Glomerulonephritis

Glomerulonephritis is a topic covered in the 5-Minute Emergency Consult.

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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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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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