Glomerulonephritis (GN) caused by rheumatoid arthritis may manifest as various pathological types; however, to the best of our knowledge, rheumatoid arthritis-associated complement 3 (C3)-GN has not been reported by any previous studies. C3GN is caused by dysregulation of the alternative pathway of complements, which is completely different from activation of the classic pathway of a typical autoimmune disease to cause renal damage. The present study describes a patient with a history of rheumatoid arthritis for 18 years, who presented with edema, proteinuria, hematuria, hypoproteinemia and a hypocomplementemic state. The pathological diagnosis was C3GN based on histological examination of a renal biopsy specimen. Hormone treatment on its own appeared to be effective and achieved complete clinical remission, while the follow-up of the condition remained stable.
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http://dx.doi.org/10.3892/etm.2018.6476 | DOI Listing |
Naunyn Schmiedebergs Arch Pharmacol
January 2025
Pharmacology Department, Medical and Clinical Research Institute, National Research Centre, Dokki, Cairo, 12622, Egypt.
Rheumatoid arthritis (RA) is one of the most common systemic autoimmune inflammatory diseases, with a progressive etiology that results in serious complications and a higher chance of early death. Visfatin, an adipokine, is correlated with disease pathologic features and becomes a key biomarker and therapeutic target for RA. This study aimed to evaluate the anti-arthritic activity of metformin (an antidiabetic drug with anti-inflammatory activities) and methotrexate (the first choice for disease-modifying antirheumatic drugs in RA, with diverse adverse effects) in complete Freund's adjuvant (CFA)-induced arthritis in female rats.
View Article and Find Full Text PDFFront Immunol
January 2025
The Catholic University of Korea and Ho-Youn Kim's Clinic for Arthritis Rheumatism, Seoul, Republic of Korea.
Introduction: Our aim was to investigate the insufficiently understood differences in the immune system between anti-citrullinated peptide antibody (ACPA)-positive (ACPA) and ACPA-negative (ACPA) early rheumatoid arthritis (eRA) patients.
Methods: We performed multiple cytokine assays using sera from drug-naïve ACPA and ACPA eRA patients. Additionally, we conducted single-cell RNA sequencing of CD45 cells from peripheral blood samples to analyze and compare the distribution and functional characteristics of the cell subsets based on the ACPA status.
Front Immunol
January 2025
Rheumatology Unit, Department of Medicine and Surgery, University of Perugia, Perugia, Italy.
This pilot study investigates distinctive features within the nail-enthesis complex among Psoriatic arthritis (PsA), Psoriasis (PSO), Rheumatoid Arthrit is (RA), and Healthy Control (HC) groups, utilizing a combined approach of ultrasound (US) and nailfold videocapillaroscopy (NVC). Clinical assessments and comprehensive US and NVC evaluations of the nail-enthesis complex were conducted on 72 subjects (18 PsA, 16 PSO, 19 RA, 19 HC). Unsupervised clustering models and factor analysis were employed to identify patterns and interrelationships between US and NVC parameters.
View Article and Find Full Text PDFFront Immunol
January 2025
Department of Odontology, Section for Molecular Periodontology, Umeå University, Umeå, Sweden.
Introduction: Periodontitis is associated with rheumatoid arthritis (RA). One hypothesis posits that this connection arises from the formation of autoantibodies against citrullinated proteins (ACPA) in inflamed gums, possibly triggered by . We previously demonstrated an increased antibody response to arginine gingipains (anti-Rgp IgG), not only in individuals with severe periodontitis compared to controls, but in RA versus controls, with an association to ACPA.
View Article and Find Full Text PDFJ Transl Autoimmun
June 2025
Medical University of Vienna, Borschkegasse 8a, 1090, Vienna, Austria.
Autoimmune rheumatic diseases (ARDs) are a heterogeneous group of conditions characterized by excessive and misdirected immune responses against the body's own musculoskeletal tissues. Their exact aetiology remains unclear, with genetic, demographic, behavioural and environmental factors implicated in disease onset. One prominent hypothesis for the initial breach of immune tolerance (leading to autoimmunity) is molecular mimicry, which describes structural or sequence similarities between human and microbial proteins (mimotopes).
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