The most likely diagnosis is membranous glomerulopathy (MG). This patient has evidence of the nephrotic syndrome, with significant protein loss in the urine, hypoalbuminemia, and edema. He also has a pulmonary embolism, a common complication of the nephrotic syndrome. The clinical presentation of MG is indistinguishable from other causes of the nephrotic syndrome, although the propensity for venous thromboembolism, and particularly renal vein thrombosis, is much higher in MG than other disorders associated with the nephrotic syndrome, such as focal segmental glomerulosclerosis or minimal change glomerulopathy. The pathophysiology of hypercoagulability in the nephrotic syndrome is not well understood, nor has the mechanism underlying the higher propensity for thromboembolism in MG been well defined. The risk appears to be inversely related to the serum albumin level in MG, and prophylactic anticoagulation is frequently given to patients with MG with a serum albumin level of ≤2.8 g/dL (28 g/L). MG is the most common cause of idiopathic nephrotic syndrome in adult white persons but may also be associated with infections, systemic lupus erythematosus, medications, and certain malignancies. Definitive diagnosis is by kidney biopsy.

The hypercoagulable state is associated with the nephrotic syndrome only, not other kidney syndromes such as acute interstitial nephritis or poststreptococcal glomerulonephritis. Additionally, these disorders typically present with evidence of inflammation on urinalysis and kidney failure, neither of which is present in this patient.

The site of thrombosis in thrombotic microangiopathy is the microvasculature, leading to clinical manifestations such as microangiopathic hemolytic anemia, thrombocytopenia, and organ dysfunction (including kidney failure). Large-vessel thrombosis does not occur as is present in this case.