Defect in urinary acidification induced in vitro by amphotericin B
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In this article, an experimental defect in urinary acidification was induced in the isolated turtle bladder by amphotericin B and the nature of the defect was examined and it was suggested that impaired acidification is caused by increased passive permeability of the luminal membrane and increased back diffusion of hydrogen ion rather than by failure of active transport.Abstract:
An experimental defect in urinary acidification was induced in the isolated turtle bladder by amphotericin B and the nature of the defect was examined. Net hydrogen ion secretion was little affected by amphotericin when passive electrochemical forces across the epithelium were held at a minimum in the short-circuited state under isohydric conditions. Hydrogen ion secretion against a gradient, however, was markedly reduced by amphotericin and abolished at gradients of more than 2 pH units.The results suggest that impaired acidification is caused by increased passive permeability of the luminal membrane and increased back diffusion of hydrogen ion rather than by failure of active transport. This interpretation is supported by evidence that amphotericin causes a large increase in the permeability to potassium and smaller increases in the sodium and chloride permeabilities. This mechanism of impaired acidification in vitro may have bearing on the renal tubular defect observed in patients treated with amphotericin B.read more
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Renal tubular acidosis.
F J Gennari,J J Cohen +1 more
TL;DR: Renal tubular acidosis (RTA) represents a clinical syndrome characterized by a state of renal tubular insufficiency with regard to the re absorption of bicarbonate, the excretion of net hydrogen ion, or both, and includes a large number of etiologies.
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Amphotericin B nephrotoxicity.
Ramzi Sabra,Robert A. Branch +1 more
TL;DR: In the clinical situation, and in long term models of nephrotoxicity in the rat, salt loading protects against deterioration in renal function; recommendations are made for the optimisation of amphotericin B therapy by salt loading.
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Nephrotoxicity of amphotericin B with emphasis on changes in tubular function
Janis L. Burgess,Robert Birchall +1 more
TL;DR: The most consistent change in proximal tubular function was an increase in the clearance of uric acid which rose with increasing dosage of amphotericin B and varied inversely with the glomerular filtration rate.
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Renal Tubular Acidosis Associated with Toluene Sniffing
TL;DR: A life-threatening complication of toluene sniffing may be the induction of a renal tubular acidification defect, which was demonstrated on several occasions during avoidance and use of toLUene "sniffing".
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TL;DR: Nephrotoxicity, the major complication of long-term therapy with amphotericin B, is attributed to drug-induced renal vasoconstriction plus a direct toxic action on renal tubules.
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