Evidence map›Paper›PMID 37036003›Full record

ArticleJCI insight2023

suPAR links a dysregulated immune response to tissue inflammation and sepsis-induced acute kidney injury.

Christian Nusshag, Changli Wei, Eunsil Hahm, Salim S Hayek, Jing Li, Beata Samelko, Christoph Rupp, Roman Szudarek, Claudius Speer, Florian Kälble and 14 more

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 1 pooled it
7.7field-weighted citation impact, top 2% 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

30 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.

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  18. Integrins in the kidney - beyond the matrix.Nature reviews. Nephrology · 2025
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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

24 authors at 5 institutions in 3 countries.

Christian NusshagDepartment of Internal Medicine, RUSH University Medical Center, Chicago, Illinois, USA.
Changli WeiDepartment of Internal Medicine, RUSH University Medical Center, Chicago, Illinois, USA.
Eunsil HahmDepartment of Internal Medicine, RUSH University Medical Center, Chicago, Illinois, USA.
Salim S HayekDepartment of Medicine, Division of Cardiology, University of Michigan, Ann Arbor, Michigan, USA.
Jing LiDepartment of Internal Medicine, RUSH University Medical Center, Chicago, Illinois, USA.
Beata SamelkoDepartment of Internal Medicine, RUSH University Medical Center, Chicago, Illinois, USA.
Christoph RuppDepartment of Anesthesiology, and.
Roman SzudarekDepartment of Anesthesiology, and.
Claudius SpeerDepartment of Nephrology, Heidelberg University Hospital, Heidelberg, Germany.
Florian KälbleDepartment of Nephrology, Heidelberg University Hospital, Heidelberg, Germany.
Matthias SchaierDepartment of Nephrology, Heidelberg University Hospital, Heidelberg, Germany.
Florian UhleDepartment of Anesthesiology, and.
Felix Cf SchmittDepartment of Anesthesiology, and.
Mascha O FiedlerDepartment of Anesthesiology, and.
Ellen KrautkrämerDepartment of Nephrology, Heidelberg University Hospital, Heidelberg, Germany.
Yanxia CaoDepartment of Internal Medicine, RUSH University Medical Center, Chicago, Illinois, USA.
Ricardo RodriguezDepartment of Internal Medicine, RUSH University Medical Center, Chicago, Illinois, USA.
Uta MerleDepartment of Gastroenterology, Heidelberg University Hospital, Heidelberg, Germany.
Jesper Eugen-OlsenDepartment of Clinical Research, Copenhagen University Hospital Hvidovre, Hvidovre, Denmark.
Martin ZeierDepartment of Nephrology, Heidelberg University Hospital, Heidelberg, Germany.
Markus A WeigandDepartment of Anesthesiology, and.
Christian MorathDepartment of Nephrology, Heidelberg University Hospital, Heidelberg, Germany.
Thorsten BrennerDepartment of Anesthesiology, and.
Jochen ReiserDepartment of Internal Medicine, RUSH University Medical Center, Chicago, Illinois, USA.
Rush University Medical Center · USHeidelberg University · DEHvidovre Hospital · DKUniversity of Duisburg-Essen · DEUniversity of Michigan · US

Funding

Role of SuPAR in the Intersection between Cardiovascular and Kidney DiseaseR01HL153384 · NHLBI · UNIVERSITY OF TEXAS MED BR GALVESTON · PI HAYEK, SALIM · 2020 to 2024
$2.5M
NHLBI NIH HHS R01 HL153384
6 · The paper itself

Abstract

Acute kidney injury (AKI) secondary to sepsis results in poor outcomes and conventional kidney function indicators lack diagnostic value. Soluble urokinase plasminogen activator receptor (suPAR) is an innate immune-derived molecule implicated in inflammatory organ damage. We characterized the diagnostic ability of longitudinal serum suPAR levels to discriminate severity and course of sepsis-induced AKI (SI-AKI) in 200 critically ill patients meeting Sepsis-3 criteria. The pathophysiologic relevance of varying suPAR levels in SI-AKI was explored in a polymicrobial sepsis model in WT, (s)uPAR-knockout, and transgenic suPAR-overexpressing mice. At all time points studied, suPAR provided a robust classification of SI-AKI disease severity, with improved prediction of renal replacement therapy (RRT) and mortality compared with established kidney biomarkers. Patients with suPAR levels of greater than 12.7 ng/mL were at highest risk for RRT or death, with an adjusted odds ratio of 7.48 (95% CI, 3.00-18.63). suPAR deficiency protected mice against SI-AKI. suPAR-overexpressing mice exhibited greater kidney damage and poorer survival through inflamed kidneys, accompanied by local upregulation of potent chemoattractants and pronounced kidney T cell infiltration. Hence, suPAR allows for an innate immune-derived and kidney function-independent staging of SI-AKI and offers improved longitudinal risk stratification. suPAR promotes T cell-based kidney inflammation, while suPAR deficiency improves SI-AKI.

Indexed as

Acute Kidney InjurySepsisAnimalsBiomarkersInflammationMiceMice, TransgenicReceptors, Urokinase Plasminogen ActivatorBiomarkersReceptors, Urokinase Plasminogen ActivatorClinical practiceDiagnosticsInflammationNephrologyT cells

Identifiers

PMID37036003
PMCPMC10132159
OpenAlexW4362724295

What OpenQuestion holds

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LicenceCC BY
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.