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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 causes acute kidney injury and renal dysfunction following kidney transplantation and contributes to the development of chronic kidney disease. Renal ischemia-reperfusion also causes drastic changes in pH and ion concentrations. GPR30 is a newly identified bicarbonate-sensing G protein-coupled receptor and elicits cellular responses in a pH-independent manner. In the brain, GPR30 is highly expressed in pericytes and regulates blood flow recovery after ischemia-reperfusion. This study aims to clarify the involvement of GPR30 in the pathophysiology of renal ischemia-reperfusion.
To examine the expression of GPR30 in the kidney, in situ RNA hybridization analysis was performed. Male C57BL/6 mice were used to establish a unilateral nephrectomy and contralateral renal ischemia-reperfusion (I/R) injury model. The mice were sacrificed at 24 hours or 7 days after I/R. To evaluate renal dysfunction, blood urea nitrogen (BUN) was measured at 24 hours and/or 7 days after reperfusion. Histological analyses using Periodic acid-Schiff (PAS) staining determined proximal tubule injury classification: necrotic, injured, recovery, and healthy. Laser doppler flowmetry was used to measure renal blood flow during renal I/R.
In situ RNA hybridization analysis showed GPR30 was expressed in kidney vessels. BUN levels at 24 hours after renal I/R were lower in GPR30-deficient mice than those in control mice. GPR30-deficient mice presented even prominent recovery in kidney function at day 7. PAS staining demonstrated that control mice presented more necrotic or injured tubules than GPR30-deficient mice. The percentage of tubules in the recovery phase at day 1 was higher in GPR30-deficient mice than in control mice. At day 7, more tubules were in the healthy phase in GPR30-deficient mice than in in control mice. Laser doppler flowmetry revealed renal blood flow changes before and after I/R. In ischemia phase, renal blood flow was reduced immediately after clamping the renal pedicle. After reperfusion, renal blood flow recovered within ten minutes and stabilized.
(1) GPR30 was expressed in kidney vessels. (2) A unilateral nephrectomy and contralateral renal I/R model was established. (3) GPR30-deficient mice showed mild renal dysfunction. (4) Renal tubule injury was mild in GPR30-deficient mice. (5) Laser doppler flowmetry was able to measure renal blood flow changes in the I/R model.
There is no specific treatment for acute kidney injury so far. This study suggests that GPR30 is related to renal I/R injury and that GPR30 inhibition is a promising target for kidney injury and repair.
