Evidence map›Paper›PMID 38106604›Full record

ArticleKidney international reports2023

Prompt Thrombo-Inflammatory Response to Ischemia-Reperfusion Injury and Kidney Transplant Outcomes.

Gabriel Strandberg, Carl M Öberg, Anna M Blom, Oleg Slivca, David Berglund, Mårten Segelmark, Bo Nilsson, Ali-Reza Biglarnia

Open access · goldAbstract read
In one paragraph

Article in Kidney international reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

6 citing papers in PubMed, 10 citations in OpenAlex.

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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

8 authors at 3 institutions in 1 country.

Gabriel StrandbergDepartment of Surgery, Department of Clinical Sciences Malmö, Skåne University Hospital, Lund University, Malmö, Sweden.
Carl M ÖbergDepartment of Nephrology, Department of Clinical Sciences Lund, Skåne University Hospital, Lund University, Lund, Sweden.
Anna M BlomDepartment of Translational Medicine, Lund University, Malmö, Sweden.
Oleg SlivcaDepartment of Surgery, Department of Clinical Sciences Malmö, Skåne University Hospital, Lund University, Malmö, Sweden.
David BerglundDepartment of Immunology, Genetics, and Pathology (IGP), Rudbeck Laboratory C5:3, Uppsala University, Uppsala, Sweden.
Mårten SegelmarkDepartment of Nephrology, Department of Clinical Sciences Lund, Skåne University Hospital, Lund University, Lund, Sweden.
Bo NilssonDepartment of Immunology, Genetics, and Pathology (IGP), Rudbeck Laboratory C5:3, Uppsala University, Uppsala, Sweden.
Ali-Reza BiglarniaDepartment of Surgery, Department of Clinical Sciences Malmö, Skåne University Hospital, Lund University, Malmö, Sweden.
Lund University · SEUppsala University · SESkåne University Hospital · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: In kidney transplantation (KT), the role of the intravascular innate immune system (IIIS) in response to ischemia-reperfusion injury (IRI) is not well-understood. Here, we studied parallel changes in the generation of key activation products of the proteolytic cascade systems of the IIIS following living donor (LD) and deceased donor (DD) transplantation and evaluated potential associations with clinical outcomes. Methods: In a cohort study, 63 patients undergoing LD ( Results: DD kidneys exhibited a prompt and interlinked activation of all 3 cascade systems of IIIS postreperfusion, indicating a robust and local thrombo-inflammatory response to IRI. In this initial response, the complement activation product sC5b-9 exhibited a robust correlation with other IIIS activation markers and displayed a strong association with short-term and mid-term (24-month) graft dysfunction. In contrast, LD kidneys did not exhibit this thrombo-inflammatory response. The use of HMP was associated with reduced thromboinflammation and preserved mid-term kidney function. Conclusion: Kidneys from DD are vulnerable to a prompt thrombo-inflammatory response to IRI, which adversely affects both short-term and long-term allograft function. Strategies aimed at minimizing graft immunogenicity prior to reperfusion are crucial to mitigate the intricate inflammatory response to IRI.

Indexed as

delayed graft functionintravascular innate immune systemischemia-reperfusion injurykidney transplantationorgan preservationthromboinflammation

Identifiers

PMID38106604
PMCPMC10719603
OpenAlexW4386992762

What OpenQuestion holds

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LicenceCC BY
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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.