Note: Oral dose equivalency (approximate) for patients with normal renal function (Brater 1983; Cody 1994; Vargo 1995): Torsemide 20 mg = bumetanide 1 mg = furosemide 40 mg = ethacrynic acid 50 mg
Edema:
Chronic renal failure: Oral: Initial: 20 mg once daily; may increase gradually by doubling dose until the desired diuretic response is obtained; doses >200 mg/day have not been adequately studied.
Heart failure:
Oral: Initial: 10 to 20 mg once daily; may increase gradually by doubling dose until the desired diuretic response is obtained. Maximum dose: 200 mg/day (ACCF/AHA [Yancy 2013]).
Hepatic cirrhosis: Oral: Initial: 5 to 10 mg once daily; may increase gradually by doubling dose until the desired diuretic response is obtained (maximum recommended single dose: 40 mg). Note: Administer with an aldosterone antagonist or a potassium-sparing diuretic.
Hypertension (alternative agent): Oral: Initial: 5 mg once daily; may increase to 10 mg once daily after 4 to 6 weeks if inadequate antihypertensive response (ACC/AHA [Whelton 2017]).
Dosage adjustment for concomitant therapy: Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.
There are no dosage adjustments provided in the manufacturer’s labeling. Higher doses may be required to achieve diuretic response.
There are no dosage adjustments provided in the manufacturer’s labeling; use with caution. Use is contraindicated in hepatic coma.
Refer to adult dosing.
Excipient information presented when available (limited, particularly for generics); consult specific product labeling. [DSC] = Discontinued product
Tablet, Oral:
Demadex: 10 mg [DSC] [scored]
Demadex: 20 mg [DSC]
Soaanz: 20 mg, 40 mg, 60 mg
Generic: 5 mg, 10 mg, 20 mg, 100 mg
Yes
Soaanz tablets: FDA approved June 2021; anticipated availability is currently unknown. Soaanz is indicated for the treatment of edema associated with heart failure or renal disease in adults. Information pertaining to this product within the monograph is pending revision. Consult the prescribing information for additional information.
Oral: May administer with or without food.
Oral: Administer without regard to meals.
Edema: Treatment of edema associated with heart failure and hepatic or renal disease.
Hypertension: Management of hypertension.
Note: Not recommended for the initial treatment of hypertension (ACC/AHA [Whelton 2017]).
Torsemide may be confused with furosemide
Demadex may be confused with Denorex
Beers Criteria: Diuretics are identified in the Beers Criteria as potentially inappropriate medications to be used with caution in patients 65 years and older due to the potential to cause or exacerbate syndrome of inappropriate antidiuretic hormone secretion (SIADH) or hyponatremia; monitor sodium concentration closely when initiating or adjusting the dose in older adults (Beers Criteria [AGS 2019]).
Loop diuretics, including torsemide, may lead to acute kidney injury (AKI) due to fluid loss (Ref). May be associated with less risk of AKI compared to furosemide (Ref).
Mechanism: Dose-related; related to the pharmacologic action (ie, volume depletion) (Ref).
Risk factors:
• Excessive doses (Ref)
• Concurrent administration of nephrotoxic agents (Ref)
• Older adults (Ref)
• Preexisting volume depletion (Ref)
• Reduced blood flow to the kidney or depletion of effective blood volume (eg, bilateral renal artery stenosis, cirrhosis, nephrotic syndrome, heart failure) (Ref)
Loop diuretics, including torsemide, may lead to profound diuresis (especially if given in excessive amounts), resulting in hypovolemia and electrolyte loss. Electrolyte disturbances (eg, hypocalcemia, hypokalemia, hypomagnesemia) may predispose a patient to serious cardiac arrhythmias. May be associated with less risk of hypokalemia than furosemide (Ref).
Mechanism: Dose-related; related to the pharmacologic action (Ref).
Risk factors:
• Excessive doses with initiation or dose adjustment (Ref)
• Reduced dietary fluid and/or electrolyte intake (Ref)
• Concurrent illness leading to excessive fluid loss (eg, diarrhea, vomiting) (Ref)
• Concomitant administration of an additional diuretic (Ref)
• Very high or very restricted dietary sodium (Ref)
Delayed hypersensitivity reactions, including Stevens-Johnson syndrome and toxic epidermal necrolysis, have been reported. A photosensitive lichenoid eruption has also been reported (Ref).
Mechanism: Delayed hypersensitivity reactions: Non–dose-related; immunologic (ie, involving a T-cell mediated drug-specific immune response) (Ref).
Onset: Delayed hypersensitivity reactions: Varied; typically occurs days to 8 weeks after drug exposure (Ref) but may occur more rapidly (usually within 1 to 4 days) upon reexposure (Ref).
