Membranoproliferative glomerulonephritis pathophysiology: Difference between revisions

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{{Membranoproliferative glomerulonephritis}}
{{Membranoproliferative glomerulonephritis}}
{{CMG}}{{APM}} {{AE}} {{OO}}.Nazia Fuad, M.D
{{CMG}}{{APM}} {{AE}} {{OO}},{{N.F}}
==Overview:==
==Overview:==
MPGN membrano proliferative glomerulonephritis, also known as mesangiocapillary glomerulonephritis, It is a [[glomerular]] injury on light [[microscopy]] that is characterized by [[mesangial hypercellularity]], endocapillary [[proliferation]], and double-contour formation along the glomerular [[capillary]] walls. "MPGN"  includes two characteristic histologic changes:Thickened [[glomerular basement membrane]] (GBM) due to deposition of [[immune complexes]] and/or complement factors, intrusion of the [[Mesangial cell|mesangial cells]] and other cellular elements between the [[glomerular basement membrane]] and the [[endothelial cells]], and new basement membrane formation. [[Mesangial cell|Mesangial]] and endocapillary cellularity is increased resulting in [[lobular]] appearance of the glomerular tuft. Proliferation of mesangial cells and circulating [[monocytes]] results in increased cellularity.Two mechanisms are involved in the pathogenesis of MPGN,Immune complex deposition leading to activation of [[Complement (biology)|complement]] (immune complex-mediated) and dysregulation and persistent activation of the [[alternative complement pathway]].
MPGN membrano proliferative glomerulonephritis, also known as mesangiocapillary glomerulonephritis, is a [[glomerular]] injury on light [[microscopy]] that is characterized by [[mesangial hypercellularity]], endocapillary [[proliferation]], and double-contour formation along the glomerular [[capillary]] walls. "MPGN"  includes two characteristic histologic changes:Thickened [[glomerular basement membrane]] (GBM) due to deposition of [[immune complexes]] and/or complement factors, intrusion of the [[Mesangial cell|mesangial cells]] and other cellular elements between the [[glomerular basement membrane]] and the [[endothelial cells]], and new basement membrane formation. [[Mesangial cell|Mesangial]] and endocapillary cellularity is increased resulting in [[lobular]] appearance of the glomerular tuft. Proliferation of mesangial cells and circulating [[monocytes]] results in increased cellularity.Two mechanisms are involved in the pathogenesis of MPGN,Immune complex deposition leading to activation of [[Complement (biology)|complement]] (immune complex-mediated) and dysregulation and persistent activation of the [[alternative complement pathway]].


==Pathophysiology==
==Pathophysiology==

Latest revision as of 18:07, 29 July 2018

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Ali Poyan Mehr, M.D. [2] Associate Editor(s)-in-Chief: Olufunmilola Olubukola M.D.[3],Nazia Fuad M.D.

Overview:

MPGN membrano proliferative glomerulonephritis, also known as mesangiocapillary glomerulonephritis, is a glomerular injury on light microscopy that is characterized by mesangial hypercellularity, endocapillary proliferation, and double-contour formation along the glomerular capillary walls. "MPGN" includes two characteristic histologic changes:Thickened glomerular basement membrane (GBM) due to deposition of immune complexes and/or complement factors, intrusion of the mesangial cells and other cellular elements between the glomerular basement membrane and the endothelial cells, and new basement membrane formation. Mesangial and endocapillary cellularity is increased resulting in lobular appearance of the glomerular tuft. Proliferation of mesangial cells and circulating monocytes results in increased cellularity.Two mechanisms are involved in the pathogenesis of MPGN,Immune complex deposition leading to activation of complement (immune complex-mediated) and dysregulation and persistent activation of the alternative complement pathway.

Pathophysiology

  • Type III MPGN:
    • It is thought to be due to a slow-acting nephritic factor that stabilizes a properdin dependent C5-convertase, (Cb3)2BbP.
    • (Cb3)2BbP activates the terminal pathway of the complement system.
    • This nephritic factor has not been reported in healthy subjects.unnlike C3NeF.
    • In addition, the deposits present in renal biopsies of patients with type III MPGN are closely associated with the circulating nephritic factor-stabilized convertase and with hypocomplementemia suggesting that NeFt is fundamental to the pathogenesis of type III MPGN.
  • Cryoglobulinemic MPGN :

Histologic Findings

Light microscopy:

Source:By Nephron [CC BY-SA 3.0 (https://creativecommons.org/licenses/by-sa/3.0) or GFDL (http://www.gnu.org/copyleft/fdl.html)], from Wikimedia Commons

References

  1. Sethi S, Fervenza FC (July 2011). "Membranoproliferative glomerulonephritis: pathogenetic heterogeneity and proposal for a new classification". Semin. Nephrol. 31 (4): 341–8. doi:10.1016/j.semnephrol.2011.06.005. PMID 21839367.
  2. Glassock, Richard J. (2010). "The Pathogenesis of Idiopathic Membranous Nephropathy: A 50-Year Odyssey". American Journal of Kidney Diseases. 56 (1): 157–167. doi:10.1053/j.ajkd.2010.01.008. ISSN 0272-6386.

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