[2] Most people will present as nephrotic syndrome, with the triad of albuminuria, edema and low serum albumin (with or without kidney failure).

It is likely that instead the field will move to novel classification on the basis of the specific autoantigen detected, though given the current lack of clinical assays (other than for PLA2R autoantibodies) this may be several years off still.

In 2014, a second autoantigen was discovered, the thrombospondin type 1 domain-containing 7A (THSD7A) system that might account for an additional 1% of membranous nephropathy cases, and appears to be associated with malignancies.

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".

[17] 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.

[citation needed] The defining point of MGN is the presence of subepithelial immunoglobulin-containing deposits along the glomerular basement membrane (GBM).

Given spontaneous remission is common, international guidelines recommend a period of watchful waiting before considering immunosuppressive treatment.

[20] Likelihood of achieving spontaneous remission is much higher if anti-proteinuric therapy with ace inhibitors or angiotensin II receptor blockers is commenced.

[citation needed] The twin aims of treating membranous nephropathy are first to induce a remission of the nephrotic syndrome and second to prevent the development of end-stage kidney failure.