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Systemic lupus erythematosus (SLE) is a chronic inflammatory autoimmune disease and can affect several organs and systems. It is characterized by high production of autoantibodies against nuclear compounds. TLR7/8/9 are responsible for nucleic acid recognition and they trigger proinflammatory responses through activation of NK-kappaB and Type I IFN production, making a bridge between the innate and the adaptative immune systems. We analyzed the frequency of TLR7 rs179008, TLR8 rs3764880, TLR9 rs5743836 and rs352140 in 370 patients with SLE and 415 healthy controls from southern Brazil. All analyses were conducted with regard to gender and ethnicity. Genotypic and allelic frequencies were different for TLR7 rs179008 (0.253 vs. 0.163, p = 0.020 and p = 0.003, OR for T allele: 1.74 CI 95% 1.12–2.70) and TLR9 rs5743836 (0.174 vs. 0.112, p = 0.045 and p = 0.017, OR for C allele: 1.59, CI 95% 0.99–2.57) between European-derived female groups. A higher frequency was observed for the presence of Anti-SSa/Ro for TRL9 rs5743836 C allele carriers (0.228 vs 0.126, Bonferroni corrected p = 0.06). No statistical differences were found for TLR9 haplotypic analyses. We suggest that TLR7 rs179008 and TLR9 rs5743836 can be considered SLE susceptibility factors for women of European descent in our population.

Vitamin D deficiency has been described in systemic lupus erythematosus (SLE). BsmI VDR (vitamin D receptor) gene polymorphism was associated with SLE in Asian patients. Studies in Brazilian populations have not been realized. A case-control study with 195 SLE patients and 201 healthy controls was conducted to investigate the influence of BsmI and FokI VDR gene polymorphisms on susceptibility to SLE. In addition, 25-hydroxyvitamin D [25(OH)D] was measured in SLE patients to evaluate possible associations with VDR polymorphic variants and clinical and laboratory expressions of disease. Genotyping was performed by RFLP-PCR. The measurement of 25(OH)D was performed by chemiluminescence. There was no statistically significant difference in genotype and allelic frequencies of BsmI and FokI polymorphisms between European-derived cases and controls. The mean serum levels of 25(OH)D were 25.51 ± 11.43 ng/ml in SLE patients. According to genotype distribution, 25(OH)D concentrations were significantly higher in patients carrying the FokI f/f genotype compared with patients carrying the F/F genotype (31.6 ± 14.1 ng/ml versus 23.0 ± 9.2 ng/ml, p = 0.004), reinforcing its role in the functional activity of VDR. This feature may be considered in future clinical and experimental studies involving vitamin D measurements. Therefore, genetic-specific definitions of ideal levels of vitamin D in SLE need to be established in future studies.

Background:Systemic lupus erythematosus (SLE) is a complex and heterogenous autoimmune disease characterised by periods of worsening symptoms, known as flares. Flares and long-term glucocorticoid (GC) therapy are both associated with increased risk of long-term damage. This significantly impacts health-related quality of life and increases emergency hospital visits and healthcare costs. The challenges facing SLE patients worldwide have garnered significant attention from patient groups and clinical experts, driving robust consensus work on their unmet needs [1,2,3]. Key challenges include poor recognition of symptoms, leading to delays in diagnosis, cycling between healthcare professionals, and receiving suboptimal care. Patient access to approved treatments for SLE also remains limited. The publication of updated EULAR recommendations for the management of SLE provides an opportunity for the lupus community to advocate for improved standards of care by championing their implementation. Key recommendations include GC-sparing approaches and early use of biological therapies to achieve remission or lower disease activity, preserve renal function, and reduce flares and organ damage.Objectives:To unite and empower patients, patient groups and healthcare professionals to advocate for improvements in the care and treatment received by people with SLE.Methods:Representatives from patient groups, professional organisations and the treatment community came together to develop a Patient Charter.Results:The Patient Charter identifies four principles of care and associated recommendations to improve care:Principle 1: I deserve recognition and understanding of early symptoms of SLE to drive timely, accurate diagnosis and assessment so that I can receive the best care available as soon as possible.Recommendations: Improve public, patient and clinical education on SLE; develop a standard list of diagnostic criteria and clinical investigation tools; implement referral pathways.Principle 2: I deserve access to information about my SLE, so I can play an active role in the management of my condition, minimise flares and reduce the impact of SLE on my life.Recommendations: Improve access to patient information and self-management tools; co-create