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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.
Hepatorenal syndrome (HRS) is a serious form of acute kidney injury (AKI) in cirrhosis. Vasoconstrictor (VC) therapy is the cornerstone of its pharmacological treatment. However, here are no optimal biomarkers to predict therapeutic response (TR) to VC therapy in HRS-AKI. We hypothesized that utilizing fractional excretion of urinary sodium (FENa) (as functional biomarker) and/or evidence of acute tubular insult (ATI) by urinary sediment microscopy (uSEDI) (as injury biomarker) may allow predicting TR to VC in HRS-AKI.
In a prospective observational cohort of AKI in cirrhosis, we searched for patients who met criteria for HRS and: 1) had a FENa < 1%, 2) did not have ≥ 6 “muddy brown” granular casts (MBGC) per low power field (lpf) by uSEDI [deemed overt ATI)], 3) were treated with a VC [midodrine/octreotide (M/O), norepinephrine (NE) or terlipressin (T)], and 4) achieved ≥ 5 mmHg rise in mean arterial pressure (MAP); over a 7.5-year period. ATI score by uSEDI was classified as: 0: bland or hyaline casts (HyC); 1: HyC >> MBGC or MBGC 0-1/lpf; 2: MBGC 2-5/lpf and ≥ HyC. Renal tubular epithelial cell casts (RTECC) were also recorded. TR to VC was defined as ≥ 30% reduction in serum creatinine (sCr) within 7 days without need for dialysis by day 14. Area under the receiver-operator curve (AUROC) for FENa and uSEDI as predictors of TR were estimated.
A total of 84 patients with HRS treated with a VC (60 NE, 20 T, 4 M/O) were included (39% women, mean age 54, sCr 3.8 mg/dL, MELD 32). Median MAP rise was 14 mmHg (5-25). TR was achieved by 40 (48%). TR was proportional to MAP rise (p=0.0003) and inversely proportional to sCr (p=0.0056). Median FENa was 0.18% (0.07-0.63). FENa AUROC for TR was 0.74 (cutoff 0.20%, p=0.003). uSEDI score 0 (n=46) was associated with -38% fall in sCr vs -2% for those with score 2 (n=19) (p=0.002). uSEDI AUROC for TR was 0.68 (p=0.007). RTECC were not discriminatory (p=0.98). Combining FENa and uSEDI led to an improved AUROC for TR of 0.80 (p<0.001). When restricting the analysis to MAP rise ≥ 15 mmHg (n=37), the AUROC for combining FENa and uSEDI ATI score to predict TR improved to 0.91 (p=0.006).
The combination of very low FENa (< 0.20%), absence of overt ATI by uSEDI, and sustained rise in MAP leads to high probability of TR to VC in HRS-AKI. Utilizing FENa value and uSEDI findings may facilitate proper patient selection for the use of VC in HRS-AKI.
