Publications by authors named "Shanklin N"

Acute treatment of hyperkalemia in patients with end-stage renal disease requires temporizing measures to shift potassium rapidly from the extracellular to the intracellular fluid compartments until hemodialysis can be initiated. Whereas insulin and albuterol are effective in lowering plasma potassium acutely, bicarbonate by itself is not. Bicarbonate administration may, however, potentiate the effects of insulin and albuterol on plasma potassium.

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End-stage renal disease patients presenting with severe hyperkalemia are frequently treated with albuterol to lower their plasma potassium acutely, until emergent hemodialysis can be initiated. Such treatment stimulates potassium shifts from the extracellular to the intracellular fluid compartments. The resulting reduction of potassium concentration gradient between the blood and dialysate may potentially attenuate the efficacy of potassium removal during the ensuing hemodialysis treatment.

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Purpose: Extrarenal potassium disposal plays an important role in the tolerance of an acute potassium load and is particularly critical in patients with renal failure. Insulin is known to stimulate this disposal by enhancing potassium uptake into the cells. Since dietary potassium is generally ingested in combination with carbohydrates, the predictable stimulation of endogenous insulin release may blunt the expected increase in plasma potassium.

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Extrarenal potassium disposal is an important defense against hyperkalemia in patients with end-stage renal disease. Both insulin and epinephrine are important modulators of this process. Hemodialysis patients are prone to developing hyperkalemia during fasting.

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In normal subjects, beta-adrenergic stimulation lowers the serum potassium, whereas alpha-stimulation raises it. Epinephrine, a mixed alpha and beta agonist, acutely lowers the blood potassium in normal subjects, but not in patients with end-stage renal disease. This study was designed to determine whether the resistance to the hypokalemic effect of epinephrine in dialysis patients is due to a blunted beta-adrenergic response, or to an augmented alpha-adrenergic response.

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