Drug reference

Torsemide

Loop Diuretic · Antihypertensive

Also known as Torasemide

START

Confirm edema or hypertension indication. Baseline electrolytes (K+, Na+, Mg2+, uric acid), creatinine, BUN, glucose, BP. Start 5-10 mg PO daily.

TYPICAL MAX

200 mg/day (edema); 10 mg/day (hypertension). Higher doses in CHF require close monitoring.

STOP IF

Severe hypokalemia (K+ <3.0), severe hyponatremia (Na+ <125), anuria, severe hypotension (SBP <90), severe dehydration, acute pancreatitis

WATCH

Electrolytes (K+, Na+, Mg2+) at baseline, 1 week, then monthly; creatinine/BUN; BP (sitting and standing); glucose; uric acid (gout); weight; signs of volume depletion

CDSCO approvedSchedule HJan AushadhiNPPA price-controlledATC C03CA04

Dose laddermg/d

Renal dose adjustmenteGFR mL/min/1.73m²

KDIGO 2024 + manufacturer label

Pharmacokineticsplasma · t hours

ONSET: 1h · 1 h (oral); 10 min (IV)
PEAK: 1.5h · 1-2 h (oral); 30 min (IV)
t½: 3.5h · 3.5 h (normal); 6-12 h (CHF/cirrhosis)
DURATION: 7h · 6-8 h (longer than furosemide)

EXCRETION

~20% renal unchanged; ~71% hepatic metabolism (CYP2C9); fecal

route + CYP

INTERACTIONS

7 major

SEVERE in our sources

PREGNANCY

FDA PLLR: Animal studies showed no teratogenicity. Limited human data. Crosses placenta. May cause fetal electrolyte disturbances and reduce placental perfusion. Use only if benefit clearly outweighs risk.

FDA category + note

Top interactionssee all 12 →

CarboplatinSevereTextbookG&G 14e · p566
CisplatinSevereTextbookG&G 14e · p566
Digitalis GlycosidesSevereTextbookG&G 14e · p566
PaclitaxelSevereTextbookG&G 14e · p566

Available in India

312 branded formulations and 3 fixed-dose combinations. Look up specific brands in the Drugs workspace.

Jan Aushadhi — generic available at GoI pharmacies

Mechanism

Torsemide is a high-ceiling (loop) diuretic that inhibits the Na+-K+-2Cl- cotransporter (NKCC2) in the thick ascending limb of the Loop of Henle in the kidney. By blocking this transporter, torsemide prevents reabsorption of sodium, potassium, and chloride ions, resulting in: (1) increased excretion of water, sodium, chloride, potassium, calcium, and magnesium; (2) reduced medullary hypertonicity, impairing urinary concentration; and (3) decreased vascular responsiveness to catecholamines (venodilation), reducing preload. Unlike furosemide, torsemide has a longer half-life, more predictable bioavailability, and some hepatic metabolism (CYP2C9), giving it a pharmacokinetic profile intermediate between furosemide and bumetanide. It also has mild antihypertensive effects independent of diuresis.

Indications

Edema associated with congestive heart failure (CHF)Edema associated with chronic renal failureEdema associated with hepatic cirrhosisEssential hypertension (monotherapy or combination)Acute pulmonary edema (off-label, IV)Ascites in cirrhosis (off-label, with spironolactone)Nephrotic syndrome (off-label)

Dosing

Adult: CHF edema: 10-20 mg PO once daily; titrate by doubling dose; max 200 mg/day. Chronic renal failure: 20 mg PO once daily; titrate; max 200 mg/day. Hepatic cirrhosis: 5-10 mg PO once daily with aldosterone antagonist; max 40 mg/day. Hypertension: 5 mg PO once daily; titrate to 10 mg; max 10 mg/day.
Pediatric: Not recommended <18 years (safety/efficacy not established).
Renal adjustment: No adjustment for mild-moderate renal impairment. Severe renal impairment: higher doses may be needed but efficacy decreases as GFR falls. Not dialyzable.
Hepatic adjustment: Start 5-10 mg/day; monitor electrolytes and mental status closely (risk of hepatic encephalopathy).
Geriatric: Start 5 mg/day; titrate slowly. Monitor electrolytes, renal function, and orthostatic BP.
Max dose: 200 mg/day (edema); 10 mg/day (hypertension)

Pharmacokinetics

Onset

Oral: diuresis within 1 hour. IV: within 10 minutes.

Peak effect

Oral: peak diuresis at 1-2 hours. IV: peak at 30 minutes.

Duration

Oral/IV: 6-8 hours (longer than furosemide's 4-6 hours).

Half-life

~3.5 hours (normal); prolonged in CHF (6-8 hours), hepatic cirrhosis (up to 12 hours), and renal impairment.

