In some critically ill patients, conventional doses of loop diuretics do not always result in optimal diuresis. In such cases, patients are considered diuretic resistant. Three mechanisms of the phenomenon of diuretic resistance have been suggested. The
most common is the concept of rebound sodium retention. After administration of loop diuretics, sodium absorption is blocked at the loop of Henle, leading to a pronounced reabsorption of sodium at the distal sites of the nephron. This reabsorption may be suffcient to nullify the prior blockade. Studies in rats have shown that six to eight
days of continuous furosemide infusion caused hypertrophy of the distal convulated tubule, the connecting tubule, and the collecting ducts of the nephron.