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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.
In acute ischemic stroke (AIS)—particularly among patients admitted to intensive care—the risk of acute kidney injury (AKI) is high. Although blood pressure variability (BPV) has been associated with adverse outcomes and independently predicts incident AKI in general populations, evidence directly relating acute‑phase BPV to AKI after cerebral infarction remains limited.
We analyzed 2,415 hospitalized AIS patients. Exposures were Variation Independent of the Mean (VIM)‑based BPV for diastolic (DBP) and systolic (SBP) blood pressure. Outcomes were in‑hospital AKI (KDIGO 1–3) and severe AKI (KDIGO 2–3). We prespecified four multiple logistic regression models: Model 1 (BPV only), Model 2 (+ age, sex, baseline kidney function as CKD grade, mean BP), Model 3 (+ heart failure, diabetes, hypertension), and Model 4 (+ NIHSS).
Incidence was 2.9% (70/2,415) for any AKI and 1.37% (33/2,415) for AKI 2–3. Across DBP‑VIM quartiles, AKI rates increased from 1.3% to 4.6% for any AKI (p=0.005) and from 0.5% to 2.5% for AKI 2–3 (p=0.027); higher NIHSS categories were also more frequent with higher DBP‑VIM (p<0.001). After multivariable adjustment, DBP VIM remained associated with severe AKI even after NIHSS (Model 4 OR 1.308; 95% CI 1.003–1.707; p=0.048). In contrast, its association with any AKI was attenuated (OR 1.109; p=0.313), and SBP VIM was not significant for either outcome in Model 4 (AKI p=0.263; AKI 2–3 p=0.674).
In AIS, diastolic BP variability (DBP VIM) shows a residual association with severe AKI after adjustment for clinical severity (NIHSS), whereas its association with any AKI appears largely explained by severity. Systolic BP variability was not independently associated with AKI after full adjustment.
