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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.
Lupus nephritis (LN) is a severe complication of systemic lupus erythematosus and a major cause of chronic kidney disease (CKD). Despite advances with immunosuppressive therapy, many patients continue to develop progressive renal impairment. Glucagon-like peptide-1 receptor agonists (GLP-1RAs), approved for diabetes and CKD, have shown renoprotective effects, but their potential in LN remains undefined.
We evaluated the renoprotective effects of liraglutide in lupus-prone MRL/lpr mice using functional, histopathological, and molecular analyses integrated with single-nucleus transcriptomics. Mechanistic studies involved ferroptosis inhibition and pharmacological blockade of cAMP signaling. To provide translational perspective, a patient with class III+V LN who initiated semaglutide during immunosuppressant tapering was included.
In lupus-prone MRL/lpr mice, liraglutide reduced proteinuria, improved renal function, and ameliorated histopathological injury without altering systemic autoantibody levels. Single-nucleus transcriptomics revealed cell type–specific remodeling, including suppression of inflammatory and metabolic pathways in podocytes, mesangial, and tubular cells, alongside signatures of tubular repair. Liraglutide treatment was associated with reduced immune infiltration, NF-κB and NLRP3 signaling, fibrosis, oxidative stress, and ferroptosis, as well as enhanced autophagy. Mechanistically, liraglutide activated cAMP signaling; ferroptosis inhibition recapitulated, whereas cAMP blockade abrogated, its protective effects on renal function, inflammation, oxidative stress, and ferroptosis. Clinically, semaglutide initiation was temporally associated with sustained proteinuria reduction during immunosuppressant tapering in one patient.
GLP-1RAs improved renal outcomes in lupus-prone mice through antioxidant, anti-inflammatory, and anti-ferroptotic effects, independent of direct immunosuppression. These findings suggest GLP-1RAs as potential adjunctive candidates for LN and warrant evaluation in prospective clinical studies.