Risk factors:
• Cross-reactivity: Cross-reactivity between antibiotic sulfonamides and nonantibiotic sulfonamides (such as torsemide) may not occur, or at the very least this potential is extremely low (Ref). Cross-reactivity due to antibody production (anaphylaxis) is unlikely to occur with antibiotic sulfonamides and nonantibiotic sulfonamides (Ref). There is limited published information regarding cross-reactivity between torsemide and other sulfonamide loop diuretics (Ref).
Loop diuretics, including torsemide, have been associated with hearing loss (deafness) and tinnitus, which are generally reversible (lasting from 30 minutes to 24 hours after administration) (Ref).
Mechanism: Dose-related; related to the pharmacologic action (ie, inhibition of a secretory isoform of the Na-K-2Cl co-transporter in the inner ear and impacts on ionic composition of cochlear fluids) (Ref).
Risk factors:
• Concurrent kidney disease (Ref)
• Excessive doses (Ref)
• Concurrent use of other ototoxic agents (eg, aminoglycosides) can lead to ototoxicity at lower doses (Ref)
The following adverse drug reactions and incidences are derived from product labeling unless otherwise specified.
1% to 10%: Renal: Polyuria (7%; dose-related)
Frequency not defined:
Endocrine & metabolic: Hyperuricemia (Hagos 2007), hypokalemia, increased serum cholesterol, increased serum glucose, increased serum triglycerides
Otic: Hearing loss (Bagshaw 2007), tinnitus (Bagshaw 2007)
Postmarketing:
Dermatologic: Lichenoid eruption (Byrd 1997), pruritus, skin photosensitivity, Stevens-Johnson syndrome, toxic epidermal necrolysis
Endocrine & metabolic: Gout (Choi 2005), increased gamma-glutamyl transferase, vitamin B deficiency
Gastrointestinal: Abdominal pain, anorexia, pancreatitis (Juang 2006)
Genitourinary: Acute urinary retention
Hematologic & oncologic: Anemia, leukopenia, thrombocytopenia
Hepatic: Increased serum transaminases
Nervous system: Confusion, paresthesia
Ophthalmic: Visual impairment
Renal: Acute kidney injury (Liu 2021)
Hypersensitivity to torsemide or any component of the formulation; anuria; hepatic coma.
Concerns related to adverse effects:
• Hyperuricemia: Asymptomatic hyperuricemia may occur; gout may be precipitated (rarely).
• Sulfonamide (“sulfa”) allergy: The FDA-approved product labeling for many medications containing a sulfonamide chemical group includes a broad contraindication in patients with a prior allergic reaction to sulfonamides. There is a potential for cross-reactivity between members of a specific class (eg, 2 antibiotic sulfonamides). However, concerns for cross-reactivity have previously extended to all compounds containing the sulfonamide structure (SO2NH2). An expanded understanding of allergic mechanisms indicates cross-reactivity between antibiotic sulfonamides and nonantibiotic sulfonamides may not occur or at the very least this potential is extremely low (Brackett 2004; Johnson 2005; Slatore 2004; Tornero 2004). In particular, mechanisms of cross-reaction due to antibody production (anaphylaxis) are unlikely to occur with nonantibiotic sulfonamides. T-cell-mediated (type IV) reactions (eg, maculopapular rash) are not well understood and it is not possible to completely exclude this potential based on current insights. In cases where prior reactions were severe (Stevens-Johnson syndrome/TEN), some clinicians choose to avoid exposure to these classes.
Disease-related concerns:
• Adrenal insufficiency: Avoid use of diuretics for treatment of elevated blood pressure in patients with primary adrenal insufficiency (Addison disease). Adjustment of glucocorticoid/mineralocorticoid therapy and/or use of other antihypertensive agents is preferred to treat hypertension (Bornstein 2016; Inder 2015).
• Bariatric surgery: Dehydration: Avoid diuretics in the immediate postoperative period after bariatric surgery; electrolyte disturbances and dehydration may occur. Diuretics may be resumed, if indicated, once oral fluid intake goals are met (Ziegler 2009).
• Diabetes: Use with caution in patients with diabetes; increased blood glucose levels and hyperglycemia may occur. Monitor blood glucose periodically.
• Hepatic impairment: Use with caution in patients with hepatic impairment; in patients with cirrhosis, avoid electrolyte and acid/base imbalances that may lead to hepatic encephalopathy. Administration with an aldosterone antagonist or potassium-sparing diuretic may provide additional diuretic efficacy and maintain normokalemia in patients with hepatic disease.
Special populations:
• Surgical patients: If given the morning of surgery, torsemide may render the patient volume depleted and blood pressure may be labile during general anesthesia.
