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indicationFor the treatment of edema associated with congestive heart failure, cirrhosis of the liver, and renal disease, including the nephrotic syndrome. Also for the treatment of hypertension alone or in combination with other antihypertensive agents.
pharmacologyFurosemide, a sulfonamide-type loop diuretic structurally related to bumetanide, is used to manage hypertension and edema associated with congestive heart failure, cirrhosis, and renal disease, including the nephrotic syndrome.
mechanism of actionFurosemide, a loop diuretic, inhibits water reabsorption in the nephron by blocking the sodium-potassium-chloride cotransporter (NKCC2) in the thick ascending limb of the loop of Henle. This is achieved through competitive inhibition at the chloride binding site on the cotransporter, thus preventing the transport of sodium from the lumen of the loop of Henle into the basolateral interstitium. Consequently, the lumen becomes more hypertonic while the interstitium becomes less hypertonic, which in turn diminishes the osmotic gradient for water reabsorption throughout the nephron. Because the thick ascending limb is responsible for 25% of sodium reabsorption in the nephron, furosemide is a very potent diuretic.
toxicityProfound diuresis may cause fluid and electrolyte depletion. Excessive dehydration and potassium depletion may occur. Excessive diuresis may cause rapid weight loss, orthostatic hypotension or acute hypotensive episodes. May also cause tinnitus, reversible or permanent hearing loss or reversible deafness.
biotransformationOnly a small amount is hepatically metabolized to the defurfurylated derivative, 4-chloro-5-sulfamoylanthranilic acid.
absorption60% absorbed in patients with normal renal function
half life2 hours
route of eliminationFurosemide is excreted in urine. Significantly more furosemide is excreted in urine following the I.V. injection than after the tablet or oral solution.
drug interactionsAmikacin: Increased ototoxicity
Cisplatin: Increased ototoxicity
Colesevelam: Bile acid sequestrants such as colesevelam may decrease the absorption of loop diuretics such as furosemide. 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
Ethotoin: The hydantoin decreases the effect of furosemide
Fosphenytoin: The hydantoin decreases the effect of furosemide
Gentamicin: Increased ototoxicity
Ginseng: Ginseng decreases the therapeutic effect
Ibuprofen: The NSAID, ibuprofen, may antagonize the diuretic and antihypertensive effects of the loop diuretic, furosemide.
Indomethacin: The NSAID, indomethacin, may decrease the diuretic and antihypertensive effects of the loop diuretic, furosemide.
Kanamycin: Increased ototoxicity
Mephenytoin: The hydantoin decreases the effect of furosemide
Netilmicin: Increased ototoxicity
Phenytoin: The hydantoin decreases the effect of furosemide
Streptomycin: Increased ototoxicity
Sulindac: The NSAID, sulindac, may decrease the diuretic and antihypertensive effects of the loop diuretic, furosemide.
Tobramycin: Increased ototoxicity
Trandolapril: The loop diuretic, Furosemide, may increase the hypotensive effect of Trandolapril. Furosemide may also increase the nephrotoxicity of Trandolapril.
Treprostinil: Additive hypotensive effect. Monitor antihypertensive therapy during concomitant use.