Glomerulonephritis, Acute

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Basics

Description

  • Acute glomerulonephritis (GN) is an inflammatory process involving the glomerulus of the kidney, resulting in a clinical syndrome consisting of sudden-onset of hematuria, proteinuria, and renal insufficiency, often in association with hypertension and edema.
  • Acute GN may be caused by primary glomerular disease or secondary to systemic disease.
  • Clinical severity ranges from self-limited asymptomatic microscopic or gross hematuria to a rapidly progressive loss of kidney function over days to weeks, termed rapidly progressive GN (RPGN).
ALERT
Urgent investigation and treatment are required to avoid irreversible loss of kidney function.

Epidemiology

  • Infection-related GN
    • Postinfectious GN most commonly manifests after resolution of group A β-hemolytic Streptococcus infection.
    • Can also occur as a result of other bacterial infections, such as infective endocarditis, VP shunt nephritis, or less commonly with viral, helminthic, or parasitic infections
  • IgA nephropathy
    • Most common primary GN in the world
    • Most common in the 2nd and 3rd decades
    • Incidence differs geographically: Asia > United States
    • HSP, the form with extrarenal manifestations, typically occurs in children <10 years old.
  • Anti-GBM disease
    • Goodpasture syndrome: a notable cause of pulmonary–renal syndrome
    • Peak distribution in 3rd and 6th decades
  • ANCA-associated GN
    • Often has a relapsing and remitting course
    • Four disease presentations:
      • Granulomatosis with polyangiitis (GPA), formerly Wegener granulomatosis
      • Microscopic polyangiitis (MPA)
      • Isolated pauci-immune GN—when isolated to kidneys
      • Eosinophilic GPA, formerly Churg-Strauss disease—GN relatively common but renal involvement rarely severe
  • MPGN
    • May be primary or secondary to systemic diseases
    • Epidemiology varies depending on the mechanism of injury and is more often a subacute or chronic presentation
  • Lupus nephritis
    • About 60% of systemic lupus patients will have renal involvement.
    • Incidence of lupus nephritis is higher among black and Hispanic populations in comparison to white populations.
    • 6 classes
      • Minimal mesangial disease
      • Mesangial proliferation
      • Focal proliferative (active) and/or sclerosing (chronic) disease
      • Diffuse segmental or global proliferative (active) and/or sclerosing (chronic) disease
      • Membranous lupus nephritis
      • Advanced sclerosis lupus nephritis
  • Cryoglobulin-associated vasculitis
    • 80% of cases with hepatitis C virus (HCV) infection
    • May also be associated with autoimmune disease or dysproteinemia

Prevalence

  • In patients >65 years of age, with an average age of 75 years, about 1.2% of people are affected by either primary or secondary GN.
  • In patients between the ages of 37 and 65 years of age, GN was much less commonly seen, with only about 0.12% of people affected by either primary or secondary GN (1).
  • The incidence and prevalence of GN in children is unknown. Acute postinfectious GN is the most common type but has diminished over the years.

Etiology and Pathophysiology

  • Systemic and/or local immune activation causes glomerular injury.
  • Immune-complex mediated: antigen–antibody formation and deposition in the kidneys. Immune complexes are seen on immunofluorescence.
    • Postinfectious GN
    • IgA nephropathy
    • MPGN
      • Cryoglobulin-associated GN
    • Lupus nephritis
  • Direct antibody-mediated injury, linear staining on immunofluorescence
    • Anti-GBM disease
  • Pauci-immune GN, not seen on immunofluorescence staining
    • ANCA-associated GN
  • Alternative complement pathway dysregulation
    • C3 glomerulopathy

Risk Factors

  • Epidemics of nephritogenic strains of streptococci are triggers for postinfectious GN.
  • Anti-GBM disease has been associated with prior pulmonary injury and inhalation exposures, such as hydrocarbon solvents.
  • ANCA-associated GN may be drug induced (e.g., hydralazine, levamisole-contaminated cocaine) and is also associated with environmental exposures such as silica.
  • Hepatitis B is associated with MPGN. Hepatitis C is associated with both MPGN and cryoglobulinemic GN.

