A loop diuretic with bioavailability ranging from 10-90% with absorption decreasing in patients with severe congestive heart failure and associated gut edema.

Has erratic oral absorption, with a bioavailability of 11% to 90%.

Furosemide increases excretion of water by interfering with the chloride-binding cotransport system, which, in turn, inhibits sodium and chloride reabsorption in the ascending loop of Henle and distal renal tubule.


Sold under the brand name Lasix among others.

A. medication used to treat fluid build-up due to heart failure, liver insufficiency, or kidney disease.

Also be used for the treatment of hypertension.

It can be taken by intravenously, intramuscularly, or by mouth.

A loop diuretic that acts by inhibiting the luminal Na-K-Cl cotransporter in the thick ascending limb of the loop of Henle, by binding to the chloride transport channel, thus causing sodium, chloride, and potassium loss in urine.

The action on the distal tubules is independent of any inhibitory effect on carbonic anhydrase or aldosterone

It abolishes the corticomedullary osmotic gradient and blocks negative, as well as positive, free water clearance.

Diuresis is not limited by development of acidosis, as it is with the carbonic anhydrase inhibitors.

When taken orally, it typically begins working within an hour.

When given intravenously, it typically begins working within five minutes.

Pregnancy category US: C (Risk not ruled out).

Bioavailability 43–69%.

Metabolism liver and kidney glucuronidation.

Elimination half-life up to 100 minutes

Excretion renal 66%, biliary 33%.

Common side effects include: feeling lightheaded with standing, ringing in the ears, and sensitivity to light.

Potentially serious side effects include electrolyte abnormalities, low blood pressure, and hearing loss.

Works by decreasing the reabsorption of sodium by the kidneys.

Primarily used for the treatment of edema, but also in some cases of hypertension, when there is also kidney or heart impairment.

A first-line agent in most people with edema caused by congestive heart failure.

Used for liver cirrhosis, kidney impairment, nephrotic syndrome, as adjunct therapy for swelling of the brain or lungs where rapid diuresis is required, and in the management of severe hypercalcemia in combination with adequate rehydration.

It is used along with albumin in nephrotic syndrome to reduce edema.

It is mainly excreted by tubular secretion in the kidney, and with kidney impairment, clearance is reduced, increasing the risk of adverse effects.

Lower initial doses are recommended in older patients, and high doses may be needed in kidney failure.

Diuresis is usually complete within 6–8 hours of oral administration.

Can lead to gout caused by hyperuricemia.

Hyperglycemia is also a common side effect.

The tendency to cause hypokalemia.

Other electrolyte abnormalities that can result from furosemide use include hyponatremia, hypochloremia, hypomagnesemia, and hypocalcemia.

Long-term use of furosemide can cause varying degrees of thiamine deficiency, so thiamine supplementation is also suggested.

It is considered ototoxic with large intravenous doses and rapid administration and in renal impairment.

Associated with sulfur allergy.


Furosemide greatly inhibits platelet aggregation, with ADP, epinephrine, collagen, ristocetin, thrombin and serotonin. 

With large doses increases free thyroid hormone effects.

It has potential interactions with:

Aspirin and other salicylates

Other diuretics-ethacrynic acid, hydrochlorothiazide.

Synergistic effects with other antihypertensives.


Potentially hazardous interactions with other drugs:

Increased risk of kidney damage with nonsteroidal anti-inflammatory drugs

Antagonism of diuretic effect with NSAIDs

Risk of cardiac toxicity exists with antiarrhythmics if hypokalemia occurs.

The effects of lidocaine and mexiletine are antagonized.

Has increased risk of ototoxicity with aminoglycosides, polymyxins and vancomycin.

Enhanced hypotensive effect with MAOIs.

Increased risk of postural hypotension with tricyclic antidepressants.

Increased risk of hyponatremia with carbamazepine.

Increased risk of hypokalemia with amphotericin

Enhanced hypotensive effect with anti hypertensives.

Increased risk of first dose hypotensive effect with alpha-blockers.

Increased risk of ventricular arrhythmias with sotalol if hypokalemia occurs.

Increased risk of ventricular arrhythmias with antipsychotic meds.

Enhanced hypotensive effect with phenothiazines.

Increases cardiac glycoside toxicity if hypokalemia occurs.

It is a noncompetitive subtype-specific blocker of GABA-A receptors.

% Bioavailability 47-70%

Bioavailability with end-stage renal disease 43 – 46%.

% Protein binding 91–99.

Volume of distribution may be higher in patients with cirrhosis or nephrotic syndrome.

% Excreted in urine 60 – 90.

% Excreted in feces 7 – 9.

% Excreted in bile 6 – 9.

Approximately 10% is metabolized by the liver.

Liver metabolism may be greater in individuals with severe kidney failure.

Elimination half-life 2 hours.

Half-life prolonged in congestive heart failure with a mean of 3.4 hrs.

Prolonged in severe kidney failure 4 – 6 hrs.

Time to peak concentration

Intravenous administration 0.3 hours

Oral solution 0.83 hours

Oral tablet 1.45 hours.

Its pharmacokinetics are not significantly altered by food.

There is no direct relationship has been between furosemide concentration in the plasma and furosemide efficacy, but depends upon the concentration of furosemide in urine.

It should be used with caution when combined with corticosteroids, aminoglycoside antibiotics and trimethoprim sulfa.

It decreases the kidneys’ ability to excrete aspirin, so dosages will need to be adjusted if combined with that drug.

Furosemide may increase the risk of digoxin toxicity due to hypokalemia.

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