Membranous Nephropathy

Membranous nephropathy is characterized by diffuse thickening of the glomerular capillary basement membrane by subepithelial immune complex deposition. This results in damage and increased permeability of the basement membrane to plasma proteins and hence nephrotic range proteinuria.

Disease pathophysiology: 

Autoantibodies to PLA2R1, usually of IgG4 subclass, are found in about 80% of patients with primary MN. These autoantibodies bind to genetically determined, conformational epitopes on PLA2R1, form immune complexes in situ and induce proteinuria, via the mannose-binding lectin pathway. The level of autoantibody to PLA2R correlates with the severity of the clinical disease.

Disease statistics:

In the US, the prevalence of membranous nephropathy is close to 2000 patients per year. In contrast to other primary glomerular diseases, the incidence of MN has remained constant since the 1980s. It is one of the most common causes of nephrotic syndrome globally, just behind focal segmental glomerular sclerosis, which is the most common aetiology. 

Disease treatment:

Immunotherapy to treat immune-mediated kidney disease including Membranous Nephropathy. It is a comprehensive treatment with the treating process of blocking the undue inflammatory response, clearing up the immune complex, protecting the healthy renal cells and tissues, recovering the impaired kidney function and regulating the immune system. 

Major research on disease:

MN, a rare kidney disease in which the immune system attacks a protein found in the kidneys, causing thickening of the small blood vessels in the kidney, proteinuria, and sometimes kidney failure. The scientists discovered the site where antibodiesbind to this protein, known as PLA2R, as well as the peptides, or small molecules, that could prevent binding.