ObjectiveMembranous nephropathy can be categorised into idiopathic membranous nephropathy (iMN) and secondary membranous nephropathy (sMN). However, it should be noted that a subset of patients initially diagnosed with iMN may develop secondary etiologies during longitudinal follow-up, even in the absence of systemic manifestations at initial presentation.MethodsThis is a single-center retrospective analysis. From January 2017 to April 2024, patients who were diagnosed with iMN at the time of their initial renal biopsy, had no extrarenal lupus manifestations at that time, and subsequently developed lupus nephritis (LN) or systemic lupus erythematosus (SLE) during the follow-up period at our center were included. Patients with sMN and incomplete SLE at the time of the initial renal biopsy were excluded from the study.ResultsA total of six patients were included. Of these, five were female and one was male. The mean age of the patients was 30.00 ± 10.39 years. At the initial renal biopsy, the proteinuria level was 6.45 ± 1.83 g/L, the serum albumin level was 21.77 ± 3.69 g/L, and the estimated glomerular filtration rate was within the normal range. Notably, one patient exhibited a positive test result for the PLA2R antibody, with a titer of 135.5 RU/ml. Following the administration of immunotherapy, all six patients achieved remission. However, after a follow-up period of 7.00 ± 5.21 years, five of the patients experienced a recurrence. Repeat renal biopsies in four relapsed patients confirmed histopathological progression to LN (class Ⅲ+Ⅴ in two cases, class V in two cases). Two patients subsequently fulfilled the 2019 EULAR/ACR SLE classification criteria.ConclusionThe diagnosis of membranous nephropathy does not entirely exclude the possibility of secondary nephropathy, even in patients with a high PLA2R antibody titer. Consequently, close longitudinal follow-up for occult autoimmune disease remains a necessity in clinical practice.

ObjectivesTo clarify risk factors for cytomegalovirus (CMV) reactivation and disease in patients with systemic lupus erythematosus (SLE).MethodsWe reviewed patients with SLE who received remission induction therapy at our institution between May 2010 and October 2022 and enrolled those whose CMV pp65 antigen-positive cell counts were measured within 3 months of admission. Patients with CMV reactivation were divided into CMV disease (with any symptoms or end-organ disease due to CMV reactivation) and asymptomatic CMV reactivation. Risk factors for CMV reactivation and CMV disease were examined.ResultsWe observed CMV reactivation in 64 of 130 patients. Age (hazard ratio [HR], 2.03; 95% confidence interval [CI], 1.09-3.78; p = 0.026), albumin (HR, 2.35; 95% CI, 1.09-5.07; p = 0.029), a high Systemic Lupus Erythematosus Disease Activity Index (SLEDAI) (HR, 1.73; 95% CI, 1.00-2.98; p = .048), and immunosuppressive drug use (HR, 1.94; 95% CI, 1.12-3.35; p = 0.018) were risk factors for CMV reactivation. CMV reactivation occurred more frequently when two or more risk factors were present. Among the 64 cases of CMV reactivation, 25 with disease had a higher number of CMV pp65 antigen-positive cells (6 vs 2; p = 0.02). The cut-off value for developing organ damage was 12 cells on two slides.ConclusionIn SLE patients, age, albumin, a high SLEDAI, and immunosuppressive drug use were possible risk factors for CMV reactivation. Patients who develop organ damage have high numbers of CMV pp65 antigen-positive cells and are prone to be symptomatic with an antigenemia count >12 per two slides.

