[Skip to Content]
Access to paid content on this site is currently suspended due to excessive activity being detected from your IP address Please contact the publisher to request reinstatement.
[Skip to Content Landing]
June 8, 1970

Diabetic Ketoacidosis

Author Affiliations

Loyola University Chicago

JAMA. 1970;212(10):1706. doi:10.1001/jama.1970.03170230108024

This article is only available in the PDF format. Download the PDF to view the article, as well as its associated figures and tables.


To the Editor.—  There is absolutely no evidence to support Dr. Zwillich's statement that patients with renal diseases who are hyperkalemic have increased body stores of potassium. As a matter of fact, these patients usually are potassium deficient. The deficits are produced by the same mechanisms which produce potassium deficits in patients with diabetic ketoacidosis. The extracellular acidosis results in transfer of potassium from intracellular sites and probably bone and connective tissue to the extracellular compartment with subsequent loss for the body. It is not unusual to observe patients with hyperkalemia subsequent to renal disease who have severe potassium depletion. Furthermore, it is not possible to replete these individuals by administration of potassium unless the acidosis is corrected, even if the potassium is administered as the chloride salt.Therefore, a good principle of patient management is not to administer potassium to any hyperkalemic patient, until the underlying cause is corrected