Evidence map›Paper›PMID 40524147›Full record

ArticleJournal of translational medicine2025

Proteomic analysis of human kidney biopsies unveils emerging acute kidney injury very early after liver graft reperfusion.

Åsa Norén, Roberto Boi, Rille Pullerits, Johan Mölne, Kerstin Ebefors, Styrbjörn Friman, Carina Sihlbom, Gustaf Herlenius, Jenny Nyström, Mihai Oltean

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In one paragraph

Article in Journal of translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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.

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

3 citing papers in PubMed.

  1. 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.

Åsa NorénThe Transplant Institute, Sahlgrenska University Hospital, 413 45, Gothenburg, Sweden.
Roberto BoiInstitute of Neuroscience and Physiology, Department of Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Rille PulleritsInstitute of Medicine, Department of Rheumatology and Inflammation Research, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Johan MölneClinical Pathology, Sahlgrenska University Hospital, Gothenburg, Sweden.
Kerstin EbeforsInstitute of Neuroscience and Physiology, Department of Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Styrbjörn FrimanThe Transplant Institute, Sahlgrenska University Hospital, 413 45, Gothenburg, Sweden.
Carina SihlbomProteomics Core Facility, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Gustaf HerleniusThe Transplant Institute, Sahlgrenska University Hospital, 413 45, Gothenburg, Sweden.
Jenny NyströmInstitute of Neuroscience and Physiology, Department of Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Mihai OlteanThe Transplant Institute, Sahlgrenska University Hospital, 413 45, Gothenburg, Sweden. mihai.oltean@surgery.gu.se.ORCID 0000-0003-3783-5207

Funding

Västra Götalandsregionen ALFGBG-1005046Västra Götalandsregionen ALFGBG-96501
6 · The paper itself

Abstract

backgroundAcute kidney injury (AKI) is a frequent complication after liver transplantation (LT) and is associated with morbidity, mortality, and late development of chronic kidney disease. Risk factors for AKI after LT include patient, perioperative and graft-related factors. The exact renal molecular mechanisms behind AKI in LT are unclear.

methodsAlterations in the proteome were investigated in kidney biopsies from 21 patients undergoing LT using quantitative proteomics. The most upregulated protein was validated using immunohistochemistry. In addition, serum levels of interleukin (IL)-33, insulin-like growth factor binding protein (IGFBP)-7 and high-mobility group box (HMGB)-1 were analyzed. In silico data validation was performed using 14 recently published proteomics and transcriptomics datasets.

resultsIn post-reperfusion biopsies, we identified 731 differentially regulated proteins between patients with and without AKI. The most upregulated pathways were related to inflammation, integrin signaling and extracellular matrix (ECM) remodeling. The most downregulated pathways were traceable to a mitochondrial origin. HMGB-1 was found to be already upregulated (15%) 2 h after LT in patients who later developed AKI. The AKI group also showed upregulation of the alarmin IGFBP-7, caspases 1, 4 and 8, nuclear factor kappa B subunits, and the inflammasome adaptor protein PYCARD. Circulating IL-33 and HMGB-1 (but not IGFBP-7) increased during LT but returned to normal levels within 24 h. Altogether, these findings indicate ongoing inflammatory signaling activity in the kidneys of LT recipients who ultimately develop moderate or severe AKI shortly after liver graft reperfusion.

conclusionsLT induces extensive alarmin signaling and ECM remodeling in the kidneys of recipients who develop postoperative AKI. Further strategies to curtail this phenomenon are mandated. Trial registration https://www.researchweb.org/is/en/vgr/project/278585 , Registered 24 May 2022 (Retrospectively registered).

Indexed as

Acute Kidney InjuryKidneyLiver TransplantationProteomicsReperfusionAdultBiopsyFemaleHMGB1 ProteinHumansLiverMaleMiddle AgedHMGB1 Protein

Identifiers

PMID40524147
PMCPMC12172208

What Socratic holds

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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 Socratic graph.