interventions with SLE patients to improve their uptake.Principle 3: I deserve access to a coordinated multi-disciplinary care team who fully understands my condition and my experience, regardless of who am I or where I live.Recommendations: Ensure patient access to multi-disciplinary teams; implement personalised care plans for every patient; establish shared care infrastructure; adopt telehealth solutions.Principle 4: I deserve access to appropriate and comprehensive pharmacological and non-pharmacological care, which reduces the burden of my SLE and allows me to have a high quality of life for as long as possible.Recommendations: Encourage clinical trial participation; minimise or monitor GC use to the lowest possible dose; update and implement clinical guidelines.Conclusion:SLE places a significant burden on the lives of millions of people worldwide, significantly impacting a patient’s quality of life, mental health and relationships. It has a substantial impact on healthcare systems due to suboptimal disease management, and on society, through the loss of productivity caused by the debilitating long-term symptoms and impact of SLE. The principles and recommendations we have set out in this charter demonstrate the core elements of quality care that all people living with SLE should receive, regardless of health system or geography. We urge healthcare professionals, providers, health systems and policymakers around the world to swiftly implement SLE diagnosis and care guidelines which reflect these principles and ensure that the latest advancements and current approaches in SLE care reach the patients who need them.REFERENCES:[1] Cornet A et al. Lupus Science & Medicine. 2021 8(1), e000469[2] Tse, K et al. Lupus Science & Medicine. 2021 8(1), e000433[3] European Reference Network. 2018 https://reconnet.ern-net.eu/Acknowledgements:The Patient Charter was initiated by AstraZeneca to inform a discussion about what quality care should look like in the provision of SLE services. These principles were debated and refined during a discussion held on Thursday 7 July 2022, organised and funded by AstraZeneca. Nine experts from academic and patient organisations and a professional group discussed the value of establishing a Patient Charter as a potential starting point for discussions on how to improve SLE care. Writing and editing assistance, including preparation of a draft manuscript under the direction and guidance of the authors, incorporating author feedback, and manuscript submission, was provided by MHP Group and Fishawack Health. All authors commented on previous versions of the manuscript. All authors read and approved the final manuscript.Disclosure of Interests:Marta Mosca AbbVie, AstraZeneca, Bristol Myers Squibb, Janssen and Lilly, AstraZeneca, AbbVie, GSK, Idorsia, Lilly and UCB, Idorsia, Jeanette Andersen AstraZeneca, Bristol Myers Squibb and Roche, AstraZeneca, Bayer, Biogen, Bristol Myers Squibb, Boehringer Ingelheim, GSK, Idorsia, Janssen, Lilly, Merck, Novartis, Roche and UCB, Patrick Wildman: None declared, Susan Manzi AstraZeneca, Exagen Diagnostics Inc, GSK, Lilly, Novartis, UCB, AbbVie, AstraZeneca and GSK, Zahir Amoura AstraZeneca, GSK, Novartis, and Roche, AstraZeneca, GSK, Novartis, Roche; Amgen, Kezar and Otsuka, Irene Bultink GSK and UCB, Odirlei André Monticielo AbbVie, Apsen, AstraZeneca, Boehringer Ingelheim, Bristol Myers Squibb, Celltrion, GSK, Janssen, Novartis and UCB, AstraZeneca, GSK and Janssen, Sandra Navarra Astellas, AstraZeneca, Boehringer Ingelheim, GSK, Janssen, Novartis and Pfizer, Biogen, Biogen, GSK, Idorsia, Lilly and Novartis, Susanne Pettersson Novartis.

The aim of this study was to analyze the allelic and genotypic frequencies of the CCR5delta32 polymorphism in systemic lupus erythematosus (SLE) patients and to investigate a possible association of this allele with SLE susceptibility and clinical outcome. A total of 367 SLE patients and 435 healthy controls were genotyped for the CCR5delta32 polymorphism. We observed that, in European-derived individuals, the frequency of the CCR5delta32 allele was smaller in patients than in controls (2.7% vs. 7.5%, OR 0.34, 95% CI 0.17–0.65, p Bonf = 0.002), suggesting that this allele could be considered a protective factor for the disease. Regarding clinical manifestations, we observed that CCR5delta32 female African-derived carrier patients presented a higher predisposition to class IV nephritis when compared with absent nephritis/other class group (13.8% vs. 3.8%, OR 37.1, 95% CI 2.8–1854.7, p Bonf = 0.030). A multivariate analysis including all female patients and controlling for the presence or absence of anti-dsDNA antibodies, ethnicity and age at diagnosis showed an increased relative risk of 3.9 times for patients carrying the CCR5delta32 allele to develop class IV nephritis as compared with noncarriers. Our data suggest that the CCR5delta32 allele is a protective factor for the disease in European-derived patients and a susceptibility factor to class IV nephritis in African-derived female patients.

