Matz has pointed out yet another clinical situation in which refractory potassium repletion secondary to magnesium depletion may be operative, ie, in diabetic ketoacidosis. While this association has not been precisely defined, there are cases of diabetic ketoacidosis described1,2 in which profound hypokalemia has been resistant to administration of very large doses of potassium, ranging upward to 710 mEq per 24 hours. While osmotic diuresis due to glycosuria may be responsible for a portion of the potassium loss, as well as translocation of extracellular potassium in response to bicarbonate therapy, requirements for potassium repletion of this magnitude suggest the possibility of refractory potassium repletion due to magnesium deficiency as being operative.
Whang R. Refractory Potassium Repletion due to Magnesium Deficiency-Reply. Arch Intern Med. 1992;152(11):2346. doi:10.1001/archinte.1992.00400230138026
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