SOUTHWESTERN INTERNAL-MEDICINE CONFERENCE - NEPHROTIC EDEMA - PATHOGENESIS AND TREATMENT

The cardinal features of the nephrotic syndrome are albuminuria, hypoa lbuminemia, and edema. Traditionally, albuminuria was thought to be re sponsible primarily for the development of hypoalbuminemia. A decrease d plasma-albumin concentration accompanied by a decreased plasma-oncot ic pressure was thought responsible for the development of edema and s econdary salt retention by the kidney. However, new findings have prom pted a reevaluation of these relationships. For example, increased ren al 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 o f mechanisms that limit fluid movement across the capillary wall parti cipate in the pathogenesis of the nephrotic syndrome and related edema . The treatment of patients with the nephrotic syndrome should limit p roteinuria. This can be accomplished by administering angiotensin-conv erting enzyme inhibitors, lowering the protein content of the diet, an d cautiously using non-steroidal antiinflammatory agents.