Background:Neuropsychiatric lupus (NPSLE) affects the central (CNS) and peripheral (PNS) nervous system. Complications in the CNS associated with SLE include behavioral and cognitive dysfunction, and the use of animal models becomes indispensable to better understand NPSLE [1]. Pristane-induced lupus (PIL) presents multiple classification criteria of SLE, but the neuropsychiatric manifestations are poorly studied in this model [2]. In this context, vitamin D (VitD) has been studied for its immunomodulatory and neuroprotective effects in autoimmune diseases [3].Objectives:To describe neuropsychiatric manifestations in the pristane-induced lupus model and to evaluate the effect of VitD supplementation on behavior.Methods:Seventy-six BALB/c mice were divided into 3 groups: CO (control, n=24), PIL (induced at T0 with 500μL of pristane intraperitoneally, n=28), and VD (PIL with VitD supplementation [2ug/kg] every two days subcutaneously, n=28). Depressive-like behavior was assessed using the forced-swim test, measuring swimming and immobility time. Anxious-like behavior was measured with the elevated plus maze test, analyzing number of entries into and time spent in the open arms. Memory was evaluated through the Barnes maze, assessing escape latency time, number of errors, and hits on the escape/target orifice for short-term memory and long-term memory. Statistical analyzes were performed using SPSS. Kruskal-Wallis test followed by Dunn’s were used. P value was considered ≤0.05.Results:Compared with CO, both PIL and VD groups showed longer immobility time in the forced-swim test, at T90 (COvsPIL, p<0.0001; COvsVD, p<0.0001) and at T180 (COvsPIL, p<0.001; COvsVD, p<0.001) (Figure 1A), as well as a reduction in swim activity at T90 (COvsPIL, p<0.05; COvsVD, p<0.001) and at T180 (COvsPIL, p<0.05; COvsVD, p<0.01) (Figure 1B). There was a reduction in the number of entries that the animals in the PIL group sought to explore the open arms in the elevated plus maze, compared with the CO group (T90: COvsPIL, p=0.05; T180: COvsPIL, p<0.05) (Figure 1C). There was no difference in the time spent in the open arms (Figure 1D). In the Barnes maze, VD had a lower number of errors compared with the PIL group for short-term memory at T90 (PILvsVD, p<0.01) (Figure 2A). For long-term memory, PIL had a lower number of hits (PILvsCO, p<0.0001; PILvsVD, p<0.01) and a higher number of errors (COvsPIL, p<0.05; PILvsVD, p<0.0001) compared with CO and VD groups at T90 (Figure 2B/C). There was no statistically significant difference in escape latency at T90 or in the other parameters evaluated at T180.Figure 1.Data from forced-swim and elevated plus maze tests: A) Time (in seconds) mice stood immobile during the forced-swim test. B) Time (s) mice remained swimming during the forced-swim test. C) Number of open armies’ entries in the elevated plus maze. D) Time (s) mice remained in the open armies of the maze. *p≤0.05; **p<0.01; ***p<0.001; ***p<0.0001; CO: control; PIL: pristane-induced lupus; VD: pristane-induced lupus + vitamin D.Figure 2.Data from Barnes maze test for short (STM) and long-term memory (LTM): A) Times the animal explored an orifice other than the target (STM at T90); B) Times the animal explored the target orifice (LTM at T90); C) Times the animal explored an orifice other than the target (LTM at T90). *p<0.05; **p<0.01; ***p<0.0001; CO: control; PIL: pristane-induced lupus; VD: pristane-induced lupus + vitamin D.Conclusion:The PIL model exhibited neuropsychiatric manifestations, showing symptoms consistent with anxiety, depression, and memory deficit. While VitD supplementation did not impact anxious and depressive-like behavior, it demonstrated a potential positive effect on memory parameters.REFERENCES:[1] Vo A et al. J Cereb Blood Flow Metab. 2014 Aug;34(8):1315-20. doi: 10.1038/jcbfm.2014.85[2] Freitas EC, de Oliveira MS, Monticielo OA. Clin Rheumatol. 2017 Nov;36(11):2403-2414. doi: 10.1007/s10067-017-3811-6[3] Karnopp TE et al. Adv Rheumatol. 2024 Jan 2;64(1):2. doi: 10.1186/s42358-023-00344-wAcknowledgements:Douglas dos Santos Soares (Laboratório de Pesquisa Cardiovascular at HCPA); Unidade de Experimentação Animal (HCPA); Diretoria de Pesquisa (HCPA); and Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES).Disclosure of Interests:None declared.

