DONALD E. BUTKUS, M.D.
To the editor: The elegant study by DeFronzo and colleagues in the March issue (1) reports a significant decrease in potassium excretion in a group of patients with sickle-cell hemoglobinopathies when compared with a group of comparably studied control patients after sodium sulfate infusion, intravenous potassium infusion, and furosemide administration. They further document that neither hyperkalemia nor increased fecal potassium excretion occur during intravenous or oral potassium loading, respectively, and suggest that the potassium load administered intravenously is handled by increased tissue uptake. Of the potential mechanisms, the authors fail to consider, that their patients were relatively potassium depleted compared
BUTKUS DE. Renal Potassium Handling in Sickle-Cell Disease. Ann Intern Med. ;91:130. doi: 10.7326/0003-4819-91-1-130_1
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Published: Ann Intern Med. 1979;91(1):130.
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