Membranous glomerulonephritis pathophysiology

Membranous glomerulonephritis Microchapters
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:

Overview

It is thought that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3].

Pathophysiology

Phospholipase A2 receptor

• The M-type PLA2R is the major antigen in human idiopathic MN. It is expressed in glomerular podocytes.
• There was no colocalization of PLA2R in secondary MN biopsies.
• PLA2R antigen detected within immune deposits by immunofluorescence of the biopsy specimen. [26]
• Detection of the immune complex specificity is 100 percent.

Thrombospondin type-1

• THSD7A has been found in patients with idiopathic MN who are negative for anti-PLA2R antibodies.

Neutral endopeptidase

• Anti-neutral endopeptidase antibodies caused MN in the neonates.
• It resolves months after birth.

• The T helper-2 predominates in MN and minimal change disease.

References

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  Membranous Glomerulonephritis: Electron micrography. An excellent example to show thickened basement membrane and immune complexes.
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  Membranous Glomerulonephritis: Micro trichrome high mag excellent to show thickened capillary basement membranes
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  Membranous Glomerulonephritis: Micro PAS high mag excellent example of this lesion
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  Membranous Glomerulonephritis: Micro PAS med mag