Related Experiment Video

Updated: Dec 20, 2025

Analyses of Proteinuria, Renal Infiltration of Leukocytes, and Renal Deposition of Proteins in Lupus-prone MRL/lpr Mice
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Treatment-resistant nephrotic syndrome in dense deposit disease: complement-mediated glomerular capillary wall

Caroline Duineveld1, Eric J Steenbergen2, Andrew S Bomback3

  • 1Department of Nephrology, Radboud University Medical Center, PO BOX 9101, 6500 HB, Nijmegen, Netherlands. caroline.duineveld@radboudumc.nl.

Pediatric Nephrology (Berlin, Germany)
|May 25, 2020
PubMed

Insights

Dense deposit disease (DDD), a C3 glomerulopathy, involves abnormal complement regulation. Two distinct pathways may cause kidney injury in DDD, one C5-independent and one C5-dependent.

Area of Science:

  • Nephrology
  • Complement System Biology
  • Glomerular Diseases

Background:

  • C3 glomerulopathies (C3G) are glomerular diseases stemming from dysregulated complement activation.
  • Dense deposit disease (DDD) is a C3G subtype characterized by electron-dense deposits in the glomerular basement membrane.
  • DDD patients exhibit hematuria, proteinuria, and kidney dysfunction, with biopsies showing inflammation and proliferation.
Abstract

Keywords:
C3 glomerulopathyDense deposit diseaseNephrotic syndromePodocyte

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