Experimental Potassium Depletion in Normal Human Subjects. I. Relation of Ionic Intakes to the Renal Conservation of Potassium*

Squires, Russell D.; Huth, Edward J.

doi:10.1172/jci103890

Cited by 84 publications

(33 citation statements)

References 14 publications

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“…But potassium depletion in man does not always result in an unequivocal extracellular alkalosis either experimentally (1) or clinically (15), and Moore and co-workers (16) have shown that loss of acid as gastric fluid and interference by adrenocortical hormones with renal compensations for internal exchanges may be at least as important in causing a manifest alkalosis.…”

mentioning

confidence: 99%

Experimental Potassium Depletion in Normal Human Subjects. Ii. Renal and Hormonal Factors in the Development of Extracellular Alkalosis During Depletion*

Huth¹,

Squires²,

Elkinton³

1959

J. Clin. Invest.

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In the preceding paper (1) experimental depletion of potassium in normal human subjects did not produce an extracellular metabolic alkalosis of the severity which usually occurs in patients with comparable potassium deficits. Much investigative study has been applied to this association but, because of the many factors involved in such patients, the relative importance of such factors in the etiology of this association in man remains unclear.Most of our knowledge of the metabolic derangements induced in mammals by potassium depletion has come from studies in rats (2-12). The depletion in rats is usually accompanied by metabolic alkalosis of varying severity. A hypothesis accounting for the alkalosis has been formulated by Darrow, Cooke and coworkers (2-4) and has been given additional support by the studies of Orloff, Kennedy and Berliner (9). In brief, the loss of potassium from cells is replaced in part by hydrogen ion from extracellular fluid, the latter shift resulting in an intracellular acidosis and an extracellular alkalosis. This primary cellular distortion of acid-base equilibrium is then maintained by the kidney by an enhancement of tubular reabsorption of bicarbonate over that of chloride and the excretion of a relatively acid urine. In these rat studies the absence or presence and degree of alkalosis appear to be related to many variables including the duration and severity of the depletion, the protein content of the diet, the acidbase composition of the diet and the use of desoxycorticosterone in promoting depletion.

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mentioning

confidence: 99%

Experimental Potassium Depletion in Normal Human Subjects. Ii. Renal and Hormonal Factors in the Development of Extracellular Alkalosis During Depletion*

Huth¹,

Squires²,

Elkinton³

1959

J. Clin. Invest.

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“…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).…”

Section: Methodsmentioning

confidence: 78%

“…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).…”

Section: Methodsmentioning

confidence: 99%

Renal potassium wasting in renal tubular acidosis (RTA)

Sebastián¹,

McSherry²,

Morris³

1971

J. Clin. Invest.

127

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A B S T R A C T In two patients with classic renal tubular acidosis (RTA) and in two patients with RTA associated with the Fanconi syndrome, renal potassium wasting persisted despite sustained correction of acidosis:(a) during moderate degrees of hypokalemia, daily urinary excretion of potassium exceeded 80 mEq in each patient; (b) during more severe degrees of hypokalemia, daily urinary excretion of potassium exceeded 40 mEq in two patients and 100 mEq in another. These urinary excretion rates of potassium are more than twice those observed in potassium-depleted normal subjects with even minimal degrees of hypokalemia. The persistence of renal potassium wasting may have resulted in part from hyperaldosteronism, since urinary aldosterone was frankly increased in two patients and was probably abnormally high in the others relative to the degree of their potassium depletion. The hyperaldosteronism persisted despite sustained correction of acidosis, a normal sodium intake, and no reduction in measured plasma volume, and was not associated with hypertension; its cause was not defined. In the two patients with classic RTA, neither renal potassium wasting nor hyperaldosteronism could be explained as a consequence of a gradient restriction on renal H' -Na' exchange because the urinary pH remained greater than, or approximately equal to, the normal arterial pH or considerably greater than the minimal urinary pH attained during acidosis. The findings provide no support for the traditional view that renal potassium wasting in either classic RTA or RTA

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“…BRUNNER and FRICK (1968) suggested that renal potassium losses constituted the main cause of hypokalemia during "massive" sodium penicillin therapy. In their paper, urinary potassium excretion did not drop below 50-70 mmol/24 hr despite frank hypokalemia during sodium penicillin administration, while urinary potassium excretion fell below 40 or even below 20 mmol/24 hr in a few days even before hypokalemia developed in normal controls depleted of potassium by a potassium deficient diet (SQUIRES and HUH, 1959). In experiments using rats, LIPNER et al (1975) suggested that a nonreabsorbable anion effect of the antibiotic may accelerate K secretion into urine.…”

mentioning

confidence: 92%

Sulbenicillin-induced kaliuresis in man.

Tomita¹,

Matsuda

Shinohara

et al. 1983

Jpn.J.Physiol

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The mechanism of kaliuresis induced by massive antibiotic administration was studied using a-sulfobenzyl penicillin (SBPC). In experimental group (n=8), urinary electrolytes excretion were compared between following the infusion of 10 g SBPC in 200 ml water at a constant rate and following the infusion of 48 mmol of NaCI (equal to that contained in 10 g SBPC) in 200 ml water. For the control group, 96 mmol NaCI in 400 ml water was infused (n=5). In the experimental group, urinary Na (UNaV) and urinary K excretion (UKV) increased relative to the control period. In the control group, UKV was not increased although UNaV was increased (p <0.05). UKV following SBPC infusion was correlated with UNaV (p<0.05) and urinary SBPC excretion (p <0.05). The ratio of urinary anion gap to urinary cation [1-{urinary Cl concentration/(urinary Na concentrations urinary K concentration)}] was significantly increased following SBPC infusion (p<0.005) but not in the control group. This increase in anion gap is possibly due to urinary SBPC, which will be ionized over 90% as nonreabsorbable anion in maximally acidic urine. We conclude that the kaliuresis induced by massive SBPC administration in man is probably caused by the nonreabsorbable anion effect of SBPC itself.

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Experimental Potassium Depletion in Normal Human Subjects. I. Relation of Ionic Intakes to the Renal Conservation of Potassium*

Cited by 84 publications

References 14 publications

Experimental Potassium Depletion in Normal Human Subjects. Ii. Renal and Hormonal Factors in the Development of Extracellular Alkalosis During Depletion*

Experimental Potassium Depletion in Normal Human Subjects. Ii. Renal and Hormonal Factors in the Development of Extracellular Alkalosis During Depletion*

Renal potassium wasting in renal tubular acidosis (RTA)

Sulbenicillin-induced kaliuresis in man.

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