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Published on: June 18, 2020
Eculizumab as a New Treatment for Severe Acute Post-infectious Glomerulonephritis: Two Case Reports
Hassib Chehade1, Gabriella Guzzo2,3,4, Francois Cachat1
1Department of Paediatrics, Lausanne University Hospital, University of Lausanne, Lausanne, Switzerland.
Insights
Acute post-infectious glomerulonephritis (APIGN) can cause severe kidney damage. Eculizumab effectively treated two children with severe APIGN, restoring kidney function and preventing dialysis.
Area of Science:
- Nephrology
- Immunology
- Pediatrics
Background:
- Acute post-infectious glomerulonephritis (APIGN) is a common cause of acute kidney injury in children, potentially leading to chronic kidney disease.
- Pathophysiology of APIGN is not fully understood, but complement system activation, particularly the alternative pathway, is implicated.
- C5 blockade has shown potential therapeutic benefits in APIGN, especially with specific autoantibodies.
Observation:
- Two children with severe APIGN and advanced renal failure were treated with eculizumab.
- The first patient had anuria, low C3, high soluble C5b-9, and a C3 Nephritic Factor (C3Nef) autoantibody.
- The second patient presented with oliguric APIGN and low C3 levels.
Findings:
- Kidney biopsies confirmed APIGN in both cases.
- Eculizumab treatment led to complete recovery of renal function in both children.
- Dialysis was successfully avoided in both treated patients.
Implications:
- Activation of alternative and terminal complement pathways may be a common mechanism in APIGN.
- Eculizumab represents a promising therapeutic option for severe cases of APIGN.
- Further research into complement-targeted therapies for APIGN is warranted.
Abstract:
Acute post-infections glomerulonephritis (APIGN) is a frequent cause of glomerulonephritis and represents the most common cause of acute glomerulonephritis in children. It can evolve to severe acute renal failure and chronic kidney disease or even end-stage kidney disease. The precise pathophysiological mechanisms of APIGN are still incompletely understood. The implication of the alternative complement pathway and the potential benefits of C5 blockade have been recently highlighted, in particular in the presence of a C3 Nephritic Factor (C3Nef), anti-Factor B or H autoantibodies. We report two children with severe APIGN, successfully treated with eculizumab. The first patient presented a severe form of APIGN with advanced renal failure and anuria, associated with a decreased level of C3 and an increased level of soluble C5b-9, in the presence of a C3NeF autoantibody. The second case had a severe oliguric APIGN associated with low C3 level. Kidney biopsy confirmed the diagnosis of APIGN in both cases. Eculizumab allowed full renal function recovery and the avoidance of dialysis in both cases. In conclusion, the alternative and terminal complement pathways activation might be common in PIGN, and in severe cases, eculizumab might help.
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