The cardinal features of the nephrotic syndrome are albuminuria, hypoalbuminemia, and edema. Traditionally, albuminuria was thought to be responsible primarily for the development of hypoalbuminemia. A decreased plasma-albumin concentration accompanied by a decreased plasma-oncotic pressure was thought responsible for the development of edema and secondary salt retention by the kidney. However, new findings have prompted a reevaluation of these relationships. For example, increased renal catabolism and blunted hepatic synthesis appear to play major roles in the development of hypoalbuminemia. Evidence suggests that primary, rather than secondary, salt retention by the kidney and activation of mechanisms that limit fluid movement across the capillary wall participate in the pathogenesis of the nephrotic syndrome and related edema. The treatment of patients with the nephrotic syndrome should limit proteinuria. This can be accomplished by administering angiotensin-converting enzyme inhibitors, lowering the protein content of the diet, and cautiously using non-steroidal antiinflammatory agents.