These results demonstrate that treatment with OCT has a renoprotective effect in ischemic AKI, possibly by suppressing cell loss. Changes in the expression of IFN-g and NHE-1 could partially link OCT to the cell survival-promoted effects.
BACKGROUND: Acute kidney injury (AKI) is a common complication of sepsis, with the burden of long hospital admission. Early prediction of AKI is the most effective strategy for intervention and improvement of the outcomes. OBJECTIVE: In our study, we aimed to investigate the predictive performance of the combined model using ultrasound indices (grayscale and Doppler indieces), endothelium injury (E-selectin, VCAM-1, ICAM1, Angiopoietin 2, syndecan, and eNOS) as well as inflammatory biomarkers (TNF-α, and IL-1β) to identify AKI. METHODS: Sixty albino rats were divided into control and lipopolysaccharide (LPS) groups. Renal ultrasound, biochemical and immunohistological variables were recorded 6 hrs, 24 hrs, and 48 hrs after AKI. RESULTS: Endothelium injury and inflammatory markers were found to be significantly increased early after AKI, and correlated significantly with kidney size reduction and renal resistance indices elevation. CONCLUSIONS: Using area under the curve (AUC), the combined model was analyzed based on ultrasound and biochemical variables and provided the highest predictive value for renal injury.
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