Internal Potassium Balance and the Control of the Plasma Potassium Concentration

Sterns, Richard H.; Cox, M.; Feig, Peter U.; Singer, Irwin

doi:10.1097/00005792-198109000-00002

Cited by 221 publications

(81 citation statements)

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“…The usual mechanism is the export of cations created by the electrogenic Na C -K C -ATPase extruding three Na C ions for every two K C ions that enter the cells (20). Hyperthyroidism can induce an increase in the number and activity of the Na C -K C pump (21) and also increase b-adrenergic sensitivity (22), further enhancing the activity of the Na C -K C pump.…”

Section: Discussionmentioning

confidence: 99%

Therapeutic analysis in Chinese patients with thyrotoxic periodic paralysis over 6 years

Shiang¹,

Cheng²,

Tsai³

et al. 2009

European Journal of Endocrinology

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Objective: To characterize the course of therapy in a large cohort of Chinese patients with thyrotoxic periodic paralysis (TPP), a reversible electrolyte emergency fraught with therapeutic challenges. Design and methods: In this prospective interventional study, 78 patients with TPP (75 males and three females with an age range of 16-48 years) were consecutively enrolled over a 6-year period. Intravenous KCl at a rate of 10 mmol/h was administered until muscle strength recovered. Serum potassium (K C ) and phosphorus concentrations were measured hourly during the paralytic attack and for 6 h after recovery. Results: The serum potassium (K C ) on attack was 2.1G0.2 mmol/l. The dose of KCl administered to restore muscle strength was 63G32 mmol, and peak serum K C concentration after recovery was 5.3G0.5 mmol/l. A paradoxical fall in serum K C concentration O0.1 mmol/l difference between presentation and treatment nadir was observed in approximately one-fourth of TPP patients (nZ20). These patients had significantly higher serum-free thyroxine concentration, systolic blood pressure, and heart rate on presentation, as well as serum phosphate concentration on recovery. They not only needed much more KCl supplementation (104G34 vs 48G19 mmol, P!0.001), but also had significantly more severe rebound hyperkalemia (5.8G0.5 vs 5.1G0.4 mmol/l, P!0.001) on recovery than those who did not have paradoxical hypokalemia. There was a positive correlation between the dose of KCl administered and the difference between peak and nadir serum K C (D K C ) (rZ0.68, P!0.001). Conclusions: TPP patients who do not develop paradoxical hypokalemia need a smaller KCl dose to achieve recovery, whereas those who develop paradoxical hypokalemia have more severe hyperthyroidism and hyperadrenergic activity and may require blockage of intracellular K C shift to prevent rebound hyperkalemia. European Journal of Endocrinology 161 911-916

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Section: Discussionmentioning

confidence: 99%

Therapeutic analysis in Chinese patients with thyrotoxic periodic paralysis over 6 years

Shiang¹,

Cheng²,

Tsai³

et al. 2009

European Journal of Endocrinology

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“…Fluxes of potassium among the fluid compartments were previously thought to be solely determined by changes in acidity. Other factors, however, have been identified as modulators of the plasma potassium response (5); prominent among them is the nature of the anion escorting the protons responsible for acidemia (6)(7)(8)(9). In sharp contrast with mineral acid acidosis that consistently leads to hyperkalemia, acute organic acid acidosis is not associated with a significant increase in plasma potassium (10).…”

Section: Introductionmentioning

confidence: 99%

Role of the endocrine pancreas in the kalemic response to acute metabolic acidosis in conscious dogs.