Bioavailability

~80-90% (oral; more predictable than furosemide's variable 10-100%). Food does not significantly affect absorption.

Protein binding

~97-99% (highly bound to albumin).

Metabolism

Hepatic via CYP2C9 (primary — hydroxylation to M1 and M3 metabolites, both inactive) and CYP2C8/2C18/2C19 (minor pathways). ~20% excreted unchanged in urine.

Excretion

Renal: ~24% (20% unchanged, 4% as glucuronide conjugates). Hepatic/biliary: ~71% (as metabolites). Fecal: ~20-30%.

Contraindications

Hypersensitivity to torsemide, sulfonamides, or other loop diuretics
Anuria (no urine output)
Hepatic coma or precoma (electrolyte disturbances may worsen encephalopathy)
Severe electrolyte depletion (hypokalemia, hyponatremia, hypochloremic alkalosis)
Severe renal impairment with declining renal function (may worsen azotemia)

Side effects

Common

Hypokalemia (dose-related; most common electrolyte abnormality)HyponatremiaHypotension, orthostatic hypotensionDizziness, headacheDehydrationHyperglycemia (especially in diabetics)Hyperuricemia (gout risk)Tinnitus, hearing loss (rare, usually with rapid IV administration)Muscle cramps

Serious

Severe hypokalemia (arrhythmia risk, especially with digoxin)
Severe hyponatremia (seizures, confusion, cerebral edema)
Hypochloremic metabolic alkalosis
Ototoxicity (deafness, usually reversible — rapid IV, renal impairment, aminoglycoside co-administration)
Severe dehydration and prerenal azotemia
Pancreatitis (rare)
Agranulocytosis, thrombocytopenia (rare)
Hepatic encephalopathy (in cirrhosis)
Anaphylaxis, severe hypersensitivity (sulfonamide cross-reactivity)

Pregnancy & lactation

Pregnancy

Lactation

Excreted in breast milk in low concentrations. May reduce milk production. Compatible with breastfeeding per AAP with monitoring. Monitor infant for dehydration and electrolyte disturbances.

Drug interactions

Carboplatin

Severe

Textbook

Increased risk of ototoxicity (e.g., tinnitus, hearing impairment, deafness, vertigo).

Not explicitly stated, but implies careful monitoring or avoidance if possible.

Source: G&G 14e · p566

Cisplatin

Severe

Textbook

Enhanced ototoxicity.

Not explicitly stated, but implies careful monitoring or avoidance if possible.

Source: G&G 14e · p566

Digitalis Glycosides

Severe

Textbook

Increased digitalis-induced arrhythmias.

Not explicitly stated, but implies careful monitoring of potassium levels.

Source: G&G 14e · p566

Paclitaxel

Severe

Textbook

Increased risk of ototoxicity (e.g., tinnitus, hearing impairment, deafness, vertigo).

Not explicitly stated, but implies careful monitoring or avoidance if possible.

Source: G&G 14e · p566

Aminoglycosides

Severe

Database

Additive ototoxicity and nephrotoxicity. Loop diuretics increase aminoglycoside concentrations in the inner ear and kidney. Both cause electrolyte disturbances that worsen each other's toxicity.

Avoid concurrent use if possible. If unavoidable, monitor renal function daily, serum aminoglycoside levels, and hearing. Keep course as short as possible.

Source: Kimi deep-research + Cla · p566

Digoxin

Severe

Database

Loop diuretics cause hypokalemia and hypomagnesemia, which increase myocardial digoxin sensitivity and risk of digoxin toxicity (arrhythmias, nausea, visual disturbances) even with therapeutic digoxin levels.

Monitor potassium and magnesium closely. Supplement K+ and Mg2+ to maintain K+ >4.0 and Mg2+ >1.8. Monitor digoxin levels and clinical signs of toxicity.

Source: Kimi deep-research + Cla · p949

Lithium

Severe

Database

Loop diuretics reduce renal lithium clearance by causing sodium depletion, which increases proximal tubular lithium reabsorption. Lithium levels can increase by 50-100%, causing toxicity (tremor, ataxia, confusion, nephrotoxicity, encephalopathy).

Avoid loop diuretics in patients on lithium if possible (thiazides are safer alternatives with lithium). If unavoidable, monitor lithium levels weekly and reduce lithium dose by 50%.

Source: Kimi deep-research + Cla · p949

Tetracycline

Moderate

Textbook-cited

Azotemia (elevated blood urea)

Avoid concurrent use

Source: KDT 7e · p949

Aceclofenac + Paracetamol

Moderate

Textbook

Blunted diuretic response; also, with high doses of salicylates, potential salicylate toxicity.

Not explicitly stated, but suggests caution or avoiding concomitant use.