Back
For best output, select "Paper Size" as "A4" and "Margin" as "0" or "None".
To save or print to PDF, please select Print Destination > Save as PDF, enable Background Graphics under "More Settings", then click "Save".
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.
Remission of proteinuria in focal segmental glomerulosclerosis (FSGS) and minimal change disease (MCD) is closely linked to disease progression. However, the metabolic mechanisms underlying FSGS/MCD remain largely unknown, and predicting treatment response remains challenging. Acylcarnitines (ACs) are key intermediates in energy metabolism, facilitating the transport of fatty acids into mitochondria for β-oxidation. In kidney diseases, mitochondrial dysfunction and impaired fatty acid oxidation contribute to disease pathophysiology and are associated with dysregulated acylcarnitine profiles. We hypothesized that ACs could serve as predictive biomarkers of treatment response in FSGS/MCD.
A total of 97 participants with FSGS or MCD were included from the Nephrotic Syndrome Study Network (NEPTUNE) cohort. We analyzed 96 plasma and 96 urine samples collected within 45 days of kidney biopsy. Untargeted metabolomics using liquid chromatography–mass spectrometry (LC–MS) identified 21 ACs in plasma and 25 in urine. Associations between ACs and time to complete remission of proteinuria (CR, UPCR < 0.3) were evaluated using univariate, unadjusted Cox proportional hazards models, and multivariable Cox models adjusted for baseline covariates (eGFR, log-transformed UPCR, and immunosuppressive use). Prediction models for time to CR were constructed using a Cox elastic net algorithm with repeated cross-validation (CV). Across 20 iterations, ACs were ranked by selection frequency and mean absolute coefficient values. After removing highly correlated features, prediction models were developed using the clinical covariates above combined with the top n metabolites. Model performance was assessed using 100 repeated 5-fold CVs, and the combination of metabolites with the highest concordance index (C-index) was selected.
Among the 97 participants, 60.3% had FSGS, 64.0% were adults, and 63.2% were male. Over a median follow-up of 51.0 months, 49.5% achieved CR. Metabolomics data included 21 plasma and 25 urine ACs with diverse chain lengths, degrees of saturation, and subclasses (Figure 1). Several ACs consistently showed significant associations (p < 0.05) with CR in both plasma and urine. Models incorporating ACs markedly improved prediction of CR compared with models using only clinical covariates. The optimal models identified eight ACs with the strongest predictive value for CR in plasma—CAR(DC(10:0)), CAR(22:4(OH)), CAR(DC9:0), CAR(DC9:1), CAR(12:1(OH)), CAR(17:2), and CAR(14:2(3,5))—and eight in urine—CAR(10:2), CAR(21:4(OH)), CAR(DC5:1), CAR(7:0(OH)), CAR(19:2), CAR(DC11:2), CAR(14:2(3,5)), and CAR(17:2) (Figure 2).
Models incorporating ACs significantly improved prediction of proteinuria remission in FSGS/MCD, suggesting that ACs represent promising biomarkers for treatment response. Further mechanistic studies on AC metabolism in the kidney may provide deeper insights into disease mechanisms and potential therapeutic targets for FSGS/MCD.
