ARTHUR H. FISHER, M.D.
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To the editor: Oh and colleagues in the December issue (1) described 35 patients who developed hyperchloremic acidosis during treatment of diabetic (normochloremic) ketoacidosis. In their discussion of the pathogenetic mechanisms involved, they did not consider a renal tubular defect as a contributing cause of the hyperchloremic acidosis. Serum and total body phosphate levels are known to be severely depressed during the early treatment phase of diabetic ketoacidosis (2, 3), and phosphate depletion has been associated with renal bicarbonate wasting and systemic hyperchloremic metabolic acidosis (3, 4).
It is unfortunate that serum phosphate and urinary pH determinations were not recorded
FISHER AH. Hyperchloremic Acidosis and Diabetic Ketoacidosis. Ann Intern Med. 1979;90:722–723. doi: https://doi.org/10.7326/0003-4819-90-4-722_2
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Published: Ann Intern Med. 1979;90(4):722-723.
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