ObjectivesTo investigate the impact of time to diagnosis on damage accrual in thrombotic antiphospholipid syndrome (APS).MethodsRetrospective cohort study including 252 patients with thrombotic APS (Sydney criteria). Time to diagnosis was defined as the period from the first thrombosis to diagnosis (diagnostic delay ≥12months). Recurrent events occurred during antithrombotic therapy. Damage was assessed using the damage index for APS (DIAPS). Risk factors for diagnosis and treatment delay (≥12months) were assessed. Cox regression analysis was used to determine predictors of damage (DIAPS ≥1) and severe damage (DIAPS ≥ 3). Significance was set as α < 0.05.ResultsMost patients were female (76.7%) with primary APS (71.8%) and a median age at onset of 40.5 (28-51) years. The median time to diagnosis was 12months (≥12months, 53.6%). Damage and severe damage affected 75.4% and 21.0% of patients, respectively. Diagnosis delay was associated with higher cumulative thrombotic events, recurrent thrombosis and anticoagulation delay (all p < .001). Secondary APS (HR 2.65, 95% CI 1.52-4.62) and recurrent thrombosis (HR 2.66, 95% CI 1.52-4.66) predicted severe damage but not damage. Diagnosis delay did not predict damage but predicted severe damage (HR 2.99, 95% CI 1.25-7.16), even after multivariate analysis (aHR 3.18, 95% CI 1.24-8.12).ConclusionIn thrombotic APS, diagnosis delay is associated with increased number of thrombotic events and recurrent thrombosis, and is an independent predictor of severe organ damage.

ObjectivesTuberculosis (TB) may increase morbidity and mortality of systemic lupus erythematosus (SLE) patients. The aim of the study was to determine the risk factors associated with TB in SLE patients.MethodsThis case-control study included SLE patients from the Hasan Sadikin Lupus Registry (HSLR) cohort between 2008 and 2024. Lupus patients with TB (cases) were matched by age with those without TB (controls). TB risk was estimated as adjusted OR (aOR) with 95% CI using univariate and multivariable logistic regression analyses.ResultsIn total, 90 SLE patients with TB and 270 without TB were included, predominantly female (n = 342; 95%). The median SLE duration to TB diagnosis was 30 (range 8-95) months, of which 56.7% (n = 51) had pulmonary TB, and 21.1% (n = 19) had extrapulmonary TB with meningitis and lymphadenitis being the most prevalent. Logistic regression analysis showed that SLE duration <9 months (aOR 4.04; 95% CI 1.78-9.18), history of TB contact (aOR 3.67; 95% CI 1.31-10.30), history of methylprednisolone ≥24mg/day for ≥4 weeks (aOR 1.96; 95% CI 1.06-3.63), using <2 disease-modifying antirheumatic drugs (DMARDs) (aOR 3.34; 95% CI 1.89-5.90), and lymphopenia (aOR 2.84; CI 95% 1.65-4.91) were associated with TB (P < .05).ConclusionsAmong SLE patients living in TB endemic country, TB contact, high dose corticosteroid, and lymphopenia increase risk of TB. Of note, lower disease duration and using <2 DMARDs are also associated with TB. Further research is necessary to evaluate the need of TB prophylaxis in SLE patients with these risk factors.

BackgroundSleep disturbances are common among patients with systemic lupus erythematosus (SLE) and significantly impair quality of life. Despite increasing awareness, determinants of poor sleep in this population remain underexplored.ObjectivesThis study aimed to assess sleep quality in Tunisian SLE patients and identify associated clinical and psychological factors.MethodsA cross-sectional study was conducted at Rabta Hospital in Tunisia from February to May 2023, including 100 SLE patients fulfilling the 2019 EULAR/ACR classification criteria. Sleep quality was measured using the Pittsburgh Sleep Quality Index (PSQI). Depression, anxiety, fatigue, pain, and quality of life were assessed using validated Arabic versions of the Hospital Anxiety and Depression Scale, Fatigue Severity Scale, Numeric Pain Rating Scale, and Lupus QoL.ResultsPoor sleep quality (PSQI ≥6) was observed in 58% of participants. Univariate analysis revealed associations between poor sleep and older age, family history of SLE, depression, anxiety, fatigue, moderate-to-severe pain, and disease activity. However, multivariate analysis identified emotional health domain as the sole independent predictor of poor sleep (OR = 0.955; p = .03).ConclusionEmotional health emerged as a key determinant of sleep quality among SLE patients in Tunisia. These findings highlight the need for integrated psychosocial interventions to improve both sleep and overall quality of life. Future longitudinal studies are needed to confirm these associations and assess causal relationships.

