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During the congress, E-Posters will be accessible to all participants on the congress website 24/7, as well as in the E-poster stations in the congress center.
Preparing your E-Poster
Please review the E-Poster format requirements carefully when preparing your E-Poster. Should your E-Poster not meet the mentioned requirements, it may not be displayed as described above.
E-Poster Submission Deadline
Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
Please follow the instructions below to input your abstract title.
Abstract titles should be brief and reflect the content of the abstract.
Acute kidney injury (AKI) often triggers pathological effects that extend beyond the kidney, predisposing patients to systemic inflammation and multi-organ comorbidities. However, how renal injury communicates with the bone marrow to imprint long-lasting immune alterations remains unclear. Trained immunity—a memory-like reprogramming of innate immune cells—has emerged as a key driver of chronic inflammation and multi-organ comorbidities. Here, we investigated whether kidney injury induces trained immunity through bone marrow reprogramming and explored its contribution to kidney-related multi-organ pathology.
We utilized a mouse model of renal ischemia-reperfusion injury (IRI). Bone marrow hematopoietic stem and progenitor cells (HSPCs) and myeloid cells were analyzed. Bone marrow transplantation (BMT) from IRI or sham donors into naïve recipients was performed to assess the functional impact of bone marrow reprogramming on subsequent kidney and lung injury. Myeloid cells were challenged with LPS to evaluate trained immune responses. Transcriptomic (RNA-seq) and epigenomic (ATAC-seq) profiling of Lin⁻Sca-1⁺c-Kit⁺ (LSK) cells was conducted to investigate the mechanism.
Renal IRI induced myeloid-biased differentiation of HSPCs and a trained immunity phenotype in monocytes and macrophages, characterized by enhanced cytokine production and metabolic activation. This phenotype was conserved in human AKI monocytes. BMT from IRI donors conferred exaggerated inflammatory responses in recipient mice upon challenge. Mechanistically, we found increased chromatin accessibility at PU.1-binding motifs in bone marrow progenitors after AKI. Renal ischemia induced the release of serum amyloid A (SAA), which systemically targeted bone marrow progenitors to upregulate Kdm6b, leading to H3K27me3 demethylation and persistent transcriptional activation to induce trained immunity.
Our study defines a kidney-bone marrow axis wherein renal injury triggers SAA-mediated, KDM6B-dependent epigenetic reprogramming of bone marrow progenitors. This reprogramming establishes trained immunity in the myeloid lineage, which in turn fuels systemic inflammation and exacerbates multi-organ injury. Targeting the SAA-KDM6B pathway may represent a novel therapeutic strategy to mitigate the systemic sequelae of AKI.
