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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.
Acute kidney injury (AKI) is a common but highly mortal comorbidity in the intensive care unit; therefore, urinary biomarkers for the early diagnosis and severity prediction of AKI have been well investigated and have established their clinical utility. On the other hand, prognostic markers after AKI have been underinvestigated, and there is essentially no biomarkers so far to predict long-term prognosis after AKI. Although we have previously reported that urinary NGAL could be a potential prognostic marker to predict major adverse kidney events after dialysis requiring AKI, we hypothesized that urinary lipids could be potential biomarkers to predict the long-term prognosis of kidney function.
73 subjects with AKI diagnosis who underwent continuous renal replacement therapy (CRRT) were enrolled in the University of Tokyo Hospital. Long-term renal prognostic endpoint, major adverse kidney events (MAKEs) at 90 days were defined as eGFR decline of more than 25% compared with baseline, RRT dependence, or death within 90 days after CRRT initiation. Urine samples collected at the time of CRRT initiation and discontinuation were analyzed. Urine lipidomic analysis were conducted by LC-MS/MS to quantify lysophospholipids (glycerolysophospholipids such as lysophosphatidic acids and lysophosphatidylcholine) and eicosanoids and related mediators (eicosanoids such as PGE2, PGA, and PGI and their metabolites and omega-3 fatty acid metabolites such as resolvins). The utility of measured lipids as predicting marker for MAKEs were evaluated.
73 subjects were divided to MAKEs group (26 subjects) and non-MAKEs group (47 subjects). 104 lysophospholipids and 214 eicosanoids were detected in the urine samples. 18:2 Lysophophatidyl glycerol (LPG) was significantly higher in MAKEs group compared to non-MAKEs group (9238 ± 213.30 nmol/gCr vs 17.54 ± 74.77, p = 0.0086). Tetranor-prostaglandin A metabolite (tetranor-PGAM) was also significantly higher in MAKEs group (31.6 ± 42.5 µg/gCr vs 125.2 ± 164.5, p = 0.0008). ROC analysis showed that AUCROC of 18:2 LPG and tetranol-PGAM were 0.62 [0.47-0.76] and 0.70 [0.57-0.84], respectively.
Novel lipid biomarkers, LPG and tetranol-PGAM could be potential renal prognostic markers for post-AKI patients. Further studies with larger sample size will be warranted to establish the utility of these with external validity.
