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Assessment of Kidney Function in Mouse Models of Glomerular Disease
Published on: June 30, 2018
Complement in glomerular diseases
Ying Tan1,2,3,4, Ming-Hui Zhao1,2,3,4,5
1Renal Division, Department of Medicine, Peking University First Hospital, Beijing, China.
Insights
Complement activation is crucial in various glomerulonephritis, including lupus nephritis and vasculitis. Targeting the complement system offers potential new therapies for these kidney diseases.
Area of Science:
- Nephrology
- Immunology
- Pathophysiology
Background:
- Complement activation is implicated in the pathogenesis of numerous glomerulonephritis conditions.
- It plays a direct role in thrombotic microangiopathy and C3 glomerulopathy.
- It also contributes significantly to lupus nephritis and anti-neutrophil cytoplasmic antibody-associated vasculitis.
Purpose of the Study:
- To elucidate the role of complement activation in the pathogenesis of various glomerulonephritis.
- To explore the potential of complement system as a therapeutic target.
Main Methods:
- Review of recent studies on complement activation in glomerulonephritis.
- Analysis of the pathogenic mechanisms involved.
Main Results:
- Complement activation is a key factor in thrombotic microangiopathy, C3 glomerulopathy, lupus nephritis, and anti-neutrophil cytoplasmic antibody-associated vasculitis.
- Emerging evidence suggests a role in immunoglobulin A nephropathy and focal segmental glomerulosclerosis.
- Monoclonal immunoglobulins can interfere with complement, leading to glomerulonephritis.
Conclusions:
- Understanding complement's role in glomerulonephritis is vital for identifying new therapeutic strategies.
- Targeting the complement system presents a promising avenue for treating these kidney diseases.
Abstract:
Complement activation has been identified to play a vital role in the pathogenesis of many glomerulonephritis, either as direct complement activation-driven factor in thrombotic microangiopathy and C3 glomerulopathy, and/or as an important contributor in lupus nephritis and anti-neutrophil cytoplasmic antibody-associated vasculitis. Recent studies indicated that complement activation may also play roles in the pathogenesis of immunoglobulin A nephropathy and focal segmental glomerulosclerosis. Interestingly, monoclonal immunoglobulins/light chains from patients with monoclonal gammopathy may interfere with complement activation and thus indirectly result in complement-mediated glomerulonephritis. Understanding of the pathogenic roles of complement activation in various glomerulonephritis will facilitate the identification of potential novel therapeutic targets in complement system.
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