Bf. Palmer, SOUTHWESTERN INTERNAL-MEDICINE CONFERENCE - NEPHROTIC EDEMA - PATHOGENESIS AND TREATMENT, The American journal of the medical sciences, 306(1), 1993, pp. 53-67
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.