{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,4]],"date-time":"2026-11-04T12:28:54Z","timestamp":1793795334984,"version":"4.6.1"},"reference-count":50,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"11","content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2026,11]]},"abstract":"<jats:sec>\n                    <jats:title>OBJECTIVES:<\/jats:title>\n                    <jats:p>Acute kidney injury (AKI) is associated with central neurologic complications, notably in critical care, the mechanisms of which are poorly understood. Blood-brain barrier (BBB) disruption is a central mechanism associated with cognitive impairment in chronic kidney disease. The objectives of this study were to characterize the influence of AKI on brain alteration and BBB permeability in a preclinical model.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>DESIGN:<\/jats:title>\n                    <jats:p>We performed a mouse model of unilateral renal ischemia-reperfusion injury without or with AKI (obtained by removing the contralateral kidney before ischemia).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Subjects:<\/jats:title>\n                    <jats:p>All animals were 7-week-old male C57Bl\/6J mice, randomly assigned to groups: AKI, kidney ischemia-reperfusion alone, or control.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>INTERVENTIONS:<\/jats:title>\n                    <jats:p>\n                      We assessed neurologic impairment using the modified neurologic severity score and motricity evaluations, quantified BBB disruption by cerebral extravasation of Evans blue and positron emission tomography (PET)\/CT imaging with Gallium-68 diethylenetriaminepentaacetic acid (\n                      <jats:sup>68<\/jats:sup>\n                      Ga-DTPA), and performed immunohistochemistry and electron microscopy on brain sections.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>MEASUREMENTS AND MAIN RESULTS:<\/jats:title>\n                    <jats:p>\n                      In mice with AKI, we found neurologic impairment, decreased spontaneous motricity, and cerebral extravasation of Evans blue, which were not observed in mice with renal ischemia-reperfusion without nephrectomy. Cerebral\n                      <jats:sup>68<\/jats:sup>\n                      Ga-DTPA PET\/CT imaging with imaging confirmed the BBB disruption. In addition, we observed more extracellular vesicles in cerebral endothelial cells by electron microscopy in AKI mice compared with controls.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>CONCLUSIONS:<\/jats:title>\n                    <jats:p>AKI-induced neurologic complications are associated with an early increase in BBB permeability and transcytosis of extracellular vesicles in cerebral endothelium.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1097\/ccm.0000000000007285","type":"journal-article","created":{"date-parts":[[2026,8,6]],"date-time":"2026-08-06T17:44:53Z","timestamp":1786038293000},"page":"2984-2994","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":1,"title":["Acute Kidney Injury Induces Neurological Impairment Through Early Blood-Brain Barrier Disruption and Endothelial Transcytosis in 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