LAUSR

Background Lupus nephritis (LN) is a common feature of systemic lupus erythematosus (SLE). While LN is considered a contributor to irreversible organ damage in SLE, the magnitude of impact of active renal disease relative to other contributors to damage accrual is unknown. Objectives To determine the time-dependent association of active lupus nephritis (LN) with organ damage accrual in SLE. Methods This study was performed on patients from the Asia Pacific Lupus Collaboration (APLC) cohort. SLE Disease Activity Index-2000 (SLEDAI-2k) is collected per-visit and SLICC-ACR Damage Index (SDI) annually. Analysis was restricted to patients with ≥2 SDI scores. Active LN was defined if patients had urinary casts, proteinuria, haematuria or pyuria as indicated in the SLEDAI-2k descriptor. Organ damage accrual was defined as a change of SDI (ΔSDI>0) between baseline and final visit. Glucocorticoid (GC) categories were defined according to cumulative GC exposure at each visit as either no GC (cum.GC=0); low GC (cum.GC ≤median) or high GC (cum.GC >median). Cox regression analyses were performed. Results 1735 patients and 5593 visits were included in the analysis. 93% of patients was female with a median ([inter-quartile range (IQR), (range)] age of 40 years.31, 51 18, 77 Median study observation period was 853 days [621, 1094].98, 1443 36% were Chinese; 20% Thai and 10% Caucasian ethnicity. 82% of patients were exposed to glucocorticoids. 40% had active renal disease at least once during the study period, and active renal disease was observed in 22% of visits (n=1238 visits). 41% of patients had organ damage at baseline and 14% accrued organ damage (272 damage accrual episodes in 250 patients). Active renal disease was significantly associated with damage accrual; after adjusting for confounders, patients with active renal disease were 66% more likely to accrue organ damage compared to those without active renal disease (adjusted hazard ratio=1.66 (95% CI: 1.26, 2.19), p-value<0.01 (table 1). High cumulative GC and age were also significantly associated with damage accrual. Conclusions Active LN is an independent risk factor for damage accrual in SLE. The concomitant independent association of GC exposure with damage accrual suggests non-GC treatments to reduce active LN are needed to reduce damage burden in SLE. Disclosure of Interest None declared