The seromucoid fraction of maternal serum glycoproteins is increased in pre-eclampsia and the rise, which is proportional to the severity of the disease, may reflect progressive placental deterioration with increasing trophoblast fragmentation and deportation. The pulmonary lysis of deported trophoblast effects the local release of fetal antigens and thromboplastin in the lungs. The former, which are immunologically inert because they are complexed with maternal serum seromucoid, are released into the peripheral circulation, while the local coagulation hazard presented by the latter is countered by intensified fibrinolytic activity, the products of which are also released into the peripheral circulation. In severe pre-eclampsia the peripheral circulation contains a considerable excess of physically similar proteins derived from the seromucoid fraction and fibrin degradation products, and the conditions which then obtain in the renal glomerulus favour the physical process of coacervation. In that event the mechanism of the origin and development of the renal lesion can be described in purely physical terms.