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Pflügers Archiv

, Volume 381, Issue 2, pp 137–142 | Cite as

Lack of effect of amphotericin B on urine-bloodpCO2 gradient in spite of urinary acidification defect

  • Lal C. Garg
Transport Processes, Metabolism and Endocrinology; Kidney, Gastrointestinal Tract, and Exocrine Glands

Abstract

The alkaline urine of normal animals and humans has higher carbon dioxide tension (pCO2) than that of blood. On the other hand, the urine-bloodpCO2 gradient is decreased in some patients and experimental animals having urinary acidification defect. It has been proposed that the urine-bloodpCO2 gradient is dependent on H+ accumulation in the distal nephron to form H2CO3 which is not dehydrated to CO2 until it passes the nephrons. We produced a urinary acidification defect in rats by treating the animals with amphotericin B and studied their ability to excrete acute acid and alkali loads. The amphotericin-treated animals could not decrease their urine pH lower than 5.84, even with a plasma HCO 3 of 10.0 mEq/l. On the other hand, control animals decreased their urine pH to 5.50 with a plasma HCO 3 of 18.2 mEq/l. There was no significant differences in urine-bloodpCO2 gradient between amphotericin-treated and control rats. Thus, there was a dissociation between the pH of an acid urine andpCO2 of an alkaline urine in the amphotericin-treated rats. The possible mechanisms of this dissociation along with the mechanisms of urinarypCO2 formation are discussed. It is concluded, that the urine-bloodpCO2 gradient during alkaline infusion is not an accurate index of H+ secretory capability.

Key words

Amphotericin B Urine-bloodpCO2 gradient Urinary acidification Renal tubular acidosis 

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Copyright information

© Springer-Verlag 1979

Authors and Affiliations

  • Lal C. Garg
    • 1
  1. 1.JHM Health CenterDepartment of Pharmacology and Therapeutics, University of Florida College of MedicineGainesvilleUSA

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