Effect of Oral Glucose Administration on Serum Potassium Concentration in Hemodialysis Patients

Muto, Shigeaki; Sebata, Kiyoko; Watanabe, Hidenobu; Shoji, Fumie; Yamamoto, Yoshie; Ohashi, Michie; Yamada, Takako; Matsumoto, Hisako; Mukouyama, Tomoko; Yonekura, Takekazu; Namiki, Sachiko; Kusano, Eiji

doi:10.1053/j.ajkd.2005.06.013

Cited by 21 publications

(15 citation statements)

References 20 publications

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“…Although insulin is generally recognized for its role in macronutrient metabolism, it also helps regulate potassium distribution and balance; potassium triggers and mediates insulin release 16–18 , and insulin, in turn, shifts potassium into cells by stimulating Na + /K + -ATPase activity 19–20 . Because dietary macronutrients, in particular glucose, also stimulate insulin release, they can help shift potassium intracelluarly 21–22 . The rise in S K following potassium ingestion is greatly attenuated if glucose is provided along with it 23–24 , although studies providing potassium and glucose in kidney disease patients and normal controls have produced conflicting results.…”

Section: Distribution and Excretion Of Potassium In Kidney Diseasementioning

confidence: 99%

Nutrient Non-equivalence: Does Restricting High-Potassium Plant Foods Help to Prevent Hyperkalemia in Hemodialysis Patients?

St-Jules

Sevick

2016

Journal of Renal Nutrition

150

129

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Hemodialysis patients are often advised to limit their intake of high-potassium foods to help manage hyperkalemia. However, the benefits of this practice are entirely theoretical and not supported by rigorous randomized controlled trials. The hypothesis that potassium restriction is useful is based on the assumption that different sources of dietary potassium are therapeutically equivalent. In fact, animal and plant sources of potassium may differ in their potential to contribute to hyperkalemia. In this commentary, we summarize the historical research basis for limiting high-potassium foods. Ultimately, we conclude that this approach is not evidence-based and may actually present harm to patients. However, given the uncertainty arising from the paucity of conclusive data, we agree that until the appropriate intervention studies are conducted, practitioners should continue to advise restriction of high-potassium foods.

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Section: Distribution and Excretion Of Potassium In Kidney Diseasementioning

confidence: 99%

Nutrient Non-equivalence: Does Restricting High-Potassium Plant Foods Help to Prevent Hyperkalemia in Hemodialysis Patients?

St-Jules

Sevick

2016

Journal of Renal Nutrition

150

129

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“…In addition, raising blood glucose alone with an oral load enhances extrarenal disposal of a K + load by stimulating insulin secretion (31, 32). Oral glucose can even lower serum [K + ] in patients with end-stage renal disease; such patients have negligible renal K + excretion, demonstrating the importance of endogenous insulin secretion to prevent hyperkalemia in this group by transferring K + from the ECF to the ICF (33). In both normal and pathological conditions, the consumption of K + along with a meal containing nutrients that stimulate insulin release leads to the activation of plasma K + clearance independent of plasma [K + ]—evidence of feedforward control of extracellular K + homeostasis by insulin.…”

Section: Sensing K+ Intake: Feedforward Versus Feedback Control Of Exmentioning

confidence: 99%

Recent Advances in Understanding Integrative Control of Potassium Homeostasis

Youn

McDonough

2009

Annu. Rev. Physiol.

118

108

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The potassium homeostatic system is very tightly regulated. Recent studies have shed light on the sensing and molecular mechanisms responsible for this tight control. In addition to classic feedback regulation mediated by a rise in extracellular fluid (ECF) [K+], there is evidence for a feedforward mechanism: Dietary K+ intake is sensed in the gut, and an unidentified gut factor is activated to stimulate renal K+ excretion. This pathway may explain renal and extrarenal responses to altered K+ intake that occur independently of changes in ECF [K+]. Mechanisms for conserving ECF K+ during fasting or K+ deprivation have been described: Kidney NADPH oxidase activation initiates a cascade that provokes the retraction of K+ channels from the cell membrane, and muscle becomes resistant to insulin stimulation of cellular K+ uptake. How these mechanisms are triggered by K+ deprivation remains unclear. Cellular AMP kinase–dependent protein kinase activity provokes the acute transfer of K+ from the ECF to the ICF, which may be important in exercise or ischemia. These recent advances may shed light on the beneficial effects of a high-K+ diet for the cardiovascular system.

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“…Exogenous insulin always causes a transient reduction in serum potassium but severe hypokalaemia can occur during the treatment of diabetic ketoacidosis or in intentional overdose of insulin [33]. The fall in potassium level is independent of plasma aldosterone and epinephrine levels [35]. Insulin increases cellular potassium uptake in the liver, muscle, and adipose tissue by activating the cellular Na + -K + -ATPase pump.…”

Section: Insulinmentioning

confidence: 99%

Drug-Induced Hypokalaemia

Salem¹,

Hmouda²,

Bouraoui³

2009

CDS

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Hypokalaemia (defined as a plasma potassium concentration<3.5 mEq/L) is a common electrolyte abnormality in clinical practice. Drugs are a common cause of either asymptomatic or symptomatic hypokalaemia. Drug-induced hypokalaemia is an important problem particularly in the elderly and in patients with cardiovascular, renal or hepatic disease. Hypokalaemia can complicate the use of the drug in the therapeutic concentration range, and can also be precipitated with overdose or conditions leading to drug intoxication. Because the etiologies of hypokalaemia are numerous, the diagnosis of drug-induced hypokalaemia may be overlooked. Physicians should always pay close attention to this common side effect. Evaluation and management of a hypokalaemic patient should include a careful review of medications history to determine if a drug capable of causing or aggravating this electrolyte abnormality is present.

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Effect of Oral Glucose Administration on Serum Potassium Concentration in Hemodialysis Patients

Cited by 21 publications

References 20 publications

Nutrient Non-equivalence: Does Restricting High-Potassium Plant Foods Help to Prevent Hyperkalemia in Hemodialysis Patients?

Nutrient Non-equivalence: Does Restricting High-Potassium Plant Foods Help to Prevent Hyperkalemia in Hemodialysis Patients?

Recent Advances in Understanding Integrative Control of Potassium Homeostasis

Drug-Induced Hypokalaemia

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