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Bumetanide is a loop diuretic and works by decreasing the reabsorption of sodium by the kidneys. The main difference between bumetanide and furosemide is in their bioavailability and potency. About 60% of furosemide is absorbed in the intestine, and there are substantial inter- and intraindividual differences in bioavailability (range 10-90%).
However, for torsemide and bumetanide, their oral bioavailability is consistently higher than 90%. Torsemide has a longer half life in heart failure patients (6 hours) than furosemide (2.7 hours). A 40 mg dose of furosemide is clinically equivalent to a 20 mg dose of torsemide and to a 1 mg dose of bumetanide. [6]
bumetanide, [17] ethacrynic acid, [17] furosemide, [17] torsemide: Inhibits the Na-K-2Cl symporter: 3. medullary thick ascending limb: Osmotic diuretics: glucose (especially in uncontrolled diabetes), mannitol: Promotes osmotic diuresis 2. proximal tubule, descending limb: Potassium-sparing diuretics
This lowers blood pressure and prevents excess fluid accumulation in heart failure. Metolazone is sometimes used together with loop diuretics such as furosemide or bumetanide, but these highly effective combinations can lead to dehydration and electrolyte abnormalities. It was patented in 1966 and approved for medical use in 1974. [1]
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Furosemide is a known ototoxic agent generally causing transient hearing loss but can be permanent. Reported cases of furosemide-induced hearing loss appeared to be associated with rapid intravenous administration, high dosages, concomitant renal disease, and coadministration with other ototoxic medication.
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