Other warnings and precautions:
• Diuretic resistance: For some patients, despite higher doses of loop diuretic treatment, an adequate diuretic response cannot be attained. Diuretic resistance can usually be overcome by intravenous administration, the use of two diuretics together (eg, furosemide and chlorothiazide), or the use of a diuretic with a positive inotropic agent. When such combinations are used, serum electrolytes need to be monitored even more closely (Cody 1994, ACC/AHA [Yancy 2013]; HFSA 2010).
Substrate of CYP2C8 (minor), CYP2C9 (minor), OATP1B1/1B3 (SLCO1B1/1B3); Note: Assignment of Major/Minor substrate status based on clinically relevant drug interaction potential
Ajmaline: Sulfonamides may enhance the adverse/toxic effect of Ajmaline. Specifically, the risk for cholestasis may be increased. Risk C: Monitor therapy
Alfuzosin: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy
Allopurinol: Loop Diuretics may enhance the adverse/toxic effect of Allopurinol. Loop Diuretics may increase the serum concentration of Allopurinol. Specifically, Loop Diuretics may increase the concentration of Oxypurinol, an active metabolite of Allopurinol. Risk C: Monitor therapy
Amifostine: Blood Pressure Lowering Agents may enhance the hypotensive effect of Amifostine. Management: When used at chemotherapy doses, hold blood pressure lowering medications for 24 hours before amifostine administration. If blood pressure lowering therapy cannot be held, do not administer amifostine. Use caution with radiotherapy doses of amifostine. Risk D: Consider therapy modification
Amikacin Liposome (Oral Inhalation): Loop Diuretics may enhance the nephrotoxic effect of Amikacin Liposome (Oral Inhalation). Loop Diuretics may enhance the ototoxic effect of Amikacin Liposome (Oral Inhalation). Risk C: Monitor therapy
Aminoglycosides: Loop Diuretics may enhance the adverse/toxic effect of Aminoglycosides. Specifically, nephrotoxicity and ototoxicity. Risk C: Monitor therapy
Amphetamines: May diminish the antihypertensive effect of Antihypertensive Agents. Risk C: Monitor therapy
Angiotensin-Converting Enzyme Inhibitors: Loop Diuretics may enhance the hypotensive effect of Angiotensin-Converting Enzyme Inhibitors. Loop Diuretics may enhance the nephrotoxic effect of Angiotensin-Converting Enzyme Inhibitors. Risk C: Monitor therapy
Antidiabetic Agents: Hyperglycemia-Associated Agents may diminish the therapeutic effect of Antidiabetic Agents. Risk C: Monitor therapy
Antipsychotic Agents (Second Generation [Atypical]): Blood Pressure Lowering Agents may enhance the hypotensive effect of Antipsychotic Agents (Second Generation [Atypical]). Risk C: Monitor therapy
Arsenic Trioxide: Loop Diuretics may enhance the hypotensive effect of Arsenic Trioxide. Loop Diuretics may enhance the QTc-prolonging effect of Arsenic Trioxide. Management: When possible, avoid concurrent use of arsenic trioxide with drugs that can cause electrolyte abnormalities, such as the loop diuretics. Risk D: Consider therapy modification
Barbiturates: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy
Benperidol: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy
Beta2-Agonists: May enhance the hypokalemic effect of Loop Diuretics. Risk C: Monitor therapy
Bilastine: Loop Diuretics may enhance the QTc-prolonging effect of Bilastine. Risk C: Monitor therapy
Bile Acid Sequestrants: May decrease the absorption of Loop Diuretics. Risk C: Monitor therapy
Brigatinib: May diminish the antihypertensive effect of Antihypertensive Agents. Brigatinib may enhance the bradycardic effect of Antihypertensive Agents. Risk C: Monitor therapy
Brimonidine (Topical): May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy
Bromperidol: May diminish the hypotensive effect of Blood Pressure Lowering Agents. Blood Pressure Lowering Agents may enhance the hypotensive effect of Bromperidol. Risk X: Avoid combination
Canagliflozin: May enhance the hypotensive effect of Loop Diuretics. Risk C: Monitor therapy
Cardiac Glycosides: Loop Diuretics may enhance the adverse/toxic effect of Cardiac Glycosides. Specifically, cardiac glycoside toxicity may be enhanced by the hypokalemic and hypomagnesemic effect of loop diuretics. Risk C: Monitor therapy
Cefazedone: May enhance the nephrotoxic effect of Loop Diuretics. Risk C: Monitor therapy
Cefotiam: Loop Diuretics may enhance the nephrotoxic effect of Cefotiam. Risk C: Monitor therapy
Cefpirome: Loop Diuretics may enhance the nephrotoxic effect of Cefpirome. Risk C: Monitor therapy
Ceftizoxime: Loop Diuretics may enhance the nephrotoxic effect of Ceftizoxime. Risk C: Monitor therapy
