Effect of amphotercin B on urine acidification in rats: implications for the pathogenesis of distal renal tubular acidosis.
It has been proposed that distal renal tubular acidosis is a gradient-limited disorder an that the low urine Pco2 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 hydrogen ions 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 hydrogen ion secretion in amphotericin B-like gradient-type lesions.
D000141:Acidosis, Renal Tubular / Q000139:chemically induced / Q000209:etiology* / Q000652:urine; D000666:Amphotericin B; D000818:Animals; D002245:Carbon Dioxide / Q000652:urine; D005665:Furosemide / Q000494:pharmacology; D007668:Kidney / Q000378:metabolism; D007671:Kidney Concentrating Ability; D008297:Male; D009994:Osmolar Concentration; D051381:Rats
D002245:Carbon Dioxide; D005665:Furosemide; D000666:Amphotericin B