Nephrotic syndrome is caused by systemic diseases such as systemic lupus erythematosus and hepatitis B, as a reaction to gold therapy, and idiopathically. This syndrome affects the glomerular capillary membrane, leading to increased glomerular permeability, secondary to collagen deposits in glomeruli and thickening of the glomerular basement membrane. Proteinuria, including loss of albumin and immunoglobulins, equal to or exceeding 3.5 g/day; lipiduria (i.e., fat in the urine); low serum albumin; generalized edema due to low serum colloidal osmotic pressure; and hyperlipidemia are characteristics of nephrotic syndrome. Loss of immunoglobulins increases the chance of developing infections. As a compensatory reaction to proteinuria, the body increases albumin production and the liver increases triglycerides and cholesterol production. This puts a person with nephrotic syndrome at risk for atherosclerosis. Hypercoagulability with resultant venous clot formation, especially in the renal veins, is thought to occur because of the loss of clot-inhibiting factors from the urine.