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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.
Maladaptive repair of renal tubular epithelial cells (TECs) following acute kidney injury (AKI) leads to irreversible fibrosis, resulting in chronic kidney disease (CKD). We previously demonstrated that CD44 expression is localized in dilated and atrophic TECs within fibrotic lesions in several rat CKD models, suggesting that CD44 is specifically expressed in failed-repair TECs (FR-TECs). In this study, we investigated the detailed kinetics of CD44 expression and its pathophysiological role in the AKI-to-CKD transition.
Six-week-old male SD rats were subjected to unilateral renal ischemia/reperfusion (I/R) operation for 60 min and sacrificed at 1, 3, 5, 7, 14, and 28 days after-operation. Control rats underwent a sham operation and were sacrificed at day 28. Histopathological and immunohistochemical analyses and in situ hybridization in the kidneys were performed. Dilated/atrophic TECs were collected by laser microdissection, subjected to microarray analysis, and subsequently underwent gene ontology and pathway analyses.
In the I/R group, dilated TECs were observed from day 3, and interstitial fibrosis with dilated and atrophic TECs developed after day 14. These TECs were positive for CD44 immunostaining. Gene ontology analysis revealed activation of extracellular matrix (ECM)-related genes and suppression of transporter- and metabolism-related genes in these TECs. Immunohistochemistry showed decreased expression of aquaporin-1, a proximal tubule marker, and increased expression of vimentin, a mesenchymal marker, in CD44-positive TECs, while their basement membranes remained intact. Pathway analysis of microarray data identified CD44 as an upstream regulator of fibrosis-related genes, including Fn1, which encodes the ECM protein fibronectin. In situ hybridization demonstrated upregulation of Fn1 mRNA in the cytoplasm of dilated/atrophic TECs, whereas immunohistochemistry showed fibronectin protein deposition in the surrounding stroma of these cells.
CD44 expression in the TECs preceded the development of fibrosis, indicating its potential as a marker for the AKI to CKD transition. CD44-positive TECs exhibited decreased expression of epithelial markers and increased expression of mesenchymal markers, along with evidence of fibronectin production, suggesting that they undergo partial epithelial–mesenchymal transition (pEMT). Together with pathway analysis results, these findings implicate that CD44 may contribute to the AKI to CKD transition by promoting ECM secretion in FR-TECs undergoing pEMT.
