; therefore,
It is probable that AmB alters the permeability of
the distal tubular cells, leading to an Increase in the
passive fluxes of potassium down its electrochemical
gradient. Renin and aldosterone levels are not increased
during AmB therapy (47,50).
The defect in urinary acidification, the potassium
wasting, and the defect in maximal urinary concentrating
ability observed In patients treated with AmB
support the concept that AmB toxicity is directed at
the distal tubule. This is In agreement with the pathologic
findings of distal tubular degeneration and
nephrocalclnosis (45,5 1 ,52). Furthermore, glucosuria,
aminoaciduria, and phosphaturia, which reflect