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Chapter 28-4: Acute Glomerulonephritis (GN)

Ernie L. Esquivel

Acute GN is caused by 1 of several disease processes, all of which involve immunologically mediated proliferative GN. The classic clinical “nephritic syndrome” consists of the acute onset of hematuria (with red cell casts), proteinuria, elevated creatinine, hypertension, and edema. See Table 28-10 for an overview of etiologies and Table 28-11 for the role of complement testing in glomerular diseases.

Table 28-10.Causes of acute glomerulonephritis (GN).
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Table 28-10. Causes of acute glomerulonephritis (GN).
Type Diseases Serologic Markers Highlights
Anti-GBM disease Goodpasture syndrome

100% anti-GBM antibody +

20% ANCA +

C3 normal

Presents with abrupt onset of oliguria, hematuria, and kidney dysfunction

Bimodal age distribution: young male smokers present with a pulmonary-renal syndrome, and women in their 50s to 60s present with kidney disease

ESRD develops in 30%
Pauci-immune GN Microscopic polyangiitis

50–75% pANCA +

Anti-GBM (–)

C3 normal

Small- and medium-vessel vasculitis

Renal involvement in 80%; pulmonary involvement in 20–55%

Presents with constitutional symptoms, hematuria, and sometimes nephrotic range proteinuria

10–46% require dialysis
Granulomatosis with polyangiitis

> 90% cANCA +

Anti-GBM (–)

C3 normal

Upper and lower respiratory tract and GN

Can be indolent prior to the onset of systemic vasculitis

Seen primarily in white men and women in the fifth decade

33–50% have eye disease
Eosinophilic granulomatosis with polyangiitis (formerly Churg-Strauss syndrome)

65% pANCA +

Anti-GBM (–)

C3 normal

IgE elevated

Asthma, eosinophilia, granulomatous vasculitis, and tissue eosinophilic infiltration

Occurs in patients in their 30s and 40s

Renal involvement typically mild
Immune-complex GN SLE, poststreptococcal, membranoproliferative, endocarditis, visceral abscesses, shunt nephritis

Low C3

Anti-GBM (–)

ANCA (–)

Post-streptococcal GN is the most common postinfectious GN, occurring 10–14 days after infection with a nephritogenic strain of group A beta-hemolytic streptococci

Supportive treatment only; residual renal impairment rare
Cryoglobulinemia

Low C4

Anti-GBM (–)

ANCA (–)

Typically associated with chronic infection such as hepatitis C or hematologic malignancy

Petechial rash, livedo reticularis, arthritis, systemic involvement
IgA nephropathy, Henoch-Schönlein purpura, fibrillary GN

Normal C3, C4

Anti-GBM (–)

ANCA (–)

IgA nephropathy is the most common cause of GN

Purpura and GI symptoms seen in Henoch-Schönlein purpura

ANCA, anti-neutrophilic cytoplasmic antibody; cANCA, cytoplasmic anti-neutrophilic cytoplasmic antibody; ESRD, end-stage renal disease; GBM, glomerular basement membrane; pANCA, perinuclear anti-neutrophilic cytoplasmic antibody; SLE, systemic lupus erythematosus.

Table 28-11.Hypocomplementemia in glomerular diseases.
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Table 28-11. Hypocomplementemia in glomerular diseases.
Glomerular diseases Complement changes Pathway affected

Lupus nephritis

Mixed essential cryoglobulinemia

 C3 ↓, C4 ↓, CH50 ↓ Classical pathway activation
Membranoproliferative GN, Type I + C4 nephritic factor  
Poststreptococcal GN Endocarditis, Hepatitis B, Hemolytic uremic syndrome C3 ↓, C4 nl, CH50 ↓ Alternative pathway activation
Membranoproliferative GN, Type II + C3 nephritic factor  
  Acquired Reduced complement synthesis
  Hereditary  
Lupus nephritis C2 deficiency  
Familial hemolytic uremic syndrome Factor H deficiency  

GN, glomerulonephritis; nl, normal.

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