C3 Glomerulonephritis Associated with Monoclonal Gammopathy

Zhang, L.H.; Chen, Zhi; Xu, Feng; Zhang, T.; Zhang, H.T.; Ge, Yongchun; Yi-jie, Zhou; Zeng, Caihong; Hu, Wenrui; Liu, Z.H.; Tang, Zheng

doi:10.1016/j.hkjn.2015.09.010

Cited by 1 publication

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“…C3GN caused by congenital defects refers to a genetic abnormality or gene mutation in the alternative pathway of complements that causes excessive activation (2). Studies have indicated that monoclonal immunoglobulinopathies may also activate the alternative pathway of complements and thus induce C3GN (3,4). In addition, a study by Alexander et al (5) on C3GN and autoimmune disease suggests that an autoimmune milieu may serve as a trigger for the development of C3GN in patients who carry C3 glomerulopathy-associated risk alleles by leading to dysregulation of the alternative pathway of complements.…”

Section: Introductionmentioning

confidence: 99%

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

Wang

Han

et al. 2018

Exp Ther Med

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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.

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Section: Introductionmentioning

confidence: 99%