Idiopathic membranous nephropathy and anti-phospholipase A2 receptor antibodies

Ali Nayer; Arif Asif

doi:10.12860/JNP.2013.35

Idiopathic membranous nephropathy and anti-phospholipase A2 receptor antibodies

Ali Nayer, Arif Asif

Medicine

Research output: Contribution to journal › Editorial › peer-review

4 Scopus citations

Abstract

Membranous nephropathy (MN) is a glomerular disease due to subepithelial immune deposits and local complement activation resulting in podocyte injury and proteinuria. Patients with idiopathic (but not secondary) MN had circulating autoantibodies, predominantly of the IgG4 subclass, directed against M-type phospholipase A2 receptor (PLA2R) located on podocytes. It is also possible that the binding of anti-PLA2R antibodies to PLA2R on podocytes could alter receptor function resulting in podocyte dysfunction.

Original language	English (US)
Pages (from-to)	214-216
Number of pages	3
Journal	Journal of Nephropathology
Volume	2
Issue number	4
DOIs	https://doi.org/10.12860/JNP.2013.35
State	Published - Jan 1 2013

Keywords

Anti-phospholipase A2 receptor antibodies
End-stage renal disease
Idiopathic membranous nephropathy
Nephrotic syndrome

ASJC Scopus subject areas

Nephrology

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abstract = "Membranous nephropathy (MN) is a glomerular disease due to subepithelial immune deposits and local complement activation resulting in podocyte injury and proteinuria. Patients with idiopathic (but not secondary) MN had circulating autoantibodies, predominantly of the IgG4 subclass, directed against M-type phospholipase A2 receptor (PLA2R) located on podocytes. It is also possible that the binding of anti-PLA2R antibodies to PLA2R on podocytes could alter receptor function resulting in podocyte dysfunction.",

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AB - Membranous nephropathy (MN) is a glomerular disease due to subepithelial immune deposits and local complement activation resulting in podocyte injury and proteinuria. Patients with idiopathic (but not secondary) MN had circulating autoantibodies, predominantly of the IgG4 subclass, directed against M-type phospholipase A2 receptor (PLA2R) located on podocytes. It is also possible that the binding of anti-PLA2R antibodies to PLA2R on podocytes could alter receptor function resulting in podocyte dysfunction.

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