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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.
Renal ischemia-reperfusion (IR) injury is one of the major causes of ischemic acute kidney injury (AKI). Pathobiological mechanisms of the renal IR injury include hypoxia, oxidative stress, endoplasmic reticulum (ER) stress, and fibrosis. However, it has been unclear when these pathobiological changes occur following renal IR injury. This ambiguity hampers timely drug therapy against ischemic AKI. In this study, we aim to make clear the pathobiological mechanisms of renal IR using a rat model.
Male Sprague Dawley rats were subjected to a bilateral renal IR for 30min followed by 2 hrs, 6 hrs, 24 hrs, 3 d, or 7 d of reperfusion. Urine samples were collected for 6 hrs from all samples except for 2 hrs of reperfusion. Biochemical analyses were performed with blood and urine samples. Renal mRNA levels were evaluated using real-time PCR and RNA-seq analysis techniques.
Plasma creatinine level was elevated significantly at 24 hrs to 7 d post-IR compared to that in sham-operated rats. Increased urine output and decreased urine osmolality were observed at 24 hrs to 7 d after IR. mRNA expression level of a hypoxia marker, Glut1 (a downstream gene of Hif), was increased at 2 and 24 hrs after IR. Nqo1, an oxidative stress marker (a downstream gene of Nrf2), mRNA level peaked at 24 hrs post-IR. Grp78 mRNA, an ER stress marker, was increased only at 6 hrs post-IR. TGFb mRNA, a fibrosis marker, was gradually increased over 6 hrs to 7 d. In relation to increased urinary solutes excretions in ischemic AKI, Slc6a19 (a neutral amino acid transporter), Slc34a1 (phosphate transporter), and Sglt2 (glucose transporter) mRNAs were significantly decreased at 24 hrs post-IR. Furthermore, results from RNA seq analyses supported the above-mentioned results.
These results indicate that hypoxic response (~ 24 hrs), ER stress response (~6 hrs), and oxidative stress response (~24 hrs) occur in the early phase of renal IR. Given that decreases in amino acid, glucose, and phosphate transporters 24 hrs after renal IR, the mechanisms underlying reductions of these transporters include hypoxia, oxidative stress, ER stress, or their combination. This study may contribute to the development of an appropriate drug therapy against AKI.