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Basics

Description

  • Acute glomerulonephritis (GN) is an inflammatory process involving the glomerulus of the kidney, resulting in a clinical syndrome consisting of sudden-onset of hematuria, proteinuria, and renal insufficiency, often in association with hypertension and edema.
  • Acute GN may be caused by primary glomerular disease or secondary to systemic disease.
  • Clinical severity ranges from self-limited asymptomatic microscopic or gross hematuria to a rapidly progressive loss of kidney function over days to weeks, termed rapidly progressive GN (RPGN).
ALERT
Urgent investigation and treatment are required to avoid irreversible loss of kidney function.

Epidemiology

  • Infection-related GN
    • Postinfectious GN most commonly manifests after resolution of group A β-hemolytic Streptococcus infection.
    • Can also occur as a result of other bacterial infections, such as infective endocarditis, VP shunt nephritis, or less commonly with viral, helminthic, or parasitic infections
  • IgA nephropathy
    • Most common primary GN in the world
    • Most common in the 2nd and 3rd decades
    • Incidence differs geographically: Asia > United States
    • HSP, the form with extrarenal manifestations, typically occurs in children <10 years old.
  • Anti-GBM disease
    • Goodpasture syndrome: a notable cause of pulmonary–renal syndrome
    • Peak distribution in 3rd and 6th decades
  • ANCA-associated GN
    • Often has a relapsing and remitting course
    • Four disease presentations:
      • Granulomatosis with polyangiitis (GPA), formerly Wegener granulomatosis
      • Microscopic polyangiitis (MPA)
      • Isolated pauci-immune GN—when isolated to kidneys
      • Eosinophilic GPA, formerly Churg-Strauss disease—GN relatively common but renal involvement rarely severe
  • MPGN
    • May be primary or secondary to systemic diseases
    • Epidemiology varies depending on the mechanism of injury and is more often a subacute or chronic presentation
  • Lupus nephritis
    • About 60% of systemic lupus patients will have renal involvement.
    • Incidence of lupus nephritis is higher among black and Hispanic populations in comparison to white populations.
    • 6 classes
      • Minimal mesangial disease
      • Mesangial proliferation
      • Focal proliferative (active) and/or sclerosing (chronic) disease
      • Diffuse segmental or global proliferative (active) and/or sclerosing (chronic) disease
      • Membranous lupus nephritis
      • Advanced sclerosis lupus nephritis
  • Cryoglobulin-associated vasculitis
    • 80% of cases with hepatitis C virus (HCV) infection
    • May also be associated with autoimmune disease or dysproteinemia

Prevalence

  • In patients >65 years of age, with an average age of 75 years, about 1.2% of people are affected by either primary or secondary GN.
  • In patients between the ages of 37 and 65 years of age, GN was much less commonly seen, with only about 0.12% of people affected by either primary or secondary GN (1).
  • The incidence and prevalence of GN in children is unknown. Acute postinfectious GN is the most common type but has diminished over the years.

Etiology and Pathophysiology

  • Systemic and/or local immune activation causes glomerular injury.
  • Immune-complex mediated: antigen–antibody formation and deposition in the kidneys. Immune complexes are seen on immunofluorescence.
    • Postinfectious GN
    • IgA nephropathy
    • MPGN
      • Cryoglobulin-associated GN
    • Lupus nephritis
  • Direct antibody-mediated injury, linear staining on immunofluorescence
    • Anti-GBM disease
  • Pauci-immune GN, not seen on immunofluorescence staining
    • ANCA-associated GN
  • Alternative complement pathway dysregulation
    • C3 glomerulopathy

Risk Factors

  • Epidemics of nephritogenic strains of streptococci are triggers for postinfectious GN.
  • Anti-GBM disease has been associated with prior pulmonary injury and inhalation exposures, such as hydrocarbon solvents.
  • ANCA-associated GN may be drug induced (e.g., hydralazine, levamisole-contaminated cocaine) and is also associated with environmental exposures such as silica.
  • Hepatitis B is associated with MPGN. Hepatitis C is associated with both MPGN and cryoglobulinemic GN.

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