Abstract

Under normal circumstances the kidney regulates the body sodium content by balancing the output against the intake. In congestive heart diseases this regulation fails, the patient puts on weight and develops edema, and sodium nearly disappears from the urine. It has been maintained that not only the kidneys, but also other organs suppress the excretion of sodium in congestive heart failure. White, Gordon & Leiter( 1950) and Berger & Steele (1952) demonstrated a lowered sodium concentration in saliva, and Berger & Steele further demonstrated suppression of sodium excretion by the colon of edematous patients, and a lowered sodium concentration in the sweat. In two patients accumulating edema fluid the sweat sodium concentration was 8 and 13 mEq/l respectively, against an average of 39 mEq in normal individuals. Berger & Steele maintain that the accumulation of edema is due to a suppressed excretion of sodium through th? kidneys, the sweat and salivary glands, and the colon. In their opinion this retention iq due to an excess of a desoxycorticosteronelike hormone, capable of suppressing the excretion of sodium through various organs. Robinson & Robinson (1954), however, seriously doubt the correctness of Berger & Steele's explanation and suggest that the lowered sodium excretion through the skin may be an adaptation to salt depletion caused by carboxylic resin therapy. We have had the opportunity to study the excretion of electrolytes through the sweat in a case oi congestive heart failure. In this patient no peripheral edema appeared in spite of a very low renal sodium excretion. Our study revealed that this was due to a very heavy sweating which contained all the dietary sodium. The purpose of this paper is to report the results of the study.

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