Hypokalemia during treatment of diabetic ketoacidosis: Clinical evidence for an aldosterone-like action of insulin

摘要

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.