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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) frequently progresses to acute lung injury (ALI), significantly increasing patient mortality. However, the underlying mechanisms linking AKI to ALI remain poorly understood.
Microarray datasets of AKI and ALI were downloaded from the Gene Expression Omnibus (GEO) database, and GEO2R/Venn diagrams were used to identify common differentially expressed genes (DEGs) with consistent expression trends. Hub genes and enriched pathways were analyzed via CytoHubba and functional enrichment tools. To further validate clinical relevance, bulk-RNA sequencing was performed on bronchoalveolar lavage fluid (BALF) from AKI patients and non-AKI controls. Mechanistically, serum proteomics of AKI patients and kidney proteomics of mice were conducted to identify proteins co-upregulated in AKI kidneys and plasma. Correlation analysis was performed between renal protein expression and pulmonary IL-17 pathway molecules. A bilateral renal ischemia-reperfusion injury (bIRI) mouse model of AKI-ALI was used for validation, including experiments using Rorγt knockout (Rorγt-KO) mice to deplete Th17 cells and administration of neutralizing antibodies against IL-17A or SAA.
A total of 148 common DEGs were identified in AKI and ALI, primarily enriched in inflammation-related pathways, with the IL-17 signaling pathway top-ranked. Consistently, bulk-RNA sequencing of BALF from AKI patients versus non-AKI controls also revealed significant enrichment of the IL-17 signaling pathway. In bIRI-induced AKI-ALI mice, circulating Th17 cells and IL-17A were markedly elevated, accompanied by pulmonary IL-17 pathway activation, which were positively correlated with ALI severity. Notably, Notably, Rorγt-KO mice or administration of IL-17A neutralizing antibody alleviated ALI phenotypes compared to control mice after AKI, manifested by the reduced alveolar wall thickness and less inflammatory cells as well as cytokines. Serum and kidney proteomics analyses identified 5 proteins (SPP1, SAA1, SAA2, HAVCR1, ITIH4) co-upregulated in AKI kidneys and plasma, among which renal SAA1 and SAA2 expression was significantly correlated with most pulmonary IL-17 pathway effectors. Furthermore, systemic neutralization of SAA reduced circulating Th17 cells and IL-17A levels, while ameliorating AKI-induced ALI.
Our findings demonstrate that AKI induces upregulation of renal and circulating SAA, which promotes Th17 cell differentiation and subsequent IL-17A release. Elevated IL-17A activates pulmonary IL-17 signaling, driving ALI. Targeting SAA to inhibit Th17 cell differentiation, or directly blocking IL-17A, holds promise as a novel strategy to prevent ALI after AKI.
