The risk of pronounced hyperkalaemia after arginine infusion in the diabetic subject.

Following previous work showing that i.v. arginine induces a fall in blood phosphorus and an increase in blood potassium in normal subjects, investigation of the mechanism underlying these metabolic changes was extended to a group of 14 insulin-dependent diabetics and a further 6 normal volunteers. In the diabetics, arginine (0.5 g/kg body weight) in 30 min caused a slight, but significant fall in blood phosphorus (delta = -0.40 +/- 0.04 mg/ml p less than 0.01). This was well below the fall noted in the normal subjects, which, as demonstrated in the earlier study, is to a great extent mediated by insulin. The increase in blood potassium was much more marked than in the normal subjects (delta = + 1.42 +/- 0.15 mEq /l; p less than 0.001) and rose to pathological levels (5.6 to 6.5. mEg/l) in 9 out of 14 patients. There were no significant changes in blood pH, plasma osmolality, or plasma aldosterone. Inhibition of the glucagon response to arginine by means of a priming dose of 250 micrograms somatostatin, followed by infusion of 1,500 micrograms/hr, did not abolish the rise in blood potassium. These findings indicate that insulin protect against arginine-induced hyperkalaemia and that this metabolic alteration does not depend on glucagon, acidosis, enhance plasma osmolality, nor the suppression of aldosterone secretion. Persons with low insulin secretion due, for example, to stress or diabetes, run the risk of pathological hyperkalaemia if subjected to i.v. infusion of arginine.