Furosemide (Lasix).
Furosemide is a powerful loop diuretic used in heart failure, edema, and hypertension. Chemically it is a sulfonamide — it carries the –SO2NH2 group — but it is not an antibiotic and lacks the N4 arylamine that drives most antibiotic-type immune reactivity. Cross-reactivity in patients with sulfa antibiotic allergy is low.
- Brand
- Lasix (most common); also generic furosemide.
- Class
- Loop diuretic — inhibitor of the
Na+-K+-2Cl−cotransporter (NKCC2) in the thick ascending limb. - Common indications
- Heart failure with volume overload, pulmonary edema, peripheral edema, hypertension, hypercalcemia.
- Sulfa allergy
- Low cross-reactivity with sulfa antibiotics in published data.
What it does
Furosemide blocks the Na+-K+-2Cl− cotransporter (NKCC2) on the apical membrane of the thick ascending limb of the loop of Henle. The transporter normally reabsorbs sodium, potassium, and chloride from the urine. Blocking it produces a powerful natriuresis — sodium and water flow out — and a diuresis that is more potent than that of any other class of diuretic in routine use.
The effect is rapid: oral furosemide acts within an hour, intravenous furosemide within minutes. The duration is short, typically a few hours, which is why it is often dosed two or three times a day in chronic use. Sulfa diuretics covers the broader class.
What it is used for
Heart failure with volume overload. The cornerstone use. Furosemide is the workhorse for relieving symptomatic congestion — peripheral edema, ascites, pulmonary edema — in chronic heart failure and during acute decompensation.
Pulmonary edema. Intravenous furosemide is part of the standard initial management of acute cardiogenic pulmonary edema, alongside oxygen, vasodilators where appropriate, and treatment of the precipitating cause.
Edema in cirrhosis and nephrotic syndrome. Often combined with potassium-sparing diuretics (spironolactone for cirrhosis) for synergistic effect and to reduce potassium loss.
Hypertension. Less commonly first-line than thiazides, but used in patients with reduced kidney function or fluid overload where thiazides are less effective.
Hypercalcemia. Loop diuretics increase urinary calcium excretion. Used as adjunctive therapy in some forms of severe hypercalcemia, with attention to volume status.
Common adverse effects
The expected pharmacology brings most of the side effects:
Electrolyte loss — hypokalemia (often), hypomagnesemia, hyponatremia, occasionally hypocalcemia. Routine monitoring is part of chronic use.
Volume depletion — particularly with high doses or in older patients. Postural hypotension and dizziness can occur.
Pre-renal kidney injury — when diuresis exceeds intravascular volume tolerance. The serum creatinine rises; the kidney is not damaged but underperfused.
Hyperuricemia and gout — loop diuretics raise serum urate and can precipitate gout in susceptible patients.
Ototoxicity — at high doses, particularly intravenously and especially in combination with aminoglycosides. Hearing loss can be permanent in severe cases.
Hyperglycemia, dyslipidemia — modest effects.
Less common: photosensitivity, rashes, rare blood dyscrasias, very rare interstitial nephritis or pancreatitis.
The sulfa allergy question
Furosemide is the example most often raised in conversations about sulfa cross-reactivity. The reasoning is on antibiotic vs non-antibiotic sulfonamides: furosemide contains the –SO2NH2 group but lacks the N4 arylamine. Published data show low rates of cross-reaction with sulfa antibiotic allergy. Most prescribers will use furosemide in patients with a documented mild sulfa antibiotic allergy. More on cross-reactivity.
For patients with documented severe past reactions — Stevens-Johnson syndrome, TEN, DRESS, anaphylaxis — the calculus shifts. Ethacrynic acid, a loop diuretic without the sulfonamide group, exists as an alternative. It has its own toxicity profile and is rarely chosen routinely, but it remains in formularies for this purpose.
Interactions
Furosemide interacts with several other drug classes. The clinically important interactions include: increased ototoxicity with aminoglycosides; potentiation of nephrotoxicity with NSAIDs and ACE inhibitors in volume-depleted patients; reduced effect of antihypertensives in volume-depleted patients (paradoxical, but real); enhanced toxicity of lithium and digoxin (the latter through diuretic-induced hypokalemia); and additive hypokalemia with other diuretics or amphotericin B. Pharmacist or prescriber review at the start of furosemide is routine.