Background:Neuropsychiatric lupus affects the central and peripheral nervous system. Physiopathology includes a blood-brain barrier disruption that leads to the infiltration of autoantibodies and immune cells into the brain [1]. Vitamin D (VitD) has immunoregulatory properties that have been explored in autoimmune diseases [1]. Pristane-induced lupus (PIL) presents multiple classification criteria of SLE, but the neuropsychiatric manifestations are poorly studied [2]. The role of VitD in this context is unknown.Objectives:To characterize cerebral immunopathological changes and IFN-α1 serum levels in the pristane-induced lupus model, as well as to assess the impact of VitD supplementation on such observations.Methods:Seventy-six BALB/c mice were randomized into 3 groups: CO (Control, n=24), PIL (induced at T0 with 500μL of pristane intraperitoneally, n=28) and VD (PIL with VitD supplementation [2ug/kg] every two days subcutaneously, n=28). Brain tissue was collected and frozen following euthanasia 90 (n=38) and 180 (n=38) days after induction. Brain IgG and IgM deposits and pVDR expression were evaluated through immunofluorescence and IFN-α1 serum levels through ELISA. Statistical analyzes were performed in the SPSS program. Kruskal-Wallis test and ANOVA were used. Data are presented as mean±standard deviation. P value was considered ≤0.05.Results:PIL group exhibited a significant increase in total IgG and IgM deposits in the brain compared with the CO group at T90 (IgG: 1.70±0.43 vs. 0.48±0.05, p<0.0001; IgM: 1.92±0.39 vs. 0.71±0.30, p<0.0001) and T180 (IgG: 1.71±0.34 vs. 0.49±0.07, p<0.0001; IgM: 2.39±0.94 vs. 0.81±0.28, p<0.0001). Supplementation with VitD reduced both IgG (T90: 0.89±0.19, p<0.0001; T180: 0.88±0.20, p<0.0001) and IgM (T90: 1.35±0.47, p<0.01; T180: 1.15±0.45, p<0.0001) deposits at both time points (Figure 1). At T90, pVDR expression was similar across groups (CO: 0.71±0.16; PIL: 0.60±0.16; VD: 0.58±0.06). However, at T180, an increase in pVDR expression was observed in the CO and VD groups (CO: 0.98±0.39; PIL: 0.45±0.06; VD: 1.16±0.65, p<0.01 PIL vs. CO; p<0.001 PIL vs. VD) (Figure 2). Serum levels of IFN-α1 were elevated in both PIL and VD groups compared to the CO group (T90: CO: 5.50±2.60; PIL: 13.74±3.36; VD: 13.07±5.55, p=0.03; T180: CO: 3.22±0.41; PIL: 11.63±3.85; VD: 11.45±3.77, p=0.001). VitD supplementation did not reduce IFN-α1 serum levels.Figure 1.Total IgG and IgM deposits in the brain in a pristane-induced lupus model. A) Total IgG fluorescence intensity in brain regions. B) Total IgG fluorescence intensity in brain regions. Values are expressed as mean±SD. *p<0.05; **p<0.01; ***p<0.001; ***p<0.0001. CO3: controls 3 months after induction; PIL3: pristane-induced lupus 3 months after induction; VD3: pristane-induced lupus+vitamin D 3 months after induction; CO6: controls 6 months after induction; PIL6: pristane-induced lupus 6 months after induction; VD6: pristane-induced lupus+vitamin D 6 months after induction.Figure 2.pVDR expression fluorescence intensity in brain regions. Values are expressed as mean±SD. *p<0.05; **p<0.01; ***p<0.001; ***p<0.0001. CO3: controls 3 months after induction; PIL3: pristane-induced lupus 3 months after induction; VD3: pristane-induced lupus+vitamin D 3 months after induction; CO6: controls 6 months after induction; PIL6: pristane-induced lupus 6 months after induction; VD6: pristane-induced lupus+vitamin D 6 months after induction.Conclusion:PIL model presented increased deposits of IgG and IgM in the brain tissue. VitD was able to reduce this immunopathological finding and enhance pVDR expression in the VD group after 180 days of treatment. PIL exhibited elevated levels of IFN-α1, which VitD did not modulate. Further data analysis is required to comprehend the immunological effects and clinical implications of VitD in this murine PIL model.REFERENCES:[1] Karnopp TE, Freitas EC, Rieger A, Chapacais GF, Monticielo OA. Clin Rheumatol 2022. doi: 10.1007/s10067-022-06094-2[2] Freitas EC, de Oliveira MS, Monticielo OA. Clin Rheumatol 2017. doi: 10.1007/s10067-017-3811-6Acknowledgements:Douglas dos Santos Soares (Laboratório de Pesquisa Cardiovascular at HCPA); Unidade de Experimentação Animal (HCPA); Diretoria de Pesquisa (HCPA); and Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES).Disclosure of Interests:None declared.

