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)

Thank Youd0pa@hotmail.com@AbdulazizEnazi

http://imamu.academia.edu/AbdulazizAlanzi