The development of edema in the nephrotic syndrome has traditionally been viewed as an underfill mechanism. According to this view, urinary loss of protein results in hypoalbuminemia and decreased plasma oncotic pressure. As a result, plasma water translocates out of the intravascular space and results in a decrease in intravascular volume. In response to the underfilled circulation, effector mechanisms are then activated that signal the kidney to secondarily retain salt and water. While an underfill mechanism may be responsible for edema formation in a minority of patients, recent clinical and experimental findings would suggest that edema formation in most nephrotic patients is the result of primary salt retention. Direct measurements of blood and plasma volume or measurement of neurohumoral markers that indirectly reflect effective circulatory volume are mostly consistent with either euvolemia or a volume expanded state. The ability to maintain plasma volume in the setting of a decreased plasma oncotic pressure is achieved by alterations in transcapillary exchange mechanisms known to occur in the setting of hypoalbuminemia that limit excessive capillary fluid filtration. The intrarenal mechanism responsible for primary sodium retention is not yet known, but may involve tubular resistance to the natriuretic effect of atrial natriuretic peptide.