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. The goal of the current study was to evaluate the effect of oral glucose on the disposition of an acute oral potassium load in hemodialysis patients and in normal controls.
Patients and methods: Eight hemodialysis patients and eight normal control subjects were studied after an overnight fast. Each subject received an oral load of potassium chloride elixir (0.25 mmol/kg). Plasma potassium was measured at baseline and at 30-minute intervals for 3 hours. On a separate study day, the subjects underwent the identical protocol, with the addition of 50 g of oral glucose to the potassium load to stimulate endogenous insulin release. The identical two experimental protocols were repeated in each subject during concomitant beta blockade with propranolol.
Results: The maximal increase in plasma potassium after the potassium load was significantly greater in the hemodialysis patients than in the controls (0.93 +/- 0.08 versus 0.52 +/- 0.04 mmol/L, p < 0.001). Concomitant oral glucose markedly blunted the maximal rise in potassium levels in both experimental groups (0.40 +/- 0.09 and 0.22 +/- 0.07 mmol/L, respectively, p < 0.005 versus potassium alone). With concomitant beta blockade, the maximal increase in plasma potassium after the potassium load was significantly greater in the hemodialysis patients than in the controls (1.11 +/- 0.12 versus 0.72 +/- 0.09 mmol/L, p = 0.02). Concomitant oral glucose again markedly blunted the maximal increase in potassium in both experimental groups (0.72 +/- 0.09 and 0.39 +/- 0.06 mmol/L, respectively, p < 0.01 versus potassium alone). The potassium load in the absence of glucose did not produce changes in plasma insulin concentration in either experimental group. The potassium load in combination with oral glucose load produced more sustained hyperinsulinemia in the dialysis patients than in the control subjects.
Conclusions: Exogenous glucose, by stimulating endogenous secretion of insulin, enhances extrarenal disposal of a potassium load. This protective effect of exogenous glucose against hyperkalemia is independent of adrenergic stimulation. The beneficial effect of exogenous glucose defends against the development of severe hyperkalemia after dietary potassium ingestion, and is critically important in hemodialysis patients, due to their negligible renal potassium excretion.