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.
Lupus nephritis (LN) is a major cause of morbidity in systemic lupus erythematosus (SLE), and relapse accelerates chronic kidney disease (CKD) progression. Conventional markers such as complement and anti-dsDNA antibodies often fail to predict flares. Epstein–Barr virus (EBV), which establishes lifelong latency in B cells, has been implicated in SLE pathogenesis and may trigger reactivation. The neutrophil-to-lymphocyte ratio (NLR) has been associated with SLE activity, but its prognostic value in LN remains unclear. This study aimed to identify relapse predictors focusing on baseline NLR, treatment pattern, histological class, and EBV-DNA elevation as a potential marker of viral reactivation.
We retrospectively analyzed 109 biopsy-confirmed LN patients treated between 2006 and 2024 at Kurashiki Central Hospital. Baseline characteristics were recorded, and 62 with complete data including NLR were evaluated for relapse risk. Patients with poor adherence were excluded. Relapse was defined as disease reactivation requiring intensified immunosuppression; renal relapse as recurrence of proteinuria ≥1 g/day, hematuria, or elevated creatinine. Comparisons used the Mann–Whitney U and Fisher’s exact tests. Relapse-free survival was assessed using Kaplan–Meier and Cox regression by NLR, treatment type (steroid monotherapy vs combination), and histology (class V vs others). EBV-DNA elevation was analyzed as an exploratory endpoint.
Among 109 patients, 62 were eligible for relapse analysis (53 female, 85.4%). The mean age at onset was 39.5±20.1 years. Over a median 5.6-year follow-up, 16 (25.8%) relapsed, including 8 renal relapses (12.9%). In multivariable Cox analysis, class V histology (HR 2.12, 95% CI 0.59–7.58), steroid monotherapy (HR 0.52, 95% CI 0.11–2.54), and NLR (HR 1.06, 95% CI 0.83–1.34) were not significant. The model concordance was 0.59, and assumptions were met (GLOBAL p = 0.153). Among the 24 patients tested for EBV-DNA (23 female), 4 were EBV-DNA positive. In this subgroup, 12 patients (50%) experienced relapse, including 7 with renal relapse and 6 with extra-renal relapse. Flare-free survival was shorter with EBV-DNA elevation (median 1,195 vs 5,966 days; p = 0.361), suggesting a possible link between viral reactivation and flare.
None of the factors independently predicted relapse. However, trends toward higher relapse risk with class V histology, steroid monotherapy, and EBV-DNA positivity may indicate biological relevance. The limited sample size, heterogeneous backgrounds, and temporal treatment changes likely reduced statistical power. Larger multicenter studies are needed to validate these findings and clarify the role of EBV reactivation and inflammatory markers in LN relapse. No independent predictors were confirmed, though class V histology, steroid monotherapy, and EBV-DNA positivity tended to increase relapse risk. Combining inflammatory and virological markers may improve individualized relapse prediction in lupus nephritis.
