Kidney nontumor
Other primary glomerular diseases
Pathogenesis of glomerular injury

Topic Completed: 2 April 2012

Minor changes: 12 February 2020

Copyright: 2002-2020,, Inc.

PubMed Search: Kidney pathogenesis of glomerular injury [title] "loattrfree full text"[sb]

Nikhil Sangle, M.D.
Page views in 2019: 1,449
Page views in 2020 to date: 705
Cite this page: Sangle N. Pathogenesis of glomerular injury. website. Accessed June 1st, 2020.
Definition / general
  • Usually immune mediated via antibody deposition, cell mediated injury or activation of alternative complement pathway (Nephrol Dial Transplant 1998;13:10, Medchrome: Pathogenesis of Glomerular Injury [Accessed 12 February 2020])
  • Antibodies deposited are either to in situ antigen (intrinsic or planted) or are circulating immune complexes
  • Intrinsic: Goodpasture 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 / tables

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Pathogenesis of glomerular injury

Microscopic (histologic) description
  • Injured epithelial cells have vacuoles, retract and detach from basement membrane, lose foot processes
Immunofluorescence description
  • Granular deposits represent immune complexes that settle out of blood or form in situ; linear deposits are due to antibasement membrane antibodies or light chain nephropathy
  • Can detect via fluorescent antibodies or using fluorescence microscopy of H&E stained sections fixed in Hollande fixative (Mod Pathol 2002;15:988)
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