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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.
Pyroptosis, a form of programmed inflammatory cell death mediated by caspase activation and gasdermin D (GSDMD) pore formation, has been implicated in acute kidney injury and various renal pathologies such as diabetic nephropathy and renal fibrosis. However, whether inhibition of this signaling would be beneficial in chronic kidney disease (CKD) remains unknown. Disulfiram, a clinically approved drug for alcohol dependence, has recently been identified as a potent inhibitor of GSDMD. Herein, this study aimed to investigate the therapeutic potential of disulfiram as a novel nephroprotective agent in CKD.
Experiment1: Eight-week-old male C57BL/6JJc mice were divided into four groups: (1) control diet, (2) disulfiram (0.1% diet), (3) 0.25% adenine diet, and (4) 0.25% adenine + disulfiram diet (0.1% diet). After 14 days of feeding, kidneys, blood, and urine were collected. Histological evaluation was performed with hematoxylin–eosin and Masson’s trichrome staining to assess tubular injury. Myeloperoxidase and CD68 positive cells, as makers of neutrophil and macrophage infiltration, were evaluated by immunohistochemistry. Quantitative PCR analyses were conducted to evaluate the expression of inflammasomes and pyroptosis-related genes and senescence-associated markers. Moreover, RNA-seq data from the kidney were subjected to enrichment analysis. Experiment 2: To investigate the potential of disulfiram to promote recovery after the onset of renal injury, mice received adenine for 2 weeks and were subsequently treated with disulfiram (0.1% diet) for 4 weeks before sample collection.
In Experiment 1, elevated BUN levels and tubular injury scores in adenine-treated mice were reduced by disulfiram. Immunohistochemistry demonstrated attenuation of neutrophil and macrophage infiltration in the kidney. In addition, disulfiram downregulated gene expression of inflammasomes and pyroptosis-related markers (Nlrp3, Gsdmd, Il1b, and Tnf) and senescence-related genes (p16 and p21) in the adenine-treated mice. Furthermore, RNA-seq–based enrichment analysis revealed that disulfiram administration upregulated pathways related to fatty acid oxidation and downregulated the neutrophil extracellular traps pathway.
In Experiment 2, disulfiram treatment after the induction of adenine-induced renal injury did not improve histological damage or the expression of pyroptosis- and proinflammatory cytokine–related genes in the kidney.
Disulfiram ameliorated the innate immune response and renal senescence in this model. This drug represents a novel therapeutic approach for CKD and may be particularly beneficial for preventing disease onset and early progression.
