Hypokalemia during treatment of diabetic ketoacidosis: clinical evidence for an aldosterone-like action of insulin. (Hebbar)

J Pediatr. 2013 Jul;163(1):207-212.e1. PMID: 23410602

OBJECTIVES: To investigate whether the development of hypokalemia in patients with diabetic ketoacidosis (DKA) treated in the pediatric critical care unit (PCCU) could be caused by increased potassium (K(+)) excretion and its association with insulin treatment.

STUDY DESIGN: In this prospective observational study of patients with DKA admitted to the PCCU, blood and timed urine samples were collected for measurement of sodium (Na(+)), K(+), and creatinine concentrations and for calculations of Na(+) and K(+) balances. K(+) excretion rate was expressed as urine K(+)-to-creatinine ratio and fractional excretion of K(+).

RESULTS: Of 31 patients, 25 (81%) developed hypokalemia (plasma K(+) concentration <3.5 mmol/L) in the PCCU at a median time of 24 hours after therapy began. At nadir plasma K(+) concentration, urine K(+)-to-creatinine ratio and fractional excretion of K(+) were greater in patients who developed hypokalemia compared with those without hypokalemia (19.8 vs 6.7, P = .04; and 31.3% vs 9.4%, P = .004, respectively). Patients in the hypokalemia group received a continuous infusion of intravenous insulin for a longer time (36.5 vs 20 hours, P = .015) and greater amount of Na(+) (19.4 vs 12.8 mmol/kg, P = .02). At peak kaliuresis, insulin dose was higher in the hypokalemia group (median 0.07, range 0-0.24 vs median 0.025, range 0-0.05 IU/kg; P = .01), and there was a significant correlation between K(+) and Na(+) excretion (r = 0.67, P < .0001).

CONCLUSIONS: Hypokalemia was a delayed complication of DKA treatment in the PCCU, associated with high K(+) and Na(+) excretion rates and a prolonged infusion of high doses of insulin.

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