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Home / Drugs / Starting with B / Bumetanide


For the treatment of edema associated with congestive heart failure, hepatic and renal disease including the nephrotic syndrome.


Bumetanide is a loop diuretic of the sulfamyl category to treat heart failure. It is often used in patients in whom high doses of furosemide are ineffective. There is however no reason not to use bumetanide as a first choice drug. The main difference between the two substances is in bioavailability. It is said to be a more predictable diuretic, meaning that the predictable absorption is reflected in a more predictable effect. Bumetanide is 40 times more potent than furosemide (for patients with normal renal function).

mechanism of action

Bumetanide interferes with renal cAMP and/or inhibits the sodium-potassium ATPase pump. Bumetanide appears to block the active reabsorption of chloride and possibly sodium in the ascending loop of Henle, altering electrolyte transfer in the proximal tubule. This results in excretion of sodium, chloride, and water and, hence, diuresis.


Overdosage can lead to acute profound water loss, volume and electrolyte depletion, dehydration, reduction of blood volume and circulatory collapse with a possibility of vascular thrombosis and embolism. Electrolyte depletion may be manifested by weakness, dizziness, mental confusion, anorexia, lethargy, vomiting and cramps. Treatment consists of replacement of fluid and electrolyte losses by careful monitoring of the urine and electrolyte output and serum electrolyte levels.


45% is secreted unchanged. Urinary and biliary metabolites are formed by oxidation of the N-butyl side chain.


Bumetanide is completely absorbed (80%), and the absorption is not altered when taken with food. Bioavailability is almost complete.

half life

60-90 minutes

route of elimination

Oral administration of carbon-14 labeled Bumex to human volunteers revealed that 81% of the administered radioactivity was excreted in the urine, 45% of it as unchanged drug. Biliary excretion of Bumex amounted to only 2% of the administered dose.

drug interactions

Amikacin: Increased ototoxicity

Cisplatin: Increased ototoxicity

Colesevelam: Bile acid sequestrants such as colesevelam may decrease the absorption of loop diuretics such as bumetanide. Monitor for decreased serum concentrations/therapeutic effects of loop diuretics if coadministered with bile acid sequestrants. Separating the administration of doses by 2 or more hours may reduce (but not eliminate) the risk of interaction. The manufacturer of colesevelam recommends that drugs should be administered at least 1 hour before or 4 hours after colesevelam.

Deslanoside: Possible electrolyte variations and arrhythmias

Digitoxin: Possible electrolyte variations and arrhythmias

Digoxin: Possible electrolyte variations and arrhythmias

Gentamicin: Increased ototoxicity

Ginseng: Ginseng may decrease the therapeutic effect of diuretic, bumetanide.

Ibuprofen: The NSAID, ibuprofen, may antagonize the diuretic and antihypertensive effects of the loop diuretic, bumetanide.

Indomethacin: The NSAID, indomethacin, may decrease the diuretic and antihypertensive effects of the loop diuretic, bumetanide.

Kanamycin: Increased ototoxicity

Netilmicin: Increased ototoxicity

Streptomycin: Increased ototoxicity

Sulindac: The NSAID, sulindac, decreases the diuretic and antihypertensive effects of the loop diuretic, bumetanide.

Tobramycin: Increased ototoxicity

Trandolapril: The loop diuretic, Bumetanide, may increase the hypotensive effect of Trandolapril. Bumetanide may also increase the nephrotoxicity of Trandolapril.

Treprostinil: Additive hypotensive effect. Monitor antihypertensive therapy during concomitant use.