Underlying causes of nephrotic syndrome (NS) include primary and secondary glomerulonephritis where membranous nephropathy (MN) is the most common cause in non-diabetic Caucasian adults over 40 years of age. Although it was recognised as a distinct clinicalpathological entity in 1940 by immunofluorescence and electron microscopy, the pathogenesis and treatment have become more apparent only in the last decade. Discovery of M-type phospholipase A2 receptor (PLA2R) antibodies has given new perspectives in understanding the pathogenesis of the disease process. Increased thromboembolic risk is a well recognized complication of nephrotic syndrome and MN, with variable reported incidence of deep venous thrombosis based on data in case series that mostly were reported more than a decade ago. The pathophysiology of hypercoagulability in the nephrotic syndrome is due to an imbalance of prothrombotic and antithrombotic factors, as well as impaired thrombolytic activities. Despite the well-established risk of venous thromboembolism (VTE) in nephrotic syndrome, the most effective method of VTE prophylaxis is unclear. We discuss the key questions to prophylactically anticoagulate adults with nephrotic syndrome.