Membranous glomerulonephritis (NMG)
is an organ-specific autoimmune disease and is the main cause of nephrotic syndrome in adult.
In this nephropathy the formation of sub-epithelial immune deposits and complement activation cause alterations in the basal membrane structure and damage to the glomerular filtration barrier, causing proteinuria.
The Membranous glomerulonephritis follows three main clinical courses: in 30% of cases spontaneous remission is observed, while in the remaining 70% of cases proteinuria persists and of these, half goes with chronic terminal renal failure.
In this pathology, the receptor 1 of type-M phospholipase A2 (PLA2R) is the main podocyte antigen involved in the pathogenesis of idiopathic pathology in adults. In addition, the link between serum levels of anti-PLA2R antibodies and the clinical development of the disease (proteinuria levels, response to therapy) has been shown.
To date, standard treatment includes administration of corticosteroid drugs, immunosuppressants and monoclonal antibodies. However, there are conditions in which the administration of drug therapy alone is insufficient to counteract high levels of antibodies.
The apheresis in this clinical context, and in particular the plasmapheresis Double filtration and the cascade filtration, which through a targeted purification of plasma from antibodies involved contribute to improve the clinical condition of the patient.