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Related Experiment Video

Updated: May 20, 2026

Analyses of Proteinuria, Renal Infiltration of Leukocytes, and Renal Deposition of Proteins in Lupus-prone MRL/lpr Mice
09:43

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

Published on: June 8, 2022

C3 glomerulopathy masquerading as acute postinfectious glomerulonephritis.

Gagangeet Sandhu1, Anip Bansal, Aditi Ranade

  • 1Division of Nephrology, Department of Medicine, St. Luke's-Roosevelt Hospital Center, Columbia University College of Physicians & Surgeons, New York, NY, USA. gsandhu@chpnet.org

American Journal of Kidney Diseases : the Official Journal of the National Kidney Foundation
|July 10, 2012
PubMed
Summary

This case study highlights C3 glomerulopathy, a kidney disease mimicking post-infectious glomerulonephritis. Early diagnosis is crucial as findings can overlap significantly between these conditions.

Related Experiment Videos

Last Updated: May 20, 2026

Analyses of Proteinuria, Renal Infiltration of Leukocytes, and Renal Deposition of Proteins in Lupus-prone MRL/lpr Mice
09:43

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
  • Pathology

Background:

  • Acute kidney injury, nephrotic syndrome, and hypocomplementemia can indicate glomerular disease.
  • Post-infectious glomerulonephritis (PIGN) typically follows infections but can present atypically.

Observation:

  • A 63-year-old man presented with symptoms suggestive of PIGN, including active urine sediment and hypocomplementemia.
  • Initial kidney biopsy showed diffuse proliferative glomerulonephritis with C3-dominant staining, consistent with PIGN but with unusual features.
  • Persistent nephrotic syndrome and hypocomplementemia led to a repeat biopsy revealing C3 glomerulopathy.

Findings:

  • C3 glomerulopathy is characterized by isolated or dominant C3 complement deposition in glomeruli.
  • This case demonstrated overlapping features between PIGN and C3 glomerulopathy.
  • The patient's presentation evolved from suspected PIGN to confirmed C3 glomerulopathy over three months.

Implications:

  • Clinicians and pathologists must consider C3 glomerulopathy in atypical PIGN presentations.
  • Recognizing overlapping features is essential for accurate diagnosis and management of complement-mediated kidney diseases.
  • Further research is needed to differentiate and manage these complex glomerular conditions.