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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
Insights
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.
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.
Abstract:
We report the case of a 63-year-old man who presented with acute kidney injury, active urine sediment, nephrotic syndrome, and hypocomplementemia after a recent report of a sore throat. Kidney biopsy showed diffuse proliferative and exudative glomerulonephritis with C3-dominant staining by immunofluorescence. Taken together, clinical and pathologic findings were most suggestive of acute postinfectious glomerulonephritis, although the history of full nephrotic syndrome, presence of segmental membranoproliferative features, and absence of classic subepithelial hump-shaped deposits were unusual for this condition. Three months after the initial biopsy, the patient continued to have hypocomplementemia and nephrotic syndrome, prompting a repeated kidney biopsy that showed findings most consistent with C3 glomerulopathy. C3 glomerulopathy is a proliferative pattern of glomerulonephritis characterized by complement deposits that stain solely or dominantly for C3. A subset of cases of C3 glomerulopathy have features that overlap extensively with acute postinfectious glomerulonephritis. Clinicians and pathologists should be aware of the similar findings seen in these 2 conditions.
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