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AUGUSTO A. CÁMARA, M.D.; HENRY K. SCHOCH, M.D.; ANN REIMER, M.S.; L. H. NEWBURGH, M.D.

AMA Arch Intern Med. 1953;92(4):554-570.

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

THE RECENT clinical literature on the treatment of edema has emphasized the failure of certain patients to respond in the expected fashion to the usual therapeutic regimen of restriction of sodium and the use of acid diuretics such as ammonium chloride. It is of especial interest that refractoriness may develop in patients who at one time had demonstrated a good response to such diuretic programs. We have attempted to obtain further insight into the mechanisms that underlie this resistance to treatment.

In the various concepts regarding the formation of edema, diminished ability of the kidneys to excrete sodium is considered by many to be the primary factor.¹ But that such diminished urinary excretion of sodium is but a part of a general response to some stimulus acting through the adrenal cortex, rather than being primarily a result of altered renal hemodynamics, is evidenced by the accompanying low excretion of sodium . . . [Full Text PDF of this Article]

Author Affiliations
GREAT FALLS, MONT.; ANN ARBOR, MICH.

From the Department of Internal Medicine, the Medical School, University of Michigan.

Footnotes
This work was done under a tenure of Fellowship of the John Simon Guggenheim Memorial Foundation (Dr. Cámara).

This study has been aided by grants from the Guggenheim Memorial Foundation and the United States Public Health Service.

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