Evidence map›Paper›PMID 41469481›Full record

ArticleCommunications biology2025

The temporal gene expression landscape of rhabdomyolysis-induced acute kidney injury reveals the timing of complement activation.

Anne Grunenwald, Idris Boudhabhay, Margot Revel, Victoria Poillerat, Elodie Voilin, Amine Majdi, Khalil Chaibi, Stephane Gaudry, Trent M Woodruff, Gilles Crambert and 9 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Communications biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the 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.

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

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

19 authors.

Anne Grunenwald *Centre de Recherche des Cordeliers, Institut National de la Santé et de la Recherche Médicale, Sorbonne Université, Université de Paris Cité, Team Inflammation, Complement and cancer, Paris, France.
Idris Boudhabhay *Centre de Recherche des Cordeliers, Institut National de la Santé et de la Recherche Médicale, Sorbonne Université, Université de Paris Cité, Team Inflammation, Complement and cancer, Paris, France.ORCID http://orcid.org/0000-0002-8045-1658
Margot RevelCentre de Recherche des Cordeliers, Institut National de la Santé et de la Recherche Médicale, Sorbonne Université, Université de Paris Cité, Team Inflammation, Complement and cancer, Paris, France.
Victoria PoilleratCentre de Recherche des Cordeliers, Institut National de la Santé et de la Recherche Médicale, Sorbonne Université, Université de Paris Cité, Team Inflammation, Complement and cancer, Paris, France.
Elodie VoilinCentre de Recherche des Cordeliers, Institut National de la Santé et de la Recherche Médicale, Sorbonne Université, Université de Paris Cité, Team Inflammation, Complement and cancer, Paris, France.
Amine MajdiCentre de Recherche des Cordeliers, Institut National de la Santé et de la Recherche Médicale, Sorbonne Université, Université de Paris Cité, Team Integrative Cancer Immunology, Paris, France.ORCID http://orcid.org/0009-0006-4692-1093
Khalil ChaibiDepartment of Intensive Care, AP-HP, Hôpital Avicenne, Bobigny, France.
Stephane GaudryDepartment of Intensive Care, AP-HP, Hôpital Avicenne, Bobigny, France.
Trent M WoodruffSchool of Biomedical Sciences, Faculty of Medicine, University of Queensland, St Lucia, QLD, Australia.ORCID http://orcid.org/0000-0003-1382-911X
Gilles CrambertCentre de Recherche des Cordeliers, Institut National de la Santé et de la Recherche Médicale, Sorbonne Université, Université de Paris Cité, Team Renal Physiology and Tubulopathies, Paris, France.
Julien GuihaireCardiac and Vascular Surgery Department, Marie Lannelongue Hospital, Groupe Hospitalier Paris Saint-Joseph, Université Paris-Saclay, Paris, France.
Mohamad ZaidanDepartment of Nephrology and Renal Transplantation, Assistance Publique-Hôpitaux de Paris, Bicetre Hospital, Le Kremlin-Bicêtre, France.
Julie OniszczukDepartment of Nephrology and Renal Transplantation, Foch Hospital, Suresne, France.
Marie FrimatUniv. Lille, CHU Lille, Nephrology Department, Inserm U1167 - RID-AGE, Lille, France.
Viviane GnemmiUniversity Lille, CNRS, Inserm, CHU Lille, UMR9020-U1277 - CANTHER - Cancer Heterogeneity Plasticity and Resistance to Therapies, Lille, France.
Marc AlettiDepartment of Internal Medicine, Percy Military Teaching Hospital, Clamart, France.
Hubert NiellyDepartment of Internal Medicine, Bégin Military Teaching Hospital, Saint-Mandé, France.ORCID http://orcid.org/0000-0002-8042-5716
Laurent GilardinSorbonne Paris-Nord University (Paris 13), Bobigny, France.
Lubka T RoumeninaCentre de Recherche des Cordeliers, Institut National de la Santé et de la Recherche Médicale, Sorbonne Université, Université de Paris Cité, Team Inflammation, Complement and cancer, Paris, France. lubka.roumenina@sorbonne-universite.fr.ORCID http://orcid.org/0000-0002-9940-0324

Funding

Agence Nationale de la Recherche (French National Research Agency) ANR project CompKid (ANR-24-CE14-2619-01)Fondation pour la Recherche Médicale (Foundation for Medical Research in France) Fondation pour la Recherche Médicale FRM team label (FRM EQU202503020008)
6 · The paper itself

Abstract

Rhabdomyolysis-induced acute kidney injury (RIAKI) involves complement activation, but its role as a therapeutic target remains unclear. We analyze urine and kidney biopsies from RIAKI patients and use a glycerol-induced mouse model to investigate complement activation and its contribution to RIAKI. Here we show that complement fragments Ba, Bb, C5a, and sC5b-9 are elevated in the urine of patients with RIAKI, and C3 staining is detected in injured tubules, often surrounded by C5aR1-expressing myeloid cells. However, pharmacologic C5 or C5aR1 inhibition fail to prevent RIAKI in mice. A kinetic analysis reveal that complement activation occurs later in the disease course, following early tubular injury and immune cell infiltration. Initial cytoprotective responses are rapidly overwhelmed, leading to tubular damage and chemokine-driven C5aR1-expressing myeloid cells recruitment. These findings suggest that complement cascade is not an initiating factor in RIAKI and underscore the multifactorial nature of this disease.

Indexed as

Acute Kidney InjuryComplement ActivationRhabdomyolysisAnimalsDisease Models, AnimalFemaleHumansMaleMiceMice, Inbred C57BLMiddle AgedReceptor, Anaphylatoxin C5aReceptor, Anaphylatoxin C5a

Identifiers

PMID41469481
PMCPMC12877018

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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.