Is C3 GN nephrotic or nepritic?

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C3 GN: Nephritic Pattern (with variable nephrotic features)

C3 glomerulonephritis (C3 GN) is primarily a nephritic syndrome, but it can present across a spectrum. Here is the breakdown:

Primary Presentation: Nephritic

The classic clinical features of C3 GN are:
  • Hematuria (micro- or macrohematuria) - the dominant feature
  • Hypertension
  • Azotemia (reduced kidney function)
  • Proteinuria (usually sub-nephrotic)
  • Low C3, normal C4 (alternative complement pathway activation)
This is a nephritic picture because the hallmark is hematuria + hypertension + reduced GFR, driven by glomerular inflammation.

Can Also Have Nephrotic Overlap

From the textbooks (Comprehensive Clinical Nephrology 7th Ed. and Brenner & Rector's The Kidney):
"Patients with C3 glomerulonephritis... can present with hypertension, azotemia, hematuria, and proteinuria, with or without nephrotic syndrome."
  • In a French series, 27% of C3 GN patients had full nephrotic syndrome at presentation
  • Two-thirds had microhematuria (nephritic)
  • One-third had hypertension (nephritic)

Why It's Classified as Nephritic

C3 GN falls under the MPGN pattern of injury (membranoproliferative glomerulonephritis). MPGN is the classic "mixed" pattern - but it is primarily categorized as nephritic in most classification systems because:
  1. Hematuria and GFR reduction predominate
  2. The mechanism is complement-mediated inflammation (not podocyte injury, which drives nephrotic)
  3. Crescents can form (severe nephritic feature)

Quick Summary Table

FeatureC3 GN
HematuriaVery common (nephritic)
HypertensionCommon (nephritic)
AzotemiaCommon (nephritic)
ProteinuriaVariable
Full nephrotic syndrome~27% of cases
C3 levelOften low
C4 levelNormal (alternative pathway)
ClassificationNephritic (MPGN pattern)
Bottom line: C3 GN = nephritic. About 1 in 4 patients can additionally develop nephrotic-range proteinuria, making it a "mixed" presentation in some, but the primary classification is nephritic due to its MPGN histology and complement-driven inflammatory mechanism.
  • Brenner and Rector's The Kidney, p. 1377
  • Comprehensive Clinical Nephrology, 7th Ed., p. 325
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