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Author: Abdulaziz Rajeh Alanzi
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Pathophysiology of
Membranous GN
Mr. Abdulaziz R. AlanziMedical Student ,
Al-Imam UniversityRiyadh – Saudi Arabia
Pathophysiology
circulating IgG antibodies directed against endogenous antigens on or near podocyte foot processes form immune complexes
C5b-9 (MAC) causes cell signaling
Antigens : Phospholipase A2 Receptor (PLA2R)Major antigen in human idiopathic (82%) Neutral Endopeptidase (NEP) Intracellular Antigens Cationic bovine serum albumin Other, - dsDNA in SLE, - thyroglobulin in thyroiditis, - hepatitis B antigen, treponemal antigen and
Helicobacter pylori in the relevant infection- Carcinoembryonic antigen and prostatic specific
antigen in malignancy.
Pathogenesis of these antigens is unproved
Pathophysiology
Source : www.uptodate.com
►Glassock RJ. N Engl J Med 2009;361:81-83.
Pathophysiology
Immunohistopathology
Membranous Nephropathy thick GBM (in
relation to tubular basement membrane)
mesangial expansion (asterisks)
Normal Glomerulus thin GBM (equivalent
to tubular basement membrane)
mesangium limited to stalk of capillary tuft (double arrows)
images from www.uptodate.com
Immunofluorescence diffuse granular IgG
deposits along GBM
Silver Stain spike pattern in
GBM highlights deposits between new GBM
images from www.uptodate.com
Membranous EM thick GMB, with
deposits (D) effacement of foot
processes
Normal EM thin, homogenous GBM epithelial cell with foot
processes fenestrated endothelial
cell (arrow)
