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Glomerulonephritis, Acute

Glomerulonephritis, Acute is a topic covered in the 5-Minute Clinical Consult.

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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 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.
    • Infection-related GN (also postinfectious GN)
    • IgA nephropathy/Henoch-Schönlein purpura (HSP)
    • Antiglomerular basement membrane disease (anti-GBM disease)
    • Antineutrophil cytoplasmic antibody (ANCA)-associated GN
    • Membranoproliferative GN (MPGN)
    • Lupus nephritis
    • Cryoglobulin-associated GN
  • Clinical severity ranges from asymptomatic microscopic or gross hematuria to a rapid loss of kidney function over days to weeks, termed rapidly progressive GN (RPGN).
    • In patients with RPGN, kidney biopsy often demonstrates crescentic GN, which usually warrants urgent and aggressive treatment.

ALERT
Urgent investigation and treatment are required to avoid irreversible loss of kidney function.

Epidemiology

  • Infection-related GN
    • Most commonly manifests after resolution of group A β-hemolytic Streptococcus infection (poststreptococcal)
    • Can also occur as a result of other bacterial infections, such as infective endocarditis or shunt nephritis, or less commonly with viral or parasitic infections
    • Accounts for 80% of acute GN in children
  • IgA nephropathy
    • Most common primary GN in the world
    • Most common in the 2nd and 3rd decades but can occur at any age
    • Incidence differs geographically: Asia > United States
    • Populations of East Asian ancestry are at increased risk for IgA nephropathy, and some genetic factors have been identified.
    • HSP, the form with extrarenal manifestations, can occur at any age but typically occurs in children <10 years old.
  • Anti-GBM disease
    • Can cause Goodpasture disease, a notable cause of the 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
    • Older patients are more commonly affected, although this GN can affect any age group.
  • MPGN
    • May be primary (idiopathic) or secondary to systemic diseases
    • Epidemiology varies depending on the mechanism of injury.
  • Lupus nephritis
    • 30–70% of systemic lupus patients will have renal involvement.
    • Incidence of lupus nephritis is higher among African Americans in comparison to white Caucasian populations.
  • Cryoglobulin-associated vasculitis
    • 80% of cases with hepatitis C virus infection
    • May also be associated with autoimmune disease or dysproteinemia

Etiology and Pathophysiology

  • In general, systemic and/or local immune activation causes glomerular injury.
  • Immune-complex mediated: from antigen–antibody formation and deposition in the kidneys
    • Postinfectious GN: host immune reaction to nephritogenic streptococci strains as a trigger
    • IgA nephropathy: abnormal glycosylation of IgA, leads to its mesangial deposition; etiology poorly understood
    • MPGN: typically secondary to systemic diseases, such as chronic infections (hepatitis C), autoimmune diseases, monoclonal gammopathies, and complement dysregulation
    • Lupus nephritis: autoimmune disease
    • Cryoglobulin-associated GN: inflammation from complexes known as cryoglobulins, named for their property of precipitating as lower temperatures
  • Direct antibody-mediated injury:
    • Anti-GBM disease: caused by autoantibodies that target type IV collagen of basement membranes
  • Pauci-immune GN
    • ANCA-associated GN: autoantibodies against neutrophil granules involved in pathogenesis
  • Alternative complement pathway dysregulation:
    • C3 glomerulopathy: subtype of MPGN with predominant C3 without immunoglobulin staining on immunofluorescence; includes dense deposit disease (DDD) and C3GN

Genetics
Genetic factors are likely to play a role in susceptibility to many of the acute GNs, although these have not been sufficiently defined to be clinically useful in most circumstances.

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.
  • Infection with hepatitis B or C is associated with MPGN.
  • Infection with hepatitis C is a risk factor for developing cryoglobulinemic GN.
  • Mutations in alternate complement pathway genes are associated with increased risk of developing complement-mediated MPGN.

General Prevention

Early detection is paramount.

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Citation

Stephens, Mark B., et al., editors. "Glomerulonephritis, Acute." 5-Minute Clinical Consult, 27th ed., Wolters Kluwer, 2019. 5minute, www.unboundmedicine.com/5minute/view/5-Minute-Clinical-Consult/116246/all/Glomerulonephritis__Acute.
Glomerulonephritis, Acute. In: Stephens MB, Golding J, Baldor RA, et al, eds. 5-Minute Clinical Consult. 27th ed. Wolters Kluwer; 2019. https://www.unboundmedicine.com/5minute/view/5-Minute-Clinical-Consult/116246/all/Glomerulonephritis__Acute. Accessed July 19, 2019.
Glomerulonephritis, Acute. (2019). In Stephens, M. B., Golding, J., Baldor, R. A., & Domino, F. J. (Eds.), 5-Minute Clinical Consult. Available from https://www.unboundmedicine.com/5minute/view/5-Minute-Clinical-Consult/116246/all/Glomerulonephritis__Acute
Glomerulonephritis, Acute [Internet]. In: Stephens MB, Golding J, Baldor RA, Domino FJ, editors. 5-Minute Clinical Consult. Wolters Kluwer; 2019. [cited 2019 July 19]. Available from: https://www.unboundmedicine.com/5minute/view/5-Minute-Clinical-Consult/116246/all/Glomerulonephritis__Acute.
* Article titles in AMA citation format should be in sentence-case
TY - ELEC T1 - Glomerulonephritis, Acute ID - 116246 ED - Stephens,Mark B, ED - Golding,Jeremy, ED - Baldor,Robert A, ED - Domino,Frank J, BT - 5-Minute Clinical Consult, Updating UR - https://www.unboundmedicine.com/5minute/view/5-Minute-Clinical-Consult/116246/all/Glomerulonephritis__Acute PB - Wolters Kluwer ET - 27 DB - 5minute DP - Unbound Medicine ER -