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Updated: May 13, 2026

Isolation of Glomeruli and In Vivo Labeling of Glomerular Cell Surface Proteins

Isolation of Glomeruli and In Vivo Labeling of Glomerular Cell Surface Proteins

Published on: January 18, 2019

Recent insights into C3 glomerulopathy.

Thomas D Barbour¹, Matthew C Pickering, H Terence Cook

¹Centre for Complement & Inflammation Research (CCIR), Division of Immunology and Inflammation, Department of Medicine, Imperial College London, London W12 0NN, UK.

Nephrology, Dialysis, Transplantation : Official Publication of the European Dialysis and Transplant Association - European Renal Association

|March 13, 2013

Summary

This summary is machine-generated.

C3 glomerulopathy, a group of rare kidney diseases, involves isolated C3 deposits in the glomerulus due to complement alternative pathway dysregulation. Research highlights genetic factors and ongoing therapeutic evaluations for these conditions.

Keywords:

complement dense deposit eculizumab glomerulonephritis kidney

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Area of Science:

Nephrology
Immunology
Genetics

Background:

C3 glomerulopathy is a classification of rare glomerulonephritis characterized by isolated C3 deposits.
Dense deposit disease (DDD), C3 glomerulonephritis (C3GN), and CFHR5 nephropathy are key types within this classification.
A common etiology involves dysregulation of the complement alternative pathway (AP).

Purpose of the Study:

To review the clinical and histological features of C3 glomerulopathy.
To relate these features to underlying molecular mechanisms, emphasizing uncontrolled C3 activation.
To discuss gene testing and therapeutic strategies for C3 glomerulopathy.

Main Methods:

Review of clinical and histological findings in C3 glomerulopathy.
Analysis of molecular mechanisms, including complement alternative pathway dysregulation.
Evaluation of genetic testing methods and ongoing therapeutic trials.

Main Results:

Isolated C3 deposits in the glomerulus are a hallmark histological feature.
Genetic defects and autoantibodies are identified in a proportion of patients.
Uncontrolled C3 activation plays a significant role in pathogenesis.

Conclusions:

C3 glomerulopathy arises from dysregulated complement alternative pathway activation.
Gene testing aids in assessing individuals and families.
Effective therapies are under investigation, but knowledge gaps remain regarding natural history and treatment protocols.