Potassium and Sodium Restriction in the Normal Human 1

Abstract

Restriction of potassium intake leads to depletion of body potassium, chiefly as a result of losses of potassium in the urine (1-3). The ability of the kidney to conserve potassium has been variously assessed. Tarail and Elkinton (4) considered the renal mechanism for potassium conservation to be relatively inefficient, whereas Fourman (5) has demonstrated a U/P ratio of less than 1.0 in the normal human. Depletion of body potassium may be associated with hypokalemic alkalosis (1), shifts of sodium into potassium depleted cells (6) and retention of sodium in the extracellular phase with expansion of the extra-, cellular fluid (1, 2).The following experiments were designed to study the effects on the composition of the serum and urine, in normal humans, of 1) restricted potassium intake alone, and 2) restriction of sodium and potassium concurrently. External balances of water and electrolytes were observed, and internal balances of sodium, potassium, and water were calculated. Clearances of endogenous creatinine were calculated. EXPERIMENTAL PROCEDURES AND METHODSThree studies were carried out on two normal male subjects. Studies RW1 and RW' were similar in design. Each was divided into an Initial period when sodium and potassium intakes were maintained at normal levels, a Depletion (K) period when potassium intake was restricted, a Depletion (Na and K) period when both sodium and potassium intakes were restricted (in RW1 9 gnL of ammonium chloride were administered on the last day of this period), and a Reloading period when sodium and potassium were returned to the diet Study JD was divided into an Initial period, a Depletion (Na and K) period when both sodium and potassium intakes were restricted, and a Depletion (K) period when so-

Water Excretion in Potassium-Deficient Man*

“…A readily demonstrable defect in renal tubular function occurred with degrees of potassium depletion tolerated by other body cells with apparent impunity (27)(28)(29). This may be ascribed to an apparent critical vulnerability of the renal tubular epithelium to potassium deficiency; however, comparable techniques to examine other body cells are lacking.…”

“…The redistribution of body fluids with sodium retention, especially the increased extracellular volume that attends potassium deficiency (27)(28)(29) if sodium is not restricted, could be expected to alter the excretion of a water load. Extrarenal factors, such as production and renal responsiveness to aldosterone and changes in body fluid volumes, may be produced by potassium depletion and may exert unknown effects on these experiments.…”

Renal potassium wasting in renal tubular acidosis (RTA)

“…servation of potassium, hypokalemia may occur with The results of the present studies indicate that both in (21)(22)(23)(24)(25)(26)(27). Some of the subjects represented by 0 were mildly alkalotic and were excreting significant amounts of urinary bicarbonate (27) ; the subj ects represented by + were moderately alkalotic and were excreting more than 50 mEq of urinary bicarbonate daily (22) ; the subjects represented by X were given large amounts of desoxycorticosterone after hypokalemia supervened (27 (14,36,37).…”

“…In studies 1-5, in which arterial pH remained normal throughout (7.38-7.42 magnitude of negative potassium balance appeared to be modest as judged from cumulative urinary losses of potassium. When dietary potassium is restricted in most normal subjects, the occurrence of hypokalemia is less rapid, despite relatively greater cumulative urinary losses of potassium (21)(22)(23)(24)(25)(26). But in normal subjects, in contrast to the patients studied with RTA, urinary excretion of potassium decreases to less than 40 mEq/day when hypokalemia occurs, even when it occurs rapidly and despite relatively modest negative potassium balance (27).…”

Respiratory Acidosis and Hypochloremic Alkalosis: Origins, Differentiation, Effects and Therapy

“…Since then other workers have shown that significant degrees of potassium depletion, i.e., 5 per cent of the body stores, may be induced without production of either hypochloremia or alkalosis. 12 ' 13 Abstraction of chloride, sodium loading, or interference with sodium excretion following ACTH did. Data are too limited at present to assert that hypochloremic alkalosis associated with potassium losses always represents chloride deficiency or necessitates sodium loading.…”