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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.
Autosomal recessive polycystic kidney disease (ARPKD) is caused by mutations in the PKHD1 gene, leading to dilated collecting ducts. In PCK rats, a well-established ARPKD model, salt-related factors are known to influence the progression of collecting duct cysts. To investigate this relationship, we generated a novel ARPKD model with salt-sensitive hypertension by introducing a mutant Pkhd1 allele from PCK rats into Dahl/salt-sensitive (SS) rats. Under normal salt conditions, SS-PCK rats exhibited higher blood pressure and renal lesions than SS rats. However, unlike PCK rats, SS-PCK rats displayed markedly reduced medullary cyst formation with smaller cyst size. Therefore, this study aimed to identify factors that suppress medullary cyst development in SS-PCK rats under conditions that exacerbate medullary cystogenesis in PCK rats.
SS-PCK rats were established by introducing the Pkhd1 gene from PCK rats through crossbreeding with SS rats for five generations at the Medical College of Wisconsin. SS rats were also procured from the same institution. Both strains were subsequently bred and maintained at Fujita Health University. Sprague–Dawley (SD) rats (control), and PCK rats were obtained from The Jackson Laboratories Japan, Inc. Male rats from all four strains were fed a standard chow diet (MF: Oriental Yeast Co. Ltd.). Furthermore, SS-PCK rats were subjected to either high salt loading, or treated with desmopressin, a synthetic vasopressin analog.
SS-PCK rats fed a standard salt diet exhibited significantly elevated blood pressure and serum creatinine levels. Histologically, the kidneys showed cyst formation and glomerular lesions predominantly in the cortex, differing from PCK rats, which developed cysts mainly in the medulla. High-salt feeding (4% NaCl for 5 weeks from 5 weeks of age) further increased blood pressure and renal injury in SS-PCK rats but did not enhance medullary cyst formation. In contrast, desmopressin administration (10 ng/hour/100 g body weight via osmotic pump from 5 to 11 weeks of age) increased kidney-to-body weight ratio and cell proliferation in medullary collecting ducts.
These findings suggest that a salt-sensitive genetic background strongly suppresses medullary cyst progression of ARPKD in SS-PCK rats. We plan to further explore this mechanism by inhibiting epithelial sodium channel (ENaC) activity, which was upregulated in the collecting ducts of SS-PCK rats. Given that ENaC activation has been implicated in medullary cyst formation in PCK rats, this approach may provide key insights into the mechanisms underlying cyst suppression in SS-PCK rats.
