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Related Experiment Video

Updated: May 11, 2026

Analyses of Proteinuria, Renal Infiltration of Leukocytes, and Renal Deposition of Proteins in Lupus-prone MRL/lpr Mice

Analyses of Proteinuria, Renal Infiltration of Leukocytes, and Renal Deposition of Proteins in Lupus-prone MRL/lpr Mice

Published on: June 8, 2022

Eculizumab and recurrent C3 glomerulonephritis.

Sevgi Gurkan¹, Billie Fyfe, Lynne Weiss

¹Department of Pediatrics, Division of Pediatric Nephrology, UMDNJ-Robert Wood Johnson Medical School, New Brunswick, NJ, USA. gurkanse@umdnj.edu

Pediatric Nephrology (Berlin, Germany)

|May 22, 2013

Summary

Eculizumab partially treated C3 glomerulonephritis (C3G) in a kidney transplant patient by inhibiting the terminal complement cascade. However, alternative pathway dysregulation persisted, showing eculizumab alone is insufficient for C3G control.

Related Experiment Videos

Last Updated: May 11, 2026

Analyses of Proteinuria, Renal Infiltration of Leukocytes, and Renal Deposition of Proteins in Lupus-prone MRL/lpr Mice

Analyses of Proteinuria, Renal Infiltration of Leukocytes, and Renal Deposition of Proteins in Lupus-prone MRL/lpr Mice

Published on: June 8, 2022

Area of Science:

Nephrology
Immunology
Complement System Biology

Background:

C3 glomerulopathies (C3G) are characterized by alternative complement pathway hyperactivity.
Eculizumab, a C5 inhibitor, shows potential in managing C3G by preventing membrane attack complex formation.

Observation:

A single patient with dense deposit disease and C3 glomerulonephritis allograft recurrence received eculizumab for one year.
The patient exhibited C3 nephritic factors and elevated soluble membrane attack complex (sMAC) levels.
Proteinuria initially decreased but returned to baseline; serum creatinine remained stable, while biopsies showed disease progression.

Findings:

Eculizumab normalized sMAC levels, indicating effective terminal complement cascade inhibition.
Despite blocking the terminal cascade, alternative complement pathway dysregulation persisted.
The patient experienced only a partial response, with disease progression evident on repeat biopsies.

Implications:

Eculizumab monotherapy may not be sufficient to control C3G due to persistent alternative pathway dysregulation.
Further research is needed to develop more comprehensive anticomplement therapies for C3G.
Targeting both terminal and alternative complement pathways may be necessary for effective C3G treatment.