Evidence map›Paper›PMID 42878585›Full record

ArticleHepatology communications2026

Lower circulating angiotensinogen levels across ACLD stages are associated with hepatic dysfunction and mortality.

Marlene Hintersteininger, Benedikt Silvester Hofer, Clemens Renhardt, Benedikt Simbrunner, Oliver Domenig, Lorenz Balcar, Mathias Jachs, Georg Kramer, Christian Sebesta, Paul Thöne and 5 more

Registry-linked trialAbstract read
In one paragraph

Article in Hepatology communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03267615 (VICIS - Vienna Cirrhosis Study), which is not on this map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–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.

NCT03267615 recruitingnot on this map

VICIS - Vienna Cirrhosis Study

Typeobservational_patient_registrySponsorMedical University of ViennaRan2017 to 2027Enrolled10,000ConditionsLiver Cirrhosis, Portal Hypertension, Ascites, Variceal Hemorrhage
3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

15 authors.

Marlene HintersteiningerDivision of Gastroenterology and Hepatology, Department of Medicine III, Medical University of Vienna, Vienna, Austria.ORCID 0009-0004-5353-5102
Benedikt Silvester HoferDivision of Gastroenterology and Hepatology, Department of Medicine III, Medical University of Vienna, Vienna, Austria.ORCID 0000-0003-3403-3372
Clemens RenhardtDivision of Gastroenterology and Hepatology, Department of Medicine III, Medical University of Vienna, Vienna, Austria.ORCID 0009-0008-5784-8500
Benedikt SimbrunnerDivision of Gastroenterology and Hepatology, Department of Medicine III, Medical University of Vienna, Vienna, Austria.ORCID 0000-0001-8181-9146
Oliver DomenigAttoquant Diagnostics, Vienna, Austria.ORCID 0000-0002-5995-8753
Lorenz BalcarDivision of Gastroenterology and Hepatology, Department of Medicine III, Medical University of Vienna, Vienna, Austria.ORCID 0000-0002-6708-3061
Mathias JachsDivision of Gastroenterology and Hepatology, Department of Medicine III, Medical University of Vienna, Vienna, Austria.ORCID 0000-0003-2871-4147
Georg KramerDivision of Gastroenterology and Hepatology, Department of Medicine III, Medical University of Vienna, Vienna, Austria.ORCID 0009-0008-1736-3699
Christian SebestaDivision of Gastroenterology and Hepatology, Department of Medicine III, Medical University of Vienna, Vienna, Austria.
Paul ThöneDivision of Gastroenterology and Hepatology, Department of Medicine III, Medical University of Vienna, Vienna, Austria.ORCID 0009-0001-1618-476
Paula HöfingerDivision of Gastroenterology and Hepatology, Department of Medicine III, Medical University of Vienna, Vienna, Austria.ORCID 0009-0007-3197-4480
Michael TraunerDivision of Gastroenterology and Hepatology, Department of Medicine III, Medical University of Vienna, Vienna, Austria.ORCID 0000-0002-1275-6425
Mattias MandorferDivision of Gastroenterology and Hepatology, Department of Medicine III, Medical University of Vienna, Vienna, Austria.ORCID 0000-0003-2330-0017
Thomas ReibergerDivision of Gastroenterology and Hepatology, Department of Medicine III, Medical University of Vienna, Vienna, Austria.ORCID 0000-0002-4590-3583
Lukas HartlDivision of Gastroenterology and Hepatology, Department of Medicine III, Medical University of Vienna, Vienna, Austria.ORCID 0000-0003-3398-6120

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionThe liver produces angiotensinogen (AGT), the key upstream precursor of the renin-angiotensin system (RAS). We measured AGT levels in patients across distinct advanced chronic liver disease (ACLD) stages and investigated the impact of AGT levels on clinical outcomes.

methodsWe included clinically stable ACLD outpatients undergoing hepatic venous pressure gradient (HVPG) measurement between May 2018 and October 2023, as well as healthy controls (HCs) recruited in the prospective Vienna Cirrhosis Study (VICIS; NCT03267615). AGT was assessed by converting it to angiotensin I (Ang I) through incubation with excess recombinant human renin. RAS parameters were measured by liquid chromatography-tandem mass spectrometry. Patients were stratified as compensated (cACLD), single decompensated (sdACLD), or further decompensated ACLD (fdACLD).

resultsOverall, 60 individuals (cACLD: n=16; sdACLD: n=22; fdACLD: n=12; HC: n=10) were included. AGT levels decreased significantly compared with HC and with increasing ACLD severity (HC: 943.2 vs. cACLD: 550.4 vs. sdACLD: 476.9 vs. fdACLD: 439.8 nmol/L; p<0.001). In contrast, plasma concentrations of Ang II (cACLD: 23.1 vs. sdACLD: 156.0 vs. fdACLD: 162.4 pmol/L; p=0.002) and Ang 1-7 (cACLD: 3.0 vs. sdACLD: 3.2 vs. fdACLD: 8.5 pmol/L; p=0.022) increased significantly with ACLD severity. AGT did not correlate with Ang II (ρ=-0.23; p=0.101), but with Ang 1-7 (ρ=0.32; p=0.022) and MELD-Na (ρ=-0.29; p=0.042). Exploratory survival analyses, limited by the small sample size, showed that lower AGT was associated with all-cause mortality (adjusted for age and MELD-Na: asHR: 1.59; 95% CI: 1.09-2.27; p=0.012/adjusted for age and albumin: asHR: 1.52; 95% CI: 1.05-2.21; p=0.026).

conclusionsAGT levels decreased in ACLD, correlated with hepatic dysfunction, and were linked to all-cause mortality in exploratory survival analyses. Still, classical and alternative RAS parameters increased in parallel to ACLD severity.

Indexed as

AngiotensinogenLiver CirrhosisAdultAngiotensin IBiomarkersFemaleHumansMaleMiddle AgedProspective StudiesRenin-Angiotensin SystemSeverity of Illness IndexAGT protein, humanAngiotensin IAngiotensinogenBiomarkersalternative RASangiotensin 1-7angiotensin IIangiotensinogencirrhosisportal hypertensionRAS

Identifiers

PMID42878585
PMCPMC13668287

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Registered trials

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