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Complement 3 Glomerulopathy (C3G) in Native and Posttransplant Kidneys: A Review
Manuel Praga1, Richard J Smith2, Andrew S Bomback3
1Department of Medicine, Nephrology Department, Complutense University, Madrid, Spain.
Summary
Complement 3 glomerulopathy (C3G) is a rare kidney disease driven by complement alternative pathway (AP) overactivation. Emerging therapies targeting AP overactivation show promise for treating C3G in native and transplanted kidneys.
Area of Science:
- Nephrology
- Immunology
- Complement System Biology
Background:
- Complement 3 glomerulopathy (C3G) is a rare kidney disease caused by complement alternative pathway (AP) overactivation.
- C3G leads to glomerular C3 deposition, progressive kidney dysfunction, and kidney failure.
- Both genetic mutations and autoantibodies can drive C3G pathophysiology.
Purpose of the Study:
- To review the current understanding of C3G pathophysiology, prognosis, and treatment.
- To highlight emerging therapies targeting AP overactivation for C3G.
- To provide an update on managing native and posttransplant recurrent C3G.
Main Methods:
- Literature review of C3G pathophysiology, prognosis, and treatment options.
- Analysis of emerging therapeutic strategies targeting the complement AP.
- Synthesis of current knowledge on native and recurrent C3G management.
Main Results:
- C3G involves overactivation of the complement AP, leading to C3 deposition and kidney damage.
- C3G has a high recurrence rate in transplanted kidneys, with poor prognosis.
- Supportive care and terminal complement cascade inhibitors show limited efficacy.
Conclusions:
- Targeting AP overactivation represents a promising therapeutic strategy for C3G.
- Effective management of C3G requires addressing the underlying complement dysregulation.
- Further research into AP-targeted therapies is crucial for improving outcomes in C3G.
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