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.
Heterogeneity in the immune mediated mechanisms underlying the pathogenesis of focal segmental glomerulosclerosis (FSGS) or minimal change disease (MCD) poses challenges to identifying therapeutic targets. To address this heterogeneity and potentially advance precision medicine approaches in FSGS/MCD, we identified for further study 3 investigational agents, targeting distinct immune pathways associated with FSGS/MCD: Bruton's tyrosine kinase (BTK), CD40 ligand (CD40L), OX40 ligand (tumor necrosis factor superfamily member 4 (TNSF4)), and tumor necrosis factor α (TNFα). The Nephrotic Syndrome Study Network (NEPTUNE) is a multi-year, multi-site prospective observational collaborative study that enrolls patients with biopsy-confirmed primary FSGS, MCD, and membranous nephropathy (MN), integrating longitudinal clinical data with molecular and histologic profiles from kidney tissue, blood, and urine. In this study, we aimed to investigate the correlation of BTK, CD40L, TNSF4, and TNF gene expression levels in kidney tissue of primary FSGS and MCD patients from the NEPTUNE registry with long term kidney outcomes in an effort to strengthen the scientific rationale for their selection as therapeutic targets.
Research biopsy cores from 220 patients with biopsy-proven MCD or FSGS and baseline urine protein to creatinine ratio (UPCR) ≥ 1.5 g/g, were stored in RNAlater. Glomerular and tubulointerstitial compartments were micro-dissected, RNA isolated, and RNA-sequenced. Proteinuria and serum creatinine were measured per NEPTUNE protocols. Median follow-up was 1356 days. Cox proportional hazard (PH) analysis was used to assess the risk of progression based on expression levels of BTK, CD40L, TNF, and TNFSF4. Complete remission was defined as urine protein-to-creatinine ratio < 0.3 g/g.
In Primary FSGS and MCD patients in the NEPTUNE cohort, patients with higher BTK, CD40L, TNF, or TNFSF4 transcript levels had significantly lower likelihoods of achieving complete remission, and higher likelihoods of progressing to the composite endpoint of ESKD or 40% eGFR loss compared to those with lower transcript levels.
This correlation between gene expression and long-term kidney outcomes supports the pathogenic role of these pathways. The therapeutic potential of inhibiting each these pathways is being assessed in the Phase 2a RESULT umbrella trial in primary FSGS and MCD (NCT06500702).