Human leukocyte antigen-G (HLA-G) is a nonclassical class I major histocompatibility complex molecule which is induced at the course of inflammatory pathologies, and its expression has been suggested as a possible mechanism of tissue protection against autoimmune inflammatory responses, therefore acting as a mechanism of immune surveillance. We investigated the influence of the 14 bp polymorphism of the HLA-G gene on systemic lupus erythematosus (SLE) by analyzing 293 patients with SLE and 460 healthy controls. The patient’s group was not in Hardy–Weinberg equilibrium, presenting an excess of heterozygotes (P = 0.014). The heterozygote group exhibited lower systemic lupus erythematosus disease activity indexes than the homozygous deletion group and the homozygous insertion group (mean value = 2.29 against 2.97 and 3.4, respectively, P = 0.035). Photosensitive patients showed a higher frequency of heterozygotes and an equivalent lower frequency of homozygotes for deletion; on the other hand, patients without arthritis presented a higher frequency of heterozygotes than the arthritis group and also a lower frequency of the del/del genotype. Overall, our results support the idea of a role of the HLA-G insertion/deletion polymorphism and therefore a role for the HLA-G molecule, on the pathology of SLE.

Background:Phase III clinical trials have shown that COVID-19 vaccines are safe and effective in healthy children. There are few studies in children with juvenile autoimmune disease (AID).Objectives:The study aims to evaluate the immunogenicity and safety of the vaccine against COVID-19 in Juvenile JAID in the real life.Methods:These data are from “Safety and efficacy on COVID-19 Vaccine in Rheumatic Disease” - SAFER study, a Brazilian multicentric prospective phase IV study to evaluate COVID-19 vaccine AID. Immunogenicity and adverse events (AE) were assessed, after 3 doses, in children compared to adults with AID. Inclusion criteria were fulfilling criteria according to international classification for AID. Exclusion criteria: pregnancy, previous severe AE to any vaccine and other immunosuppression causes. Stratification of post-vaccination AE was performed using a diary, filled out daily and returned at the end of 28 days of each dose. The IgG antibodies to SARS-CoV-2 spike receptor-binding domain by chemiluminescence were measured at baseline and after first and 2nd dose. The seropositivity was defined for titers ≥ 7 BAU/mL. The Kruskal-Wallis, post-hoc Dwass-Steel-Critchlow-Fligner pairwise comparisons tests, and multiple linear regression analysis were used. The p-value ≤0.05 was considered significant.Results:A total of 123 volunteers with AID, 37 adults and 86 juvenile AID patients were included in the study.The juvenile group was aged < 18 years (adult 32.5 ±6 vs children group 14.5 ±1.7, p<0.01) and had fewer comorbidities (19 vs. 60%, p<0.01). The groups were homogeneous for sex (female 86% vs. 75%, p=0.23), ethnicity (Caucasians 47 vs. 43%, p=0.7) and degree of immunosuppression (high grade 62 vs. 60%, p=0.25). The frequency of diseases in adults was SLE= 56%, SpA= 5.41%, RA= 5.1%, others= 33.2%; and in children it was SLE= 38.4%, JIA= 41.8, others= 19.7%. The frequency of previous natural exposure to COVID-19 was higher in adults (30.6 vs. 8.1%, p<0.001). Both groups received BNT162b2 vaccine in the 1st. and 2nd. doses and in more than 90% in the 3rd. dose. The frequency of joint paint in post-1st dose (41 vs. 15%, p= 0.003) and in 2nd. dose (24 vs. 0%, p=0.003) was higher in adults. There was no difference in adverse events between the groups after the