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AMOS H. LIEBERMAN, M.D.

AMA Arch Intern Med. 1958;102(6):990-997.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

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 . . . [Full Text PDF of this Article]

Author Affiliations
San Francisco

Footnotes
Submitted for publication June 26, 1958.

From the Department of Medicine, Stanford University School of Medicine. Fellow, Giannini Foundation. This investigation was supported by a research grant (A-630 C3) from the National Institute of Arthritis and Metabolic Diseases, Public Health Service.

Read in the Symposium on Recent Advances in the Knowledge of the Causes of Edema and in Diuretic Therapy before the Joint Meeting of the Section on Experimental Medicine and Therapeutics and the Section on Internal Medicine at the 107th Annual Meeting of the American Medical Association, San Francisco, June 26, 1958.

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