Lupus nephritis (LN), a major complication in individuals diagnosed with systemic lupus erythematosus, substantially increases morbidity and mortality. Despite marked improvements in the survival of patients with severe LN over the past 50 years, complete clinical remission after immunosuppressive therapy is achieved in only half of the patients. Therefore, timely detection of LN is vital for initiating prompt therapeutic interventions and improving patient outcomes. Biomarkers have emerged as valuable tools for LN detection and monitoring; however, the complex role of these biomarkers in LN pathogenesis remains unclear. Renal biopsy remains the gold standard for the identification of the histological phenotypes of LN and guides disease management. However, the molecular pathophysiology of specific renal lesions remains poorly understood. In this review, we provide a critical, up-to-date overview of the latest developments in the field of LN biomarkers.

Systemic lupus erythematosus (SLE) is a complex autoimmune disorder characterized by the production of autoreactive B and T cells and cytokines, leading to chronic inflammation affecting multiple organs. SLE is associated with significant complications that substantially increase morbidity and mortality. Given its complex pathogenesis, conventional treatments for SLE often have significant side effects and limited efficacy, necessitating the exploration of novel therapeutic strategies. One promising approach is the use of chimeric antigen receptor (CAR)-T-cell therapy, which has shown remarkable success in treating refractory hematological malignancies. This review provides a comprehensive analysis of the current use of CAR-T-cell therapy in SLE.

Background: In systemic lupus erythematosus (SLE), detection of interferon-β (IFNβ) in B cells was found to be most prominent in patients with high anti-Smith (Sm) and renal disease, but a mechanistic connection was not clear. The objective of the present study is to determine the association of IFNβ in peripheral blood naïve B cells with the histopathological features of lupus nephritis (LN). Methods: The percentage of IFNβ⁺ cells in IgD⁺CD27⁻ naïve CD19⁺ B cells (B cell IFNβ) among peripheral blood mononuclear cells (PBMCs) from 80 SLE patients were analyzed using flow cytometry. Serological and clinical data were collected. The correlations of B cell IFNβ with LN classification and with histopathological findings (light, electron, and immunofluorescence [IF] microscopic analyses for deposition of IgM, IgG, IgA, C1q, and C3) were determined in 23 available biopsy specimens. Results: B cell IFNβ is positively associated with anti-Sm (p = 0.001), anti-DNA (p = 0.013), and LN (p < 0.001) but was negatively associated with oral/nasal ulcer (p = 0.003) and photosensitivity (p = 0.045). B cell IFNβ positively correlated with immune complex (IC) deposit in the glomerular basement membrane (GBM) (p = 0.002) but not in the mesangial (p = 0.107) or tubular region (p = 0.313). Patients with high B cell IFNβ had statistically increased development of the proliferative LN (Classes III, IV and/or V), compared to patients with low B cell IFNβ (p < 0.0001). Histopathological features positively associated with increased B cell IFNβ included active glomerular lesions as determined by fibrocellular crescents (p = 0.023), chronic glomerular lesions indicated by segmental sclerosis (p = 0.033), and a membranous pattern of renal damage indicated by spike/holes (p = 0.015). Conclusion: B cell IFNβ correlates with history of severe LN, glomerular basement membrane (GBM) IC deposition, and anatomical features of both active and chronic glomerular lesions.

