Membranous glomerulonephritis pathophysiology: Difference between revisions
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==Overview== | ==Overview== | ||
==Pathophysiology== | |||
MGN is caused by circulating [[immune complex]]. Current research indicates that the majority of the immune complexes are formed via binding of antibodies to antigens ''in situ'' to the glomerular basement membrane. The said antigens may be [[endogenous]] to (from) the basement membrane, or "planted" from systemic circulation. | |||
The immune complex serves as an activator that triggers a response from the C5b - C9 complements, which form a [[Complement_membrane_attack_complex|membrane attack complex]] (MAC) on the glomerular epithelial cells. This, in turn, stimulates release of proteases and oxidants by the mesangial and epithelial cells, damaging the capillary walls and causing them to become "leaky". In addition, the epithelial cells also seem to secrete an unknown mediator that reduces nephrin synthesis and distribution. | |||
==References== | ==References== | ||
{{reflist|2}} | {{reflist|2}} | ||
Revision as of 20:08, 27 September 2012
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Membranous glomerulonephritis Microchapters |
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Differentiating Membranous glomerulonephritis from other Diseases |
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Diagnosis |
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Treatment |
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Case Studies |
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Membranous glomerulonephritis pathophysiology On the Web |
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Directions to Hospitals Treating Membranous glomerulonephritis |
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Risk calculators and risk factors for Membranous glomerulonephritis pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Pathophysiology
MGN is caused by circulating immune complex. Current research indicates that the majority of the immune complexes are formed via binding of antibodies to antigens in situ to the glomerular basement membrane. The said antigens may be endogenous to (from) the basement membrane, or "planted" from systemic circulation.
The immune complex serves as an activator that triggers a response from the C5b - C9 complements, which form a membrane attack complex (MAC) on the glomerular epithelial cells. This, in turn, stimulates release of proteases and oxidants by the mesangial and epithelial cells, damaging the capillary walls and causing them to become "leaky". In addition, the epithelial cells also seem to secrete an unknown mediator that reduces nephrin synthesis and distribution.