#6315 CHARACTERIZATION OF BRAIN DAMAGE AFTER ACUTE KIDNEY INJURY

Abstract Background and Aims Acute kidney injury (AKI) is a very common condition in inpatients. Severe AKI frequently associated with by neurological disorders such as confusion, the mechanisms of which are poorly understood. We have shown several animal models that chronic disease impaired cognitive performance memory increased permeability blood-brain barrier (BBB), related to accumulation uremic toxin indoxyl sulfate. The goal these experiments was highlight influence on cerebral impairment mice, particularly BBB permeability, describe involved. Method performed an C57/Bl6 WT unilateral nephrectomy transient ischemia-reperfusion remaining for 20 minutes (RIRI20 group) compared them two other groups: control mice without (IR20). Modified severity score (mNSS) daily. assessed quantification Evans Blue leakage brain 68Ga-DTPA TEP/CT imaging. Cerebral immuno-histochemistry evaluate neuro-inflammatory processes. Results Glomerular filtration rate at Day 1 lower group 0.21 ± 0.26 vs. 0.94 0.13 mL/min/100g b.w (p<0.0001) IR group: 0.75 0.17 (p = 0.0007). Mice displayed day 2 post-AKI, IR20 mainly balance. Mean mNSS 2.6 4.5 group, 0.0 ±-0.0 both groups 0.002). higher than 0.10) 0.0006) blue staining. TEP imaging found similar results D1 D2 0.004 p 0.009, respectively). On immunohistochemistry, brains after more astrocytosis microglial activation mice. Conclusion specifically early damage, unlike renal alone, disruption first days AKI. appears induce altered phenotype, potentially due neuroinflammatory processes following disruption.