Evidence map›Paper›PMID 32958893›Full record

ReviewNature reviews. Nephrology2021

Immunopathophysiology of trauma-related acute kidney injury.

David A C Messerer, Rebecca Halbgebauer, Bo Nilsson, Hermann Pavenstädt, Peter Radermacher, Markus Huber-Lang

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Nephrology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 93 papers.

0numbers the graph read from it
0cells of the map it votes in
93citing papers in PubMed
8.9field-weighted citation impact, top 1% 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

93 citing papers in PubMed, 134 citations in OpenAlex.

  1. Loss of C3 and CD14 reduces region-specific neuroinflammation in a murine polytrauma model.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
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  11. Toxicological Profile of aJournal of toxicology · 2026
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  14. Bimodal distribution of trauma-related acute kidney injury (TrAKI): A clinical review.Journal of critical care medicine (Universitatea de Medicina si Farmacie din Targu-Mures) · 2026
    Review
  15. Article
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33 more citing papers are in PubMed but not listed here.

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

6 authors at 3 institutions in 2 countries.

David A C MessererInstitute of Clinical and Experimental Trauma Immunology, University Hospital Ulm, Ulm, Germany.ORCID http://orcid.org/0000-0002-0834-038X
Rebecca HalbgebauerInstitute of Clinical and Experimental Trauma Immunology, University Hospital Ulm, Ulm, Germany.ORCID http://orcid.org/0000-0001-8060-2076
Bo NilssonDepartment of Immunology, Genetics and Pathology, Rudbeck Laboratory Uppsala University, Uppsala, Sweden.
Hermann PavenstädtInternal Medicine D, University Hospital Muenster, Muenster, Germany.
Peter RadermacherInstitute of Anaesthesiological Pathophysiology and Process Development, University Hospital Ulm, Ulm, Germany.
Markus Huber-LangInstitute of Clinical and Experimental Trauma Immunology, University Hospital Ulm, Ulm, Germany. markus.huber-lang@uniklinik-ulm.de.ORCID http://orcid.org/0000-0003-2359-6516
University Hospital Ulm · DEUniversity Hospital Münster · DEUppsala University · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Physical trauma can affect any individual and is globally accountable for more than one in every ten deaths. Although direct severe kidney trauma is relatively infrequent, extrarenal tissue trauma frequently results in the development of acute kidney injury (AKI). Various causes, including haemorrhagic shock, rhabdomyolysis, use of nephrotoxic drugs and infectious complications, can trigger and exacerbate trauma-related AKI (TRAKI), particularly in the presence of pre-existing or trauma-specific risk factors. Injured, hypoxic and ischaemic tissues expose the organism to damage-associated and pathogen-associated molecular patterns, and oxidative stress, all of which initiate a complex immunopathophysiological response that results in macrocirculatory and microcirculatory disturbances in the kidney, and functional impairment. The simultaneous activation of components of innate immunity, including leukocytes, coagulation factors and complement proteins, drives kidney inflammation, glomerular and tubular damage, and breakdown of the blood-urine barrier. This immune response is also an integral part of the intense post-trauma crosstalk between the kidneys, the nervous system and other organs, which aggravates multi-organ dysfunction. Necessary lifesaving procedures used in trauma management might have ambivalent effects as they stabilize injured tissue and organs while simultaneously exacerbating kidney injury. Consequently, only a small number of pathophysiological and immunomodulatory therapeutic targets for TRAKI prevention have been proposed and evaluated.

Indexed as

Acute Kidney InjuryHumansImmunity, InnateKidneyWounds and Injuries

Identifiers

PMID32958893
OpenAlexW3087382850

What Socratic holds

Textmetadata
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 Socratic graph.