REPLY
Urea Excretion Rate as a Contributor to Trimethoprim-induced Hyperkalemia
Heino Velazquez, PhD;
David H. Ellison, MD; and
Mark A. Perazella, MD
15 January 1994 | Volume 120 Issue 2 | Pages 166-167
IN RESPONSE:
In a recent study [1], we showed that trimethoprim inhibits potassium secretion and blocks sodium channels in the renal distal tubule and that half of the patients with AIDS who were treated with trimethoprim developed hyperkalemia (plasma potassium >5.0). We attributed this finding to a decrease in renal potassium excretion caused by trimethoprim.
Drs. Schreiber and Halperin propose another possible reason, namely a low volume delivery (low osmolar delivery, specifically urea) to the distal tubule. Tubule fluid flow rate is an important determinant of potassium secretion [2] and limiting distal solute delivery can decrease potassium secretion. We do not have data on urea excretion or volume status of the patients in our study sample, but we agree that this possibility should be studied further.
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Author and Article Information
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Yale University School of Medicine; New Haven, CT 06520-8029
1. Velazquez H, Perazella MA, Wright FS, Ellison DH. Renal mechanism of trimethoprim-induced hyperkalemia. Ann Intern Med. 1993; 119:296-301.
2. Good DW, Wright FS. Luminal influences on potassium secretion: sodium concentration and fluid flow rate. Am J Physiol. 1979; 236: F192-205.
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