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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.
Polycystic kidney disease (PKD) is the most common form of inherited kidney disease and leads to a build-up of fluid-filled cysts. Progression of PKD can lead to complete kidney failure and the only treatment options for patients are dialysis or kidney transplantation. Patients with PKD have a 2-fild higher risk of developing cognitive impairment and dementia. Dementia is the second leading cause of death in Australia and a risk factor for cardiovascular disease. Currently, there are no disease modifying drugs available for dementia as the underlying causes are unclear. The pathogenesis of cognitive impairment in PKD is unknown, however periperial inflammation and vascular changes have been suggested to play a role. Therefore, the hypothesis of this study is to establish the first rat model of PKD-induced cognitive impairment and elucidate potential mechanisms that can contribute to the development of cognitive impairment.
Male and female Lewis wild-type (WT) and Lewis polycystic kidney (LPK) rats were studied at 6, 12 and 18 weeks of age. Blood pressure was measured by tail cuff. Cognition was assessed using the novel object recognition and Y-maze tests. Aortic thickening was assessed using histology. Inflammation was measured using flow cytometry.
LPKs had higher blood pressure compared to WT from 6 weeks (178±1 mmHg vs 132±1 mmHg, n=10, P<0.05) which was maintained at 12 and 18 weeks. LPK rats had heavier kidneys (P<0.001), hearts (P<0.05) and impaired kidney function (P<0.001). The thickness of the abdominal aortic wall increased in LPKs compared to WT from 6 weeks (0.36±0.01 mM vs 0.32±0.005 mM, n=9-10, P<0.05) to 18 weeks (0.64±0.06 mM vs 0.35±0.03 mM, n=6-7, P<0.05). Compared to WT, kidney T cells and macrophages were increased in LPKs at 6 weeks by 1.5-fold, and 12 weeks by 2.3- and 1.9- fold respectively (n=8-10, P<0.05). At 18 weeks, kidney T cells were similar between LPKs and WT while LPK kidney macrophages were reduced by 4-fold (n=8-10, P<0.05). LPK rats had intact recognition memory but spatial working memory was impaired at 12 and 18 weeks of age (n=9-10, P<0.05).
Cognitive impairment was observed in a rat model of PKD from 12 weeks of age after the onset of hypertension, aortic thickening and kidney inflammation. Aortic thickening is a marker of aortic stiffening which can promote cognitive impairment in other disease settings. The hypertension, aortic thickening and kidney inflammation may have contributed to the development of the cognitive impairment in this rat model of PKD.