Adrogué¹,

Chap²,

Ishida³

et al. 1985

J. Clin. Invest.

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Metabolic acidosis due to organic acids infusion fails to elicit hyperkalemia. Although plasma potassium levels may rise, the increase is smaller than in mineral acid acidosis. The mechanisms responsible for the different effects of organic acid acidosis and mineral acid acidosis remain undefined, although dissimilar hormonal responses by the pancreas may explain the phenomena. To test this hypothesis, beta-hydroxybutyric acid (7 meq/kg) or hydrochloric acid (3 meq/kg) was infused over 30 min into conscious dogs (n = 12) with chronically implanted catheters in the portal, hepatic, and systemic circulation, and flow probes were placed around the portal vein and hepatic artery. Acid infusion studies in two groups of anesthetized dogs were also done to assess the urinary excretion of potassium (n = 14), and to evaluate the effects of acute suppression of renal electrolyte excretion on plasma potassium and on the release/uptake of potassium in peripheral tissues of the hindleg (n = 17). Ketoacid infusion caused hypokalemia and a significant increase in portal vein plasma insulin, from the basal level of 27±4 uU/ml to a maximum of 84±22 ,U, ml at 10 min, without changes in glucagon levels. By contrast, mineral acid acidosis of similar severity resulted in hyperkalemia and did not increase portal insulin levels but enhanced portal glucagon concentration from control values of 132±25 pg/ml to 251±39 pg/ml at 40 min. A significant decrease in plasma glucose levels due to suppression of hepatic release was observed during ketoacid infusion, while no changes were observed with mineral acid infusion. Plasma flows in the portal vein and hepatic artery remained unchanged from control values in both acid infusion studies. Differences in renal potassium excretion were ruled out as determinants of the disparate kalemic responses to organic acid infusion compared with HCO acidosis. Evaluation of the arteriovenous potassium difference across the hindleg during ketoacid infusion demonstrates that peripheral uptake of potassium is unlikely to be responsible for the observed hypokalemia. Although the tissue responsible for the different kalemic responses could not be defined with certainty, the data are compatible with an hepatic role in response to alterations in the portal vein insulin and/or glucagon levels in both acid infusion studies. We propose that cellular uptake of potassium is enhanced by hyperinsulinemia Correspondence and reprint requests should be addressed to Dr.

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“…Some of the measured values would also be compatible with the first hypothesis, an onset of fasting at or shortly before the beginning of the study; but none of them was exclusively specific for phase-I fasting. A number of metabolic results underline the notion of a phase-II fasting as does the initial discrete increase and then substantial decrease of the BMR [22,23], as well as the persistent ketonuria which points to an elevated oxidation of stored fat [24]. In individuals with low to moderate physical activity (as in the subject) this mainly leads to elevated serum triglycerides and free fatty acids [25].…”

Section: Discussionmentioning

confidence: 99%

Nutrition with ‘Light and Water’?

Heusser

Wolf²,

Vonwiller³

et al. 2008

Forsch Komplementmed

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Background: In her book ‘Living on Light’, Jasmuheen tries to animate people worldwide to follow her drastic nutrition rules in order to boost their quality of life. Several deaths have been reported as a fatal consequence. A doctor of chemistry who believably claimed to have been ‘living on light’ for 2 years, except for the daily intake of up to 1.5 l of fluid containing no or almost no calories was interested in a scientific study on this phenomenon. Participant and Methods: The 54-year-old man was subjected to a rigorous 10-day isolation study with complete absence of nutrition. During the study he obtained an unlimited amount of tea and mineral water but had no caloric intake. Parameters to monitor his metabolic and psychological state and vital parameters were measured regularly and the safety of the individual was ensured throughout the study. The subject agreed on these terms and the study was approved by the local ethics committee. Results: The most important observations were a permanent urinary excretion of ketones, up to a 3-fold increase in free fatty acid plasma levels, a mean weight loss of 0.26 kg/d, and an initially secondary hyperaldosteronism. Additionally, his ability to exercise was reduced. The subject remained psychologically stable and testing did not reveal any relevant changes. Conclusion: The results refute the claim and indicate a phase-II fasting state.

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Internal Potassium Balance and the Control of the Plasma Potassium Concentration

Cited by 221 publications

References 0 publications

Therapeutic analysis in Chinese patients with thyrotoxic periodic paralysis over 6 years

Therapeutic analysis in Chinese patients with thyrotoxic periodic paralysis over 6 years

Role of the endocrine pancreas in the kalemic response to acute metabolic acidosis in conscious dogs.

Nutrition with ‘Light and Water’?

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Internal Potassium Balance and the Control of the Plasma Potassium Concentration

Cited by 221 publications

References 0 publications

Therapeutic analysis in Chinese patients with thyrotoxic periodic paralysis over 6 years

Therapeutic analysis in Chinese patients with thyrotoxic periodic paralysis over 6 years

Role of the endocrine pancreas in the kalemic response to acute metabolic acidosis in conscious dogs.

Nutrition with &lsquo;Light and Water&rsquo;?

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Nutrition with ‘Light and Water’?