Complement 3 glomerulonephritis in rheumatoid arthritis: A case report and follow‑up

Abstract

Abstract. 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.

C3 glomerulonephritis and systemic lupus erythematosus: A report of a patient treated with eculizumab and review of the literature

“…A few previous studies have reported the coexistence of C3GN in the setting of autoimmune diseases, including patients with SLE or with SLEassociated autoantibodies, [15][16][17] ANCA-associated vasculitis, 19 rheumatoid arthritis and autoimmune thyroiditis. 20 These findings suggest the presence of a subgroup of patients whose C3GN may be related to autoimmunity. 15 The presence of C3NeF, identified in approximately 50% of patients with C3GN, indicates the existence of autoantibodies against C3 convertase that could stabilize the complex and cause persistent activation of the alternative complement pathway 21 ; however, our patient tested negative.…”