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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.
Cholesterol crystal embolism (CCE) is a severe complication of atherosclerosis that triggers sterile inflammation and can cause immunothrombotic occlusions of renal arteries, often leading to acute kidney injury. No specific therapy exists for CCE, highlighting an unmet medical need. Kv1.3 is a voltage-gated potassium channel expressed in platelets and neutrophils that drives immune cell effector function. We hypothesized that genetic deletion of Kv1.3 attenuates the inflammatory and thrombotic responses to cholesterol crystals, thereby protecting against CCE and preserving renal function.
Kv1.3 knockout (Kv1.3 -/-) mice and wild type (WT) mice were subjected to a CCE model by direct injection of cholesterol crystals into the renal artery. We monitored 24-hour outcomes including glomerular filtration rate (GFR), histopathological injury (infarct size and obstruction of arteries by thrombi), and immune cell infiltration via flow cytometry.
Kv1.3 -/- mice were protected from CCE-induced renal injury compared to WT controls, showing a significantly smaller GFR decline, reduced infarct size, and fewer arterial occlusions. Pharmacological Kv1.3 inhibition reproduced, and even exceeded, the protection observed in knockout mice. Histological analysis revealed attenuated neutrophil infiltration in both Kv1.3 -/- and inhibitor-treated kidneys, contrasting with extensive immunothrombotic occlusion and neutrophil accumulation in WT mice. Together, these findings demonstrate that Kv1.3 activity coordinates immune cell recruitment and promotes vascular obstruction in response to cholesterol crystals.
Genetic and pharmacological Kv1.3 inhibition mitigate kidney injury from cholesterol crystal embolism by blunting the sterile inflammatory response. This is the first evidence that targeting an immune cell potassium channel can resolve crystal-induced immunothrombosis in the kidney. Our study identifies Kv1.3 as a promising therapeutic target in CCE, an area of critical need with no current treatments. Immune modulation through Kv1.3 blockade could offer a novel strategy to protect patients at risk of renal damage and improve kidney outcomes.
