Shifts of fluid from the intravascular to the extravascular compartment are facilitated by appropriate changes in venous pressure, colloidal osmotic pressure, capillary permeability, and "tissue pressure." Development and subsidence of generalized edema cannot easily be explained on the basis of these factors alone. Starling 1 invoked diminished excretion by the kidneys to explain the "hydremic plethora" found in chronic congestive heart failure. Schroeder found that the capacity to excrete sodium chloride was greatly reduced in the edematous patient.2 Restriction of salt intake to a level below urine output arrested edema accumulation or caused diuresis. Warren and Stead3 administered sodium chloride to edema-forming patients and noted extracellular fluid accumulated before any increase in venous pressure was detected. They concluded that the edema of congestive failure resulted from failure of the kidneys to excrete salt and, secondarily, water for reasons then unkonwn.
Acute reduction in glomerular filtration rate in the