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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
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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.
Apolipoprotein L1 (APOL1) was identified as a component of trypanosome lytic factors present in human plasma. With regard to kidney disease, APOL1 has one low-risk variant, termed APOL1-G0, and two high-risk variants, termed APOL1-G1 and -G2. Human populations with high-risk variants have a higher risk of developing progressive kidney disease, termed APOL1 nephropathy. Although glomerular damage is the main pathologic finding, progressive tubular injury is also common. The underlying mechanism of tubular injury in APOL1 nephropathy remains poorly understood.
Using BAC/APOL1 transgenic mice, we established an IV interferon-g model which activates expression of human APOL1 gene. We previously reported that BAC/APOL1-G1 mice develop more albuminuria than APOL1-G0 mice at 24 hours after the administration of interferon-g IV. Here we performed multi-omics analysis of kidneys and urine, including metabolomics analysis, and also bulk RNA-seq analysis of BAC/APOL1-G0 and -G1 mice 24 hours after the intravenous administration of interferon-g. In order to evaluate the effect of a candidate metabolite found in the multi-omics analysis. Human renal proximal tubular epithelial cells (HK-2 cells) were used to evaluate the effect in vitro. We reanalyzed the single-cell RNA-seq data sets publicly available at KPMP.org to confirm these findings.
Metabolomics analysis showed that glyceric acid levels were higher in kidneys and urine of BAC/APOL1-G1 mice after the administration of interferon-g, compared with APOL1-G0 mice. Bulk RNA sequencing revealed that the gene GLYCTK, encoding glycerate kinase, which catabolizes glyceric acid, was downregulated in BAC/APOL1-G1 mouse kidneys. The knock-down of GLYCTK lowered the viability of HK-2 cells, accompanied by a decrease of downstream metabolites. Further, supplementing glyceric acid accelerated the damage of HK-2 cells with GLYCTK knockdown, whereas glyceric acid did not change viability of HK-2 cells without GLYCTK knockdown. Single-cell RNA-seq dataset from KPMP showed that GLYCTK expression in the proximal tubule cells, but not in glomerular endothelial cells or in podocytes, were downregulated both in acute kidney injury samples and in chronic kidney disease samples, compared with healthy control samples.
These in vivo and in vitro experiments demonstrate upregulated glyceric acid and reduced expression of GLYCTK, suggesting metabolic alterations in proximal tubules in the setting of APOL1 nephropathy. Ongoing experiments will determine the diagnostic potential of this pathway in APOL1 nephropathy and whether it might be a therapeutic target.