Objective: This single-center clinical study identifies clusters of different phenotypes and pathophysiology subtypes of patients with gout and associated comorbidities.Methods: Patients clinically diagnosed with gout were enrolled between January 2018 and December 2019. Hierarchical cluster analyses were performed using clinical data or biological markers, inflammatory markers, and oxidative stress pathway metabolites assayed from serum and plasma samples. Subgroup clusters were compared using ANOVA for continuous data and chi-square tests for categorical data.Results: Hierarchical cluster analysis identified 3 clusters. Cluster 1 (C1; n = 24) comprised dyslipidemia, hypertension, and early-onset gout, without tophi. Cluster 2 (C2; n = 25) comprised hypertension, dyslipidemia, nephrolithiasis, and obesity. Cluster 3 (C3; n = 39) comprised multiple comorbidities and tophi. Post hoc comparisons of data obtained from samples of patients in C1, C2, and C3 revealed significant differences in the levels of oxidative stress and inflammation-related markers, including 3-nitrotyrosine, tumor necrosis factor, C-reactive protein, interleukin (IL) 1β, IL-6, platelet-derived growth factor (PDGF)–AA, and PDGF-BB. Reclustering patients based on all markers as well as on the biological markers that significantly differed among the initial clusters identified similar clusters.Conclusion: Oxidative stress and inflammatory marker levels may affect the development and clinical manifestations (ie, clinical phenotypes) of gout. Measuring oxidative stress and levels of inflammatory cytokines is a potential adjunctive tool and biomarker for early identification and management of gout.

Connective tissue disease-associated pulmonary arterial hypertension (CTD-PAH) is a progressive and high-risk subtype of PAH, with outcomes generally worse than those seen in idiopathic PAH. Early recognition and treatment are essential for improving survival, yet early-stage CTD-PAH remains challenging to identify, particularly for non-specialist clinicians. The 2022 ESC/ERS guidelines introduced several key updates that support an earlier diagnosis and more targeted management. These include a revised echocardiographic threshold for pulmonary hypertension probability (tricuspid regurgitation velocity >2.8 m/s), a lowered hemodynamic definition of PAH (mean pulmonary artery pressure >20 mmHg and pulmonary vascular resistance >2 WU), and a preference for annual screening using the DETECT algorithm in asymptomatic systemic sclerosis (SSc) patients. Additionally, novel therapeutic targets such as the activin/TGF-β pathway have been incorporated into updated treatment algorithms. Although CTD-PAH remains associated with worse outcomes than idiopathic PAH, recent advances in screening, risk assessment, and targeted therapies have begun to improve the trajectory of the disease. Early detection, personalized treatment, and comprehensive care are now key to transforming this high-risk condition into a more manageable one.

Background: Rheumatoid arthritis-associated interstitial lung disease (RA-ILD) is a well-described complication of rheumatoid arthritis (RA). The authors sought to describe the characteristics, treatment strategies, and outcomes of RA-ILD patients at 6 and 12 months. Methods: Patients treated at the medical center between 2010 and 2019 with ICD9 and ICD10 codes for RA and interstitial lung disease (ILD) meeting American College of Rheumatology 1987 or 2010 ACR/European League Against Rheumatism classification criteria were considered for inclusion. The diagnosis of RA-ILD was based on clinical features, pulmonary function testing (PFT), and high-resolution computed tomography (HRCT) findings. Baseline demographics, body mass index , serologic status, tobacco use, PFT and HRCT findings, and RA-ILD treatments at 0, 6, and 12 months were extracted and analyzed. Results: Forty-seven patients diagnosed with RA-ILD were included in this analysis. The median age at diagnosis was 64.7 years, and the median duration of follow-up was 30 months. Thirty-two patients (68.09%) had follow-up data available at 6 months and 27 (57.45%) had follow-up data at 12 months. Twenty-three (48.9%) patients received treatment for RA-ILD. Forty-three (90.6%) and 42 (88.9%) patients exhibited stability/improvement of RA-ILD at 6 and 12 months of follow-up, respectively. Progression of RA-ILD at 6 months was associated with tobacco use (P=.025); however, no specific variable was associated with RA-ILD progression at 12 months. Conclusions: Patients with RA-ILD receiving treatment tend to show improvement or stability in lung disease at 6 and 12 months, although high attrition rate and short follow-up preclude finding of additional factors associated with ILD. Trial registration: Not applicable. Cite this article as: Alduraibi FK, Haigney J, Surmachevska N, Sun D, Osborne JD, Danila MI. Profile of patients with rheumatoid arthritis-associated interstitial lung disease: A single-center. Eur J Rheumatol. 2025, 12(3), 0087, doi: 10.5152/eurjrheum.2025.24087.