third dose. The groups were homogeneous for IgG-S titers at baseline. Patients with positive or negative IgG-S at baseline were analyzed separately. There was a significant increase (p<0.001) in IgG-S levels after the 1st, 2nd and 3th doses in the juvenile AID (0.71(0.28-35.07) vs. 443.04 (36.92-2155.77) vs. 2232.38 (1207.43-3688.45) vs. 1920.72 (1383.45-5680.00)), and in the adult group ((1.14(0.14-46.86) vs. 280.17 (49.70-4991.06) vs. 3787.14 (964.28-5680) vs. 2445.24 (868.12-4.418.19)). There was no difference between groups in the 4 times of comparison (p<0.05), regardless of the antibody level at baseline and the degree of immunosuppression. The seroconversion rate was 95% and 100% in both groups, after the 2nd and 3th dose.Conclusion:BNT162b2 vaccine is effective, safe and induced high titles and seroconversion rate in juvenile AID, similar to adults, independent of immunosuppression, comorbidities or previous natural infection. Children showed more joint pain as AE than adults.REFERENCES:NIL.Table 1.IgG-S measurement after vaccination against COVID-19 in baseline, 28 days after 1st dose, 2nd and 3th doseTotalAdultsJuvenilePN=123N=37N=86IgG at inclusion, Median (IQR)0.85 (0.14-46.15)0.71 (0.28-35.07)1.14 (0.14-46.86)0.98IgG 28 days after 1st dose Median (IQR)326.96 (45.16-3887.32)443.04 (36.92-2155.77)280.17 (49.70-4991.06)0.33IgG 28 days after 2nd dose, Median (IQR)3189.32 (965.15-5245.62)2232.38 (1207.43-3688.45)3787.14 (964.28-5680.00)0.14IgG after 3th dose, Median (IQR)2287.78 (888.89-5680.00)1920.72 (1383.45-5680.00)2445.24 (868.12-4418.19)0.67Figure 1.IgG-S measurement after vaccination against COVID-19 in T1(baseline, at inclusion), T2 (28 days after 1st dose), T3 (28 days after 2nd dose) and T3 (28 days after 3th dose).Acknowledgements:We thank Safer Study Group, and the Brazilian Society of Rheumatology for supporting this study. This study was funded by Department of Science and Technology of Federal Government of Brazil.Disclosure of Interests:None declared.

Background:Lupus nephritis (LN) is one of the most common, serious manifestations of systemic lupus erythematosus (SLE) and is associated with significant morbidity and mortality.Objectives:To evaluate work productivity (WP) and activity impairment (AI) in patients with active LN at cohort entry and 12 months after treatment initiation according to their renal response.Methods:GLADEL 2.0 is an observational prevalent and incident cohort. Forty-four centers from Latin-American countries enrolled patients ≥18 years of age who fulfilled the 1982/1997 American College of Rheumatology (ACR) and/or the 2012 Systemic Lupus International Collaborating Clinics (SLICC) classification criteria for SLE. Patients from different subsets of LN were enrolled. For this analysis, patients in Group II (prevalent inactive LN), III (prevalent active LN) and IV (incident LN) and 12-month follow-up data were included. Demographic, clinical manifestations, disease activity (SLEDAI- 2k) and damage SLICC/ACR Damage Index (SDI) were examined. At baseline, WPAI scores stratified by the presence of active or inactive LN were compared. At 12 months, absenteeism, presenteeism, global work impairment in employed patients and AI in patients with active LN were compared according to their renal response. Renal responses were defined according to EULAR/KDIGO: Complete clinical response: UPCR < 0.5 g/g; Partial clinical response: ≥50% reduction in UPCR, No Response: <50% reduction in proteinuria. Descriptive analyses were performed.Results:Of the 1081 patients included in the cohort, 651 with history of LN were evaluated (423 