ObjectiveCervical cancer remains a leading cause of death among women of childbearing age despite the proven efficacy of screening in reducing mortality rates. Women with systemic lupus erythematosus (SLE) are at a higher risk for cervical cancer but tend to have lower screening rates. This study aimed to assess cervical cancer screening (CCS) rates and identify factors influencing screening uptake among Korean women of childbearing age with SLE.MethodsWomen aged 20-49 with SLE and age matched controls, randomly selected at a 1:5 ratio, were identified from the 2016-2017 Korean National Health Insurance Service-National Health Information Database (NHIS-NHID). Data from 10,981 women with SLE and 54,905 controls eligible for National Health Screening Program (NHSP) in 2018-2019 were analyzed. The CCS rate was determined based on participation in Papanicolaou test among eligible individuals for NHSP. Logistic regression was used to estimate odds ratios (ORs) for factors associated with CCS uptake.ResultsThe CCS rate was significantly lower in women with SLE compared to controls (49.6% vs 52.1%, P < .0001). Logistic regression revealed that younger age, lower income, self-employment or medical aid insurance, and rural residence were associated with reduced CCS uptake in both groups. The highest CCS uptake occurred in the 40-44 age group for both women with SLE (OR 5.09, 95% CI 4.17-6.22) and controls (OR 4.65, 95% CI 4.26-5.07). Comorbidities increased CCS uptake among controls (OR 1.18, 95% CI 1.13-1.23), but were associated with mild non-significant decrease in uptake among women with SLE (OR 0.96, 95% CI 0.87-1.04).ConclusionNational CCS program is often underutilized by Korean women of childbearing age with SLE, particularly among those with lower income and those of rural residency. Targeted interventions are needed to improve screening rates and address the unique challenges faced by this high-risk population.

IntroductionJuvenile Systemic Lupus Erythematosus (jSLE) is a rare pediatric rheumatic disease characterized by systemic inflammation that can lead to organ damage. Compared to adults, it often has a more severe course in children. Both disease activity and treatments may result in temporary or permanent damage.ObjectivesTo evaluate risk factors associated with damage occurrence in patients with jSLE.MethodsThis multicenter, retrospective study included patients with jSLE followed for at least 12 months. Low-dose corticosteroid therapy was defined as prednisolone 0.01-0.03mg/kg/day (max 7.5mg/day). The annual cumulative steroid dose was calculated by dividing the total steroid intake by 365.25 times the number of follow-up years. Collected data included SLEDAI and SDI scores at initial and final visits, laboratory parameters, and flare characteristics.ResultsA total of 158 patients (86.7% female) from 17 centers were included. Median age at diagnosis was 13.8years, with a median follow-up of 35months. Organ damage was present in 14 patients at diagnosis and in 23 at final visit. Damage types included proteinuria, cognitive dysfunction (each 3.2%), and others such as cataracts, erosive arthritis, avascular necrosis, optic atrophy, and vertebral collapse. Patients with damage had significantly higher SLEDAI scores at both time points, delayed transition to low-dose steroids, and a lower rate of achieving Lupus Low Disease Activity State (LLDAS) (p = .006).ConclusionPersistent disease activity and delayed control are major contributors to organ damage in jSLE. Early and sustained disease suppression is critical to prevent long-term complications.

A baby girl, born to a 35-year-old mother, was admitted at 14.5 hours of life due to apnoea and seizures. Diffusion-weighted magnetic resonance imaging revealed multiple ischemic lesions. Laboratory screening for thrombophilia showed elevated levels of anti-cardiolipin IgG antibodies (aCL-IgG). The mother also tested positive for aCL-IgG, raising the possibility of transplacental antibody transfer. The neonate's aCL-IgG levels gradually declined and normalized by 4months of age. Although causality cannot be established, this case suggests a potential association between transient maternal antiphospholipid antibodies and neonatal ischemic stroke.