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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.
Congenital nephrogenic diabetes insipidus (CNDI) is a hereditary disorder characterized by impaired renal response to arginine vasopressin (AVP), leading to defective urinary concentration and excessive excretion of dilute urine. Approximately 90% of CNDI cases are caused by mutations in the AVPR2 gene, which encodes the vasopressin V₂ receptor. Because Avpr2 knockout mice die within a few days after birth, conditional Avpr2 knockout mice and AVP-deficient Brattleboro rats have been used to study AVP signaling. Recent advances in genome editing have facilitated the generation of genetically modified rats. We previously created Avpr2 knockout rats, which survived long-term and exhibited a severe CNDI-like symptoms. In this study, we aimed to generate rat models carrying human AVPR2 mutations to establish physiologically relevant models of CNDI.
Two human AVPR2 mutations, D85N and S333del, were introduced into Sprague–Dawley rats using the rat Genome-editing via Oviductal Nucleic Acids Delivery (rGONAD) method, an in vivo clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR-associated protein 9 (Cas9)-based genome-editing technique. Phenotypes of wild-type and mutant rats was characterized at 8 weeks of age, including assessment of body weight, urine data, response to hydrochlorothiazide (HCTZ), and renal morphology.
Both D85N and S333del mutant rats were viable after weaning and could be maintained long-term, similar to Avpr2 knockout rats. Administration of HCTZ reduced urine output and increased urinary osmolarity in both mutant strains. D85N mutant rats showed increased urine volume compared with wild-type rats, but only about half that observed in Avpr2 knockout rats. Unlike knockout rats, D85N mutants did not display decreased body weight or thinning of the renal medulla. In contrast, S333del mutant rats exhibited severe polyuria, reduced body weight, and renal medullary thinning comparable to Avpr2 knockout rats.
The Avpr2 D85N mutant rat exhibited a stable and moderately severe CNDI phenotype without lethal complications, suggesting that it serves as a physiologically relevant model for human CNDI. These gene-edited rat models could be a valuable tool for elucidating the molecular mechanisms and for developing therapeutic strategies for AVPR2-related disorders.
