conclusionsIdentifying modifiable targets in the Fas-mediated pathway may lead to strategies for prevention and treatment of a clinically important form of AKI.

Indexed as

RiskAcute Kidney InjuryAdultAgedBiomarkersCritical Illnessfas ReceptorFemaleHospital MortalityHumansIntensive Care UnitsMaleMiddle AgedPhenotypeBiomarkersFAS protein, humanfas ReceptorAcute kidney injuryApoptosisBiomarkers

Identifiers

PMID28814331
PMCPMC5559814

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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.