with active LN and 228 with inactive LN). Of the active LN patients, 369 (87.4%) were women, were younger at cohort entry, of a lower socioeconomic status, had a higher unemployment rate and a higher SLEDAI than patients with inactive LN. Of the LN patients, 257 (39.5%) were employed (salaried work) at cohort entry and were included in this analysis. Patients with active LN showed higher rates of impairment in the WPAI score with greater impact and lower WP in all domains than in patients with inactive LN (Table 1). At 12 months, there was no evidence of a positive impact on WP as measured by the WPAI in patients who achieved renal response (Table 2).Conclusion:Patients with active LN presented a greater impairment on WP compared to patients with inactive LN. There was no evidence of a positive impact on WP in patients who achieved a complete or partial renal response after 12 months of treatment. Future analyses with a larger number of patients being followed up would be necessary to provide more definitive data.REFERENCES:NIL.Acknowledgements:Medical writing support was provided by Panita Maturavongsadit, PhD, of Lumanity Communications Inc., and was funded by Janssen Global Services, LLC.Disclosure of Interests:Guillermo Pons-Estel AstraZeneca, Boehringer Ingelheim, GSK, Janssen, Novartis, Pfizer, RemeGen, Sanofi and Werfen Diagnostics, AstraZeneca, Boehringer Ingelheim, GSK, Janssen, Novartis, Pfizer, RemeGen, Sanofi and Werfen Diagnostics, AstraZeneca, Boehringer Ingelheim, GSK, Janssen, Novartis, Pfizer, RemeGen, Sanofi and Werfen Diagnostics, Romina Nieto: None declared, Rosana Quintana: None declared, Diana Carolina Fernández Ávila: None declared, Rosa Serrano: None declared, Guillermina Harvey: None declared, Lucia Hernández: None declared, Karen Roberts: None declared, Luis Catoggio: None declared, Gislea Subils: None declared, Carla Gobbi: None declared, Florencia Bordon: None declared, Pablo David Ibañez Peña: None declared, Leonel Ariel Berbotto: None declared, María Constanza Bertolaccini: None declared, Diego O. Rinesi: None declared, Maria de los Ángeles Gargiulo: None declared, Cecilia Pisoni: None declared, Joaquín Martínez Serventi: None declared, Emilio Buschiazzo: None declared, Vitalina Barbosa: None declared, Odirlei André Monticielo: None declared, Carolina Albanez de A. Da C. Andrade: None declared, Francinne Machado Ribeiro: None declared, Eloisa Bonfa: None declared, Eduardo F. Borba: None declared, Emília I. Sato: None declared, Alexis Peralta Bondi: None declared, Silvana Donoso: None declared, Gustavo Aroca Martínez: None declared, Hellen Medina: None declared, Alex Echeverri: None declared, Sebastian Molina-Rios: None declared, Manuela Rubio Rivera: None declared, Rafael Lopez Martinez: None declared, Mario Moreno Alvarez: None declared, Olga L. Vera Lastra: None declared, Mario Pérez Cristóbal: None declared, Carlos Núñez Álvarez: None declared, Luis M. Amezcua-Guerra: None declared, Ignacio García-Valladares: None declared, Carlos Abud Mendoza: None declared, Dionicio A. Galarza-Delgado: None declared, Marcos Vázquez: None declared, Astrid Paats: None declared, Jorge N. Cieza Calderón: None declared, Ana Mabel Quiros Alva: None declared, Roberto Muñoz Louis: None declared, Carina Pizzarossa: None declared, Adriana Carlomango: None declared, Rocío V. Gamboa-Cardenas: None declared, Graciela S. Alarcón: None declared, Urbano Sbarigia Johnson & Johnson, Johnson & Johnson, Federico Zazzetti Johnson & Johnson, Johnson & Johnson, Ashley Orillion Johnson & Johnson, Johnson & Johnson, Bernardo Pons-Estel AstraZeneca, GSK, and Janssen.

