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Contrasting Effects of Various Potassium Salts on Renal Citrate Excretion^*

Center for Mineral Metabolism and Clinical Research and Nephrology Division, Department of Internal Medicine, University of Texas Southwestern Medical Center Dallas, Texas 75235
The Nephrology Section, Vanderbilt University School of Medicine Nashville, Tennessee 37232

Address all correspondence and requests for reprints to: Dr. Khashayar Sakhaee, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, Texas 75235–8885.

Mechanisms for the citraturic response to potassium citrate treatment were sought by assessing renal citrate clearance and acid-base status after oral administration of potassium citrate, potassium bicarbonate, and potassium chloride. After 2 weeks of treatment of eight patients with stones at a dose of 80 meq/day, urinary citrate rose significantly from 2.5 ± 1.6 mmol/day (no drug) to 5.1 ± 1.7 mmol/day with potassium citrate and to 4.5 ± 1.5 mmol/day with potassium bicarbonate (P < 0.05), but did not change significantly with potassium chloride. Citrate clearance increased from 8.0 to 27.4 mL/min with potassium citrate and 25.8 mL/min with potassium bicarbonate (P < 0.05), but did not ir. crease with potassium chloride. Both potassium citrate and potassium bicarbonate significantly raised urinary bicarbonate and decreased urinary ammonium, titratable acid, and net acid excretion. Potassium chloride was without effect. Effects of potassium citrate on urinary citrate, citrate clearance, and acid-base status tended to be more prominent than those of potassium bicarbonate, but these changes were not significant. Thus, the citraturic action of potassium citrate is largely accountable fo r by provision of an alkali load. Potassium itself had no effect in the absence of potassium deficiency.

^* This work was supported by USPHS Grants P01-DK-20543, M01-RR-00633, and R01-AR-16061.

Received July 2, 1990.

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