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Kidney non-tumor

Primary glomerular diseases

Pathogenesis of glomerular injury


Reviewers: Nikhil Sangle, M.D. (see Reviewers page)
Revised: 10 January 2013, last major update April 2012
Copyright: (c) 2003-2013, PathologyOutlines.com, Inc.

General
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● Usually immune mediated via antibody deposition, cell-mediated injury or activation of alternative complement pathway (Nephrol Dial Transplant 1998;13(suppl 1):10, Med Chrome)
● Antibodies deposited are either to in situ antigen (intrinsic or planted) or are circulating immune complexes
Intrinsic: Goodpasture’s disease-antigens are in basement membrane; Heymann nephritis-antigens are on visceral epithelial cells; produce linear immunofluorescence patterns
Planted antigens are deposited in basement membrane; may be exogenous (drugs, infectious agents) or endogenous (DNA, immunoglobulin, immune complexes); their cationic proteins bind to glomerular anionic sites and produce granular lumpy staining by immunofluorescence
Circulating immune complexes may be endogenous (DNA, tumors) or exogenous (infectious products); they usually localize within glomeruli and activate complement; deposits are usually mesangial or subendothelial and resolve by macrophage phagocytosis, unless there are repeated cycles of formation (Hepatitis B/C, lupus)
Cell-mediated immune injury is by sensitized nephritogenic T cells
Progression to end stage renal disease occurs when the glomerular filtration rate (GFR) is 30-50% of normal, due to compensatory hypertrophy of remaining glomeruli and systemic hypertension (inhibited by angiotensin converting enzyme inhibitors), eventually causing glomerulosclerosis

Diagrams
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Pathogenesis of glomerular injury

Micro description
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● Injured epithelial cells have vacuoles, retract and detach from basement membrane, lose foot processes

Immunofluorescence
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● Granular deposits represent immune complexes that settle out of blood or form in situ; linear deposits are due to anti-basement membrane antibodies or light chain nephropathy
● Can detect via fluorescent antibodies or using fluorescence microscopy of H&E stained sections fixed in Hollande’s fixative (Mod Pathol 2002;15:988)

End of Kidney non-tumor > Primary glomerular diseases > Pathogenesis of glomerular injury

Ref Updated: 4/9/12


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