Glomerulonephritis

Basics

Description

Syndrome characterized by:
- Hematuria
- Proteinuria
- Red blood cell casts
- Hypertension
- Renal insufficiency
Common pathway of multiple diseases resulting in intraglomerular inflammation and cellular proliferation
Contributing factors:
- Genetics
- Infectious
- Rheumatologic
- Leading to antibody deposition:
  - Antibody attaches to glomerular antigen (native or implanted)
  - Circulating antigen–antibody complex deposited
- Causing an influx and activation of inflammatory mediators:
  - Leukocytes, complement, cytokines
  - Cell-mediated immune mechanisms
Results in glomerular dysfunction
Persistent inflammation that can lead to scarring and permanent damage

Etiology

Postinfectious:
- Poststreptococcal glomerulonephritis (PSGN):
  - Usually occurs 7–21 d after Streptococcal pharyngitis or skin infection, but can occur as late as 6 wk after skin infection
  - Caused when exotoxins released by group A streptococci bind to glomeruli, activating an antibody response
  - Highest prevalence in ages 2–14 and the elderly
  - Male predominance
  - Ranges from asymptomatic hematuria to oliguric renal failure
- Can follow other bacterial, fungal, viral, or parasitic infections
IgA nephropathy (Berger disease):
- Most common in men in the third and fourth decades of life
- Possibly related to increased production of IgA after infection, usually a URI in genetically susceptible individuals
- Henoch–Schönlein purpura (HSP) has IgA nephropathy but affects a younger age and has systemic symptoms
Rapidly progressive glomerulonephritis (RPGN):
- Can destroy renal function in days
- Crescentic deposits in glomeruli destroy function
- Pauci-immune (small vessel vasculitides):
  - Necrotizing glomerulonephritis with no immune deposits
  - Often antineutrophil cytoplasmic antibody (ANCA)-positive
  - Can involve other areas (i.e., lungs, skin)
  - Wegener granulomatosis
  - Microscopic polyangiitis
  - Churg–Strauss syndrome
- Immune complex deposits:
  - Postinfectious
  - Endocarditis associated
  - Systemic disease (i.e., systemic lupus erythematosus [SLE], HSP)
- Anti-glomerular basement membrane (GBM) deposits:
  - Unclear trigger, but may be postinfectious
  - Older patients of age >60
  - Goodpasture disease with pulmonary involvement
Membranoproliferative glomerulonephritis (MPGN):
- Complement deposits in basement membrane
- Hepatitis C
- Non-Hodgkin lymphoma
- Occult infection

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