Potassium Deficiency and the Role of the Kidney in Its Production 12

Tarail, R.; Elkinton, J. R.

doi:10.1172/jci102059

Cited by 85 publications

(22 citation statements)

References 26 publications

(40 reference statements)

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“…The striking retention of potassium administered to this series of patients points to the existence of concomitant deficits of this cation in the body cells. Such an interpretation is supported by the experiments of Tarail and Elkinton which showed that amounts of potassium as great as those employed in some of our studies were not retained in the body when given by mouth to healthy adults (28). Presumably such subjects do not have potassium deficits and hence the administered potassium is promptly excreted.…”

Section: Discussionsupporting

confidence: 71%

See 1 more Smart Citation

Studies in Diabetic Acidosis and Coma, With Particular Emphasis on the Retention of Administered Potassium

Danowski¹,

Peters²,

Rathbun³

et al. 1949

J. Clin. Invest.

109

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Abnormally low concentrations of potassium, at times associated with muscular paralysis, have been observed in the serum of diabetic patients while under treatment for acidosis or coma (1)(2)(3)(4). Available data indicate that deficits of cell potassium are also present in at least some of these subjects (5). In an attempt to characterize and quantitate the magnitude of these deficits, exchanges of water, electrolytes, carbohydrate, and protein have been investigated in diabetic acidosis and coma prior to, during, and following the administration of potassium salts. EXPERIMENTAL PROCEDURE AND METHODSEight cases in all have been studied. Of these, two were adults and the remaining six juvenile diabetics 16 years of age or younger. On admission all had Kussmaul breathing, a marked reduction of the serum bicarbonate content, hyperglycemia, glycosuria, and ketonuria.Studies during treatment and recovery were divided into three periods. The first or pre-KCl period extended from admission to the point where the patients had improved sufficiently to be maintained on an oral intake. During this time insulin, 0.9 per cent saline, and, once the blood sugar began to drop, glucose solutions were administered in amounts summarized in Table I. Under this treatment ketosis diminished, overbreathing ceased, hyperglycemia decreased, and mental clarity returned. This interval lasted 12 to 25 hours in the individual subjects. During the second or KC1 period, 22 to 37 hours in length, the patients received insulin, 10.0 to 30.0 grams of KCI per os or intravenously, whole milk containing added carbohydrate, and water as desired. The third or post-KCl period began after the final dose of KC1 and lasted up to 34 hours. During this time the patients received insulin as needed, together with measured amounts of water and milk.In all subjects concentrations of the whole blood nonprotein nitrogen, blood sugar (6-8), and the levels of serum chloride, bicarbonate, sodium, potassium and water were measured at the beginning and end of each period (6,(9)(10)(11)(12). Average values for the electrolyte, carbohydrate, and protein content of fresh milk have been used in calculating the intake (13, 14). Urine excreted during each period was analyzed for nitrogen, sodium, potassium, chloride, and glucose (6, 10, 11, 15, 16). Body weight was determined when possible at the start and end of each period. METHOD OF CALCULATIONAlterations in extracellular fluid volume were calculated from changes in the chloride space, based on the external balance of this anion and corrected for changes in the serum concentrations of chloride as described by Elkinton and co-workers, and by . In view of the dehydration known to develop in the course of diabetic acidosis and coma, the initial extracellular volume was assumed for purposes of this calculation to be 15 per cent of the body weight rather than the usual value of 18.7 to 23 per cent found in non-dehydrated human subjects (20). In two instances a pre-treatment weight could not be obtained. A reasonable assumpt...

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Section: Discussionsupporting

confidence: 71%

“…Finally, the evidence to date suggests that as long as urine is being elaborated it contains potassium. This appears to be true even though deficits of cell potassium, and even extracellular hypopotassemia, are present (21,28). Hence, with the diuresis characteristic of almost all patients in coma considerable amounts of potassium are lost.…”

Section: Discussionmentioning

confidence: 99%

Studies in Diabetic Acidosis and Coma, With Particular Emphasis on the Retention of Administered Potassium

Danowski¹,

Peters²,

Rathbun³

et al. 1949

J. Clin. Invest.

109

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“…The important contribution of renal "leakage" of potassium to the development of potassium depletion in man has been emphasized (26,27 (29).…”

Section: Discussionmentioning

confidence: 99%

Metabolic and Renal Studies in Chronic Potassium Depletion Resulting From Overuse of Laxatives 12

Schwartz¹,

Relman²

1953

J. Clin. Invest.

239

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“…Under these circumstances the lowering of chloride has been interpreted as originating from dilution of chloride space, from extracellular transfers or segregation of chloride, or most likely from losses in urine. The importance of continued renal losses of potassium in the production of deficiencies of this ion have been amply established, 7 …”

mentioning

confidence: 99%

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

1956

Diabetes

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Potassium Deficiency and the Role of the Kidney in Its Production 12

Cited by 85 publications

References 26 publications

Studies in Diabetic Acidosis and Coma, With Particular Emphasis on the Retention of Administered Potassium

Studies in Diabetic Acidosis and Coma, With Particular Emphasis on the Retention of Administered Potassium

Metabolic and Renal Studies in Chronic Potassium Depletion Resulting From Overuse of Laxatives 12

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

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