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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.
Due to global warming and heat waves, heat-related illness (HRI) is now a major health concern. HRI can induce multiple organ failure, including acute kidney injury (AKI). In addition, recent studies have warranted that HRI-induced AKI could progress to chronic kidney disease (CKD) termed heat stress nephropathy (HSN). We previously reported that urinary liver fatty acid-binding protein (L-FABP) elevated in patients with severe HRI and HRI-induced AKI. Moreover, elevation in core temperature during exercise was associated with appearance of L-FABP in urine. Although our data showed that urinary L-FABP was a candidate biomarker for early detection of HRI and HRI-induced AKI, it is still unclear why urinary L-FABP elevate in these patients. Therefore, in this study, we used a mouse heat stress model to elucidate the mechanism underlying the increase in urinary L-FABP in heat-induced renal injury.
Since L-FABP gene expression is strongly suppressed in mouse tubular cells, we used human L-FABP (hL-FABP) chromosomal transgenic (Tg) mice (Patent Number: WO0073791). Male hL-FABP Tg mice (8 weeks old) were exposed to heat stress for 40 min (40°C and 40% relative humidity) without food and water. Mice were euthanized before heat exposure, on day 0 (2h after heat exposure) and day 1 (n=6, each) for collecting kidney and blood samples. Kidney and liver injury, urinary L-FABP level, and tubular L-FABP expression were assessed. Mitochondrial reactive oxygen species (ROS) production and fatty acid oxidation (FAO) function in tubular cells were analyzed using flow cytometry. Furthermore, hL-FABP Tg mice were exposed to heat stress of varying intensities (20–40 min at 40°C, 40% relative humidity), and the correlation between reactive oxygen species (ROS) production, fatty acid oxidation (FAO), and L-FABP expression in tubular cells after heat stress was investigated (day 0; n=10, day 1; n=17).
The levels of serum creatinine were significantly higher on day 1 than before heat stress. Urinary L-FABP levels and tubular L-FABP expression were significantly higher on day 0 than before stress and on day 1. Mitochondrial ROS production in tubular cell was significantly higher on day 0 than before stress and on day 1. FAO in tubular cell was impaired after heat stress. On day 0, L-FABP expression in tubular cell showed a positive correlation with ROS production level (r=0.69, p=0.03), but a negative correlation trend with FAO function (r=-0.63, p=0.05). In contrast, on day 1, L-FABP expression in tubular cell was positively correlated with FAO function (r=0.51, p=0.04).
Heat stress impairs the mitochondria tubular cells, inducing increased ROS production and FAO dysfunction. The expression of L-FABP, reported to act as a ROS scavenger, is enhanced in response to ROS production in an acute phase after heat stress. Conversely, in the sub-acute phase, L-FABP expression seems to be enhanced by recovery of FAO function because L-FABP is a transporter of fatty acid in tubular cells. These results suggest that urinary L-FABP reflects heat-induced mitochondrial impairment in tubular cells and may serve as a useful early biomarker for HRI and HRI-induced AKI.
