[PDF][PDF] Complement pathways in membranous nephropathy: complex and multifactorial

V Brglez, S Boyer-Suavet, B Seitz-Polski - Kidney International Reports, 2020 - Elsevier
V Brglez, S Boyer-Suavet, B Seitz-Polski
Kidney International Reports, 2020Elsevier
Membranous nephropathy (MN) is a rare, but severe autoimmune kidney disease and a
major cause of nephrotic syndrome in adults. Clinically defined by nephrotic syndrome,
which is persistent in about two thrid of untreated patients, it manifests histologically by
subepithelial immune deposits at the glomerular basement membrane in the kidney
containing IgGs. Membranous nephropathy can be idiopathic (or primary, iMN) without any
identified cause (70-80% of cases), or secondary (sMN) to clinical disorders such as …
Membranous nephropathy (MN) is a rare, but severe autoimmune kidney disease and a major cause of nephrotic syndrome in adults. Clinically defined by nephrotic syndrome, which is persistent in about two thrid of untreated patients, it manifests histologically by subepithelial immune deposits at the glomerular basement membrane in the kidney containing IgGs. Membranous nephropathy can be idiopathic (or primary, iMN) without any identified cause (70-80% of cases), or secondary (sMN) to clinical disorders such as hepatitis B, systematic lupus erythematosus, cancer or drug side effects. Etiology of iMN has remained elusive for decades, until recently when several groups have discovered different podocyte antigens, such as a neutral endopeptidase in rare cases in the neonate in 2002, M-type phospholipase A2 receptor (PLA2R1) in 70% of iMN patients in 2009, thrombospondin type-1 domain-© 2020 published by Elsevier. This manuscript is made available under the Elsevier user license https://www. elsevier. com/open-access/userlicense/1.0/
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