Rapidly progressive glomerulonephritis classification

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

Classification

RPGN is classified on the basis of the cause of crescent formation resulting from glomerular injury .[1][2].

Type I

  • Type I RPGN is characterized by the presence of autoantibodies directed against the glomerular basement membrane (GBM)[3].
  • Type I also known as anti-GBM glomerulonephritis.
  • The antibodies formed are known as anticollagen antibodies and react against type IV collagen of GBM.[4]
  • The antibodies can be produced by a stimulus such as viral URTI that exposes alveolar collagen membrane or it can be idiopathic.
  • The antibodies formed can act against alveolar membrane and lungs get involved in some cases such as in goodpasture syndrome.

Type II

Type III

  • Type III RPGN is also known as pauci immune RPGN[4].
  • There are no anti GBM antibodies or no immune complexes involved.
  • It is further classified into 2 types:
    • Immunogenic - ANCA positive
    • Non immunogenic- ANCA negative/ Idiopathic
  • ANCAs cause the release of lytic enzymes from neutrophils that damage the GBM.
  • Systemic vasculitis is present in most of the cases but some occur without systemic involvement and only renal findings maybe present.
  • Examples include

References

  1. Couser WG (1988). "Rapidly progressive glomerulonephritis: classification, pathogenetic mechanisms, and therapy". Am J Kidney Dis. 11 (6): 449–64. PMID 3287904.
  2. Couser WG (1998). "Pathogenesis of glomerular damage in glomerulonephritis". Nephrol Dial Transplant. 13 Suppl 1: 10–5. PMID 9507491.
  3. Heeringa P, Brouwer E, Klok PA, Huitema MG, van den Born J, Weening JJ; et al. (1996). "Autoantibodies to myeloperoxidase aggravate mild anti-glomerular-basement-membrane-mediated glomerular injury in the rat". Am J Pathol. 149 (5): 1695–706. PMC 1865281. PMID 8909258.
  4. 4.0 4.1 Cotran, Ramzi S.; Kumar, Vinay; Fausto, Nelson; Nelso Fausto; Robbins, Stanley L.; Abbas, Abul K. (2005). Robbins and Cotran pathologic basis of disease. St. Louis, MO: Elsevier Saunders. pp. pp976–8. ISBN 0-7216-0187-1.