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Glomerulonephritis, Acute

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

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  • 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.

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


  • Infection-related GN
    • Most commonly follows group A β-hemolytic Streptococcus infection (poststreptococcal) but can occur as a result of other bacterial infections, such as infective endocarditis, 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
    • Male > female (2:1)
    • Incidence differs geographically: Asia > United States
    • HSP, the form with extrarenal manifestations, 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 or secondary, as in viral illness (hepatitis B or hepatitis C), rheumatologic disease (lupus, Sjögren syndrome, systemic sclerosis), or dysproteinemia such as monoclonal gammopathy
    • Immunofluorescence aids in determining mechanism of injury (mediated by immune complex formation, monoclonal immunoglobulins, or complement).
  • Lupus nephritis
    • 30–70% of systemic lupus patients will have renal involvement.
    • Several histologic variants but diffuse proliferative GN are the most severe and require urgent treatment.
  • 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: from abnormal glycosylation of IgA, related to genetic and environmental factors
    • MPGN: typically secondary to systemic disease but otherwise idiopathic
    • 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 typically 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

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.
  • Persons of East Asian ancestry are at increased risk for IgA nephropathy, and some genetic factors have been identified.
  • 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 known to be associated with MPGN.
  • Infection with hepatitis C is a risk factor for developing cryoglobulinemic GN.
  • Mutations in alternate complement pathway genes are associated with complement-mediated MPGN.

General Prevention

Early detection is paramount.

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Stephens, Mark B., et al., editors. "Glomerulonephritis, Acute." 5-Minute Clinical Consult, 27th ed., Wolters Kluwer, 2019. Medicine Central, im.unboundmedicine.com/medicine/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://im.unboundmedicine.com/medicine/view/5-Minute-Clinical-Consult/116246/all/Glomerulonephritis__Acute. Accessed April 21, 2019.
Glomerulonephritis, Acute. (2019). In Stephens, M. B., Golding, J., Baldor, R. A., & Domino, F. J. (Eds.), 5-Minute Clinical Consult. Available from https://im.unboundmedicine.com/medicine/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 April 21]. Available from: https://im.unboundmedicine.com/medicine/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://im.unboundmedicine.com/medicine/view/5-Minute-Clinical-Consult/116246/all/Glomerulonephritis__Acute PB - Wolters Kluwer ET - 27 DB - Medicine Central DP - Unbound Medicine ER -