EFFECT OF AMPHOTERICIN-B ON URINE ACIDIFICATION IN RATS - IMPLICATIONS FOR PATHOGENESIS OF DISTAL RENAL TUBULAR-ACIDOSIS

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  • 1 January 1977
    • journal article
    • research article
    • Vol. 89  (3) , 463-470
Abstract
Distal renal tubular acidosis possibly is a gradient-limited disorder and the low urine PCO2 [partial pressure of CO2] observed in this condition is caused by back diffusion of carbonic acid. This study was designed to examine this hypothesis using the amphotericin B model of gradient-limited distal renal tubular acidosis in rats. After induction of acute metabolic acidosis the minimum urine pH in 12 of 24 amphotericin B-treated rats exceeded 5.63 (mean 5.76 .+-. 0.04), whereas it was 5.41 .+-. 0.04 in control rats. These animals with impaired urine acidification were presumed to have a gradient lesion and were studied in bicarbonate-loading experiments. The urine minus blood PCO2 gradient in these rats was 24.9 .+-. 1.5 mm Hg, a value similar to that of the control rats (26.7 .+-. 2.1 mm Hg). The presence of a normal urine minus blood PCO2 value in this experimentally induced gradient-limited type of acidification lesion indicates that a permeability defect for H+ was not associated with a similar defect for carbonic acid and that the urine minus blood PCO2 gradient is a valid index of distal nephron H+ secretion in amphotericin B-like gradient-type lesions.