younger, female patients, and indeed 1/3 of patients with class V lupus nephritis are EXT positive. Prognosis is good. Semaphorin3B predominates in children, esp <2 years old. there can be a family history of MN in these patients, it frequently causes progressive disease and it can recur in kidney transplants. Protocadherin 7 (PCDH7) in 2020. It is generallly described in older patients, who have less complement on renal biopsy and frequently have spontaneous remission. FAT1 is associated with haemopoetic stem cell transplant, and responds to treatment. NDNF is associated with syphilis (close to 100% of membranous nephrology is NDNF positive). Secondary We include the traditional list of secondary causes, though as above nomenclature is moving towards an autoantibody specific approach. Membranous nephropathy is associated with the following: autoimmune conditions (e.g., systemic lupus erythematosus). infections (e.g., syphilis, malaria, hepatitis B, hepatitis C, HIV). drugs (e.g., captopril, NSAIDs, penicillamine, probenecid, Bucillamine, Anti-TNF therapy, Tiopronin). inorganic salts (e.g. gold, mercury). tumors, frequently solid tumors of the lung and colon; hematological malignancies such as chronic lymphocytic leukemia are less common. Pathogenesis MGN is caused by immune complex formation in the glomerulus. The immune complexes are formed by binding of antibodies to antigens in the glomerular basement membrane. The antigens may be part of the basement membrane, or deposited from elsewhere by the systemic circulation. The immune complex serves as an activator that triggers a response from the C5b - C9 complements, which form a membrane attack complex (MAC) on the glomerular epithelial cells. This, in turn, stimulates release of proteases and oxidants by the mesangial and epithelial cells, damaging the capillary walls and causing them to become "leaky". In addition, the epithelial cells also seem to secrete an unknown mediator that reduces nephrin synthesis and distribution. Within membranous glomerulonephritis, especially in cases caused by viral hepatitis, serum C3 levels are low. Similar to other causes of nephrotic syndrome (e.g., focal segmental glomerulosclerosis or minimal change disease), membranous nephropathy is known to predispose affected individuals to develop blood clots such as pulmonary emboli. Membranous nephropathy in particular is known to increase this risk more than other causes of nephrotic syndrome though the reason for this is not yet clear. Morphology The defining point of MGN is the presence of subepithelial immunoglobulin-containing deposits along the glomerular basement membrane (GBM). By light microscopy, the basement membrane is observed to be diffusely thickened. Using Jones' stain, the GBM