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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.
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Abstract titles should be brief and reflect the content of the abstract.
Systemic lupus erythematosus (SLE) diagnosed at 50 years of age or older is generally defined as late-onset SLE (Medicine, 2004). This study reports a single-center cohort detailing the clinicopathological features and outcomes of patients with late-onset lupus nephritis (LN).
137 patients newly diagnosed with LN at Kitano Hospital between March 2001 and May 2023 were enrolled. Patients with onset age ≧ 50 years were classified as the late-onset group (L group, n=35), and age < 50 years as the early-onset group (E group, n=102). The late-onset matched group (L-M group, n=32) and early-onset matched group (E-M group, n=32) were extracted using propensity score matching based on past medical history (PMH) of hypertension, PMH of diabetes mellitus (DM), sex, estimated glomerular filtration rate (eGFR), and urinary protein-to-creatinine ratio (UPCR) to exclude the age-related comorbidities. Continuous variables were expressed as mean ± SD and categorical variables as percentages. Group differences were assessed using the Wilcoxon rank-sum test. Survival was analyzed using Kaplan–Meier curves and compared using the log-rank test. Hazard ratios were estimated using Cox proportional hazards models. A p-value <0.05 was considered statistically significant.
L group included older patients (62.7±9.4 vs 34.6±11.5 years, p<0.0001 ) and showed a tendency toward a lower proportion of females (88.6% vs 97.1%, p=0.07), a higher prevalence of hypertension(62.9% vs 30.4%, p<0.001) and DM (11.4% vs 2.9%, p<0.05), lower eGFR (66.0±26.6 vs 87.9±34.5 mL/min/1.73m², p<0.0005), higher UPCR (2.92 ± 4.46 g/gCr vs 2.18±3.46 g/gCr, p<0.05), and a lower frequency of hypocomplementemia (C3: 65.7% vs 83.3%, p<0.05; C4: 62.9% vs 81.4%, p<0.05; CH50: 37.1% vs 66.7%, p<0.005). NIH activity index was comparable (4.0±3.7 vs 3.3±3.0, p=0.55), but the chronicity index was higher in L group (3.2±1.0 vs 2.6±1.3, p<0.001) due to a greater score of global glomerulosclerosis (1.09±0.61 vs 0.64±0.66, p<0.0005). ISN/RPS classification was comparable. L group showed a significantly higher rate of all-cause mortality (HR=7.17, 95%CI 2.44-21.12, p<0.0001) and renal impairment, defined as a 1.5-fold increase in serum creatinine level from the time of renal biopsy (HR=2.66, 95%CI 1.22-5.81, p<0.05).
In the propensity score matching analysis, L-M group showed a tendency toward a lower frequency of hypocomplementemia (C3: 65.6% vs 84.4%, p=0.08; C4: 62.5% vs 78.1%, p=0.17; CH50: 37.5% vs 59.4%, p=0.08). There were no significant differences in NIH activity index (3.8±3.5 vs 4.3±3.2, p=0.37) or chronicity index (3.2±1.0 vs 3.4±1.7, p=0.87). L-M group had a significantly higher all-cause mortality rate (HR=5.38, 95% CI 1.16-25.02, p<0.05) and a tendency toward worse renal impairment (HR=2.57, 95% CI 0.87-7.56, p=0.07). In the multivariate analysis, late-onset, eGFR, and UPCR remained independent predictors of all-cause mortality rate, whereas late-onset remained an independent predictor of renal impairment.
Clinical features of late-onset included lower frequency of hypocomplementemia and higher NIH chronicity index. Our findings indicate that late-onset LN is associated with increased all-cause mortality and renal impairment, irrespective of disease activity or age-related comorbidities. Limitations include the difficulty to completely separate age as a prognostic factor due to the definition of late-onset LN and inability to establish causality due to the retrospective nature of this study.