Background:Lupus nephritis (LN) is one of the most common, serious manifestations of systemic lupus erythematosus (SLE) and is associated with significant morbidity and mortality. Data on treatment response among Latin American patients with LN remain limited.Objectives:To describe the rate of treatment response at 12 months in a cohort of SLE patients with active LN.Methods:GLADEL 2.0 is an observational prevalent and incident cohort. Forty-four centers from 10 Latin-American countries enrolled patients ≥18 years old who fulfilled the 1982/1997 American College of Rheumatology (ACR) and/or 2012 Systemic Lupus International Collaborating Clinics (SLICC) classification criteria. Patients were categorized into 4 subsets according to the presence of LN. For this analysis, patients in Group III (prevalent and active LN) and IV (incident LN, onset <3 months with renal biopsy) and sufficient follow-up data at 12 months were included. Baseline demographics, clinical manifestations, disease activity (SLEDAI-2k) and SLICC/ACR Damage Index (SDI) and LN treatments were examined. Partial and complete response according to EULAR/KDIGO were examined at 12 months: Complete Response Criteria (CRC): proteinuria <0.5 g/g measured as the urine protein to creatinine ratio (UPCR) from a 24-h urine collection; Partial Response Criteria (PRC): ≥50% reduction in UPCR from a 24-h urine collection and No Response (NR): <50% reduction in proteinuria.Results:One-thousand eighty-one patients were enrolled in GLADEL 2.0 with 364 patients included in this analysis: 195 (53.5%) in group III and 169 (46.4%) in group IV. At the 12-month follow-up, 13/364 (3.5%) patients had died, 14/364 (3.8%) had been lost to follow-up and 28/364 (7.6%) had incomplete data; therefore, the calculation of renal response was carried out in the remaining 309 patients. Table 1 describes the characteristics of patients with LN. Table 2 shows that patients who achieved renal response (complete or partial) had a shorter disease duration, greater use of pulse corticosteroids and IV cyclophosphamide, a lower chronicity index and all belonged to the LN incident group. When comparing complete vs partial response, patients who achieved complete response had lower baseline proteinuria and creatinine values, belonged to histological Class III and had lower SLEDAI.Conclusion:Renal response was achieved in 64% of patients having their first episode of LN, with lower chronicity rates in the biopsy and a lower SLEDAI. Pulsed corticosteroids and IV cyclophosphamide continue to be the options chosen by treating physicians. More data in the follow-up will allow us to evaluate the persistence of this response over time and what factors may influence it.REFERENCES:NIL.Acknowledgements:Medical writing support was provided by Panita Maturavongsadit, PhD, of Lumanity Communications Inc., and was funded by Janssen Global Services, LLC.Disclosure of Interests:Rosana Quintana: None declared, Romina Nieto: None declared, Diana Carolina Fernández Ávila: None declared, Rosa Serrano: None declared, Guillermina Harvey: None declared, Lucia Hernández: None declared, Karen Roberts: None declared, Marina Scolnik Speaker fees/advisory: GSK, Astrazeneca, Janssen, Roche, Pfizer, Grants: GSK, Astrazeneca, Janssen, Roche, Pfizer, Carmen Funes Soaje: None declared, Paula Alba: None declared, Verónica Saurit: None declared, Mercedes Argentina García: None declared, Guillermo Berbotto: None declared, Verónica Bellomio: None declared, Wilfredo Patiño Grageda: None declared, Graciela Gómez: None declared, Cecilia Pisoni: None declared, Ana Malvar: None declared, Vicente Juarez: None declared, Nílzio A. da Silva: None declared, Odirlei André Monticielo: None declared, Henrique Ataide Mariz: None declared, Francinne Machado Ribeiro: None declared, Eduardo F. Borba: None declared, Luciana Parente Speaker GSK, astrazeneca, Edgard Torres: None declared, Oscar Neira: None declared, Loreto Massardo: None declared, Gustavo Aroca Martínez: None declared, Carlos A. Cañas Davila: None declared, Gerardo Quintana López: None declared, Carlos Enrique Toro-Gutierrez: None declared, Mario Moreno Alvarez: None declared, Andres Zúñiga: None declared, Miguel A. Saavedra Salinas: None declared, Margarita Portela Hernandez: None declared, Hilda Fragoso Loyo: None declared, Luis Silveira: None declared, Ignacio García De La Torre: None declared, Carlos Abud Mendoza: None declared, Marcos Fonseca Hernández: None declared, Jorge Antonio Esquivel-Valerio: None declared, Isabel Acosta Colmán: None declared, Jhonatan Losanto: None declared, Claudia Mora Trujillo: None declared, Katiuska Zuñiga Corrales: None declared, Roberto Muñoz Louis: None declared, Martin Rebella: None declared, Álvaro Danza: None declared, Manuel F. Ugarte-Gil Speaker: GSK and Aztra-Zeneca, Advisory boards: Aztra-Zeneca and Ferrer, Grant support: Janssen, Graciela S. Alarcón: None declared, Urbano Sbarigia Johnson & Johnson, Johnson & Johnson, Federico Zazzetti Johnson & Johnson, Johnson & Johnson, Ashley Orillion Johnson & Johnson, Johnson & Johnson, Guillermo Pons-Estel Speaker and/or advisor: AstraZeneca, GSK, Janssen, Bernardo Pons-Estel Speaker and/or advisor and/or steering committee for the following companies: AstraZeneca, Boehringer Ingelheim, GSK, Janssen, Novartis, Pfizer, RemeGen, Sanofi and Werfen Diagnostics, Grants, consulting fees: AstraZeneca, Boehringer Ingelheim, GSK, Janssen, Novartis, Pfizer, RemeGen, Sanofi and Werfen Diagnostics.