Cephalothin: Loop Diuretics may enhance the nephrotoxic effect of Cephalothin. Risk C: Monitor therapy
Cephradine: May enhance the nephrotoxic effect of Loop Diuretics. Risk C: Monitor therapy
CISplatin: Loop Diuretics may enhance the nephrotoxic effect of CISplatin. Loop Diuretics may enhance the ototoxic effect of CISplatin. Risk C: Monitor therapy
Corticosteroids (Systemic): May enhance the hypokalemic effect of Loop Diuretics. Risk C: Monitor therapy
CycloSPORINE (Systemic): May enhance the adverse/toxic effect of Loop Diuretics. Risk C: Monitor therapy
CYP2C9 Inducers (Moderate): May decrease the serum concentration of Torsemide. Risk C: Monitor therapy
CYP2C9 Inhibitors (Moderate): May increase the serum concentration of Torsemide. Risk C: Monitor therapy
Desmopressin: May enhance the hyponatremic effect of Loop Diuretics. Risk X: Avoid combination
Dexmethylphenidate: May diminish the therapeutic effect of Antihypertensive Agents. Risk C: Monitor therapy
Diacerein: May enhance the therapeutic effect of Diuretics. Specifically, the risk for dehydration or hypokalemia may be increased. Risk C: Monitor therapy
Diazoxide: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy
Dichlorphenamide: Loop Diuretics may enhance the hypokalemic effect of Dichlorphenamide. Risk C: Monitor therapy
Dofetilide: Loop Diuretics may enhance the QTc-prolonging effect of Dofetilide. Management: Monitor serum potassium and magnesium more closely when dofetilide is combined with loop diuretics. Electrolyte replacements will likely be required to maintain potassium and magnesium serum concentrations. Risk D: Consider therapy modification
DULoxetine: Blood Pressure Lowering Agents may enhance the hypotensive effect of DULoxetine. Risk C: Monitor therapy
Empagliflozin: May enhance the hypotensive effect of Loop Diuretics. Risk C: Monitor therapy
Foscarnet: Loop Diuretics may increase the serum concentration of Foscarnet. Management: When diuretics are indicated during foscarnet treatment, thiazides are recommended over loop diuretics. If patients receive loop diuretics during foscarnet treatment, monitor closely for evidence of foscarnet toxicity. Risk D: Consider therapy modification
Fosphenytoin: May diminish the diuretic effect of Loop Diuretics. Risk C: Monitor therapy
Herbal Products with Blood Pressure Increasing Effects: May diminish the antihypertensive effect of Antihypertensive Agents. Risk C: Monitor therapy
Herbal Products with Blood Pressure Lowering Effects: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy
Hypotension-Associated Agents: Blood Pressure Lowering Agents may enhance the hypotensive effect of Hypotension-Associated Agents. Risk C: Monitor therapy
Iodinated Contrast Agents: Loop Diuretics may enhance the nephrotoxic effect of Iodinated Contrast Agents. Risk C: Monitor therapy
Ipragliflozin: May enhance the adverse/toxic effect of Loop Diuretics. Specifically, the risk for intravascular volume depletion may be increased. Risk C: Monitor therapy
Ivabradine: Loop Diuretics may enhance the arrhythmogenic effect of Ivabradine. Risk C: Monitor therapy
Levodopa-Containing Products: Blood Pressure Lowering Agents may enhance the hypotensive effect of Levodopa-Containing Products. Risk C: Monitor therapy
Levosulpiride: Loop Diuretics may enhance the adverse/toxic effect of Levosulpiride. Risk X: Avoid combination
Licorice: May enhance the hypokalemic effect of Loop Diuretics. Risk C: Monitor therapy
Lithium: Loop Diuretics may decrease the serum concentration of Lithium. Loop Diuretics may increase the serum concentration of Lithium. Risk C: Monitor therapy
Lormetazepam: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy
Mecamylamine: Sulfonamides may enhance the adverse/toxic effect of Mecamylamine. Risk X: Avoid combination
Methotrexate: May diminish the therapeutic effect of Loop Diuretics. Loop Diuretics may increase the serum concentration of Methotrexate. Methotrexate may increase the serum concentration of Loop Diuretics. Risk C: Monitor therapy
Methylphenidate: May diminish the antihypertensive effect of Antihypertensive Agents. Risk C: Monitor therapy
Molsidomine: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy
Naftopidil: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy
Neuromuscular-Blocking Agents: Loop Diuretics may diminish the neuromuscular-blocking effect of Neuromuscular-Blocking Agents. Loop Diuretics may enhance the neuromuscular-blocking effect of Neuromuscular-Blocking Agents. Risk C: Monitor therapy
Nicergoline: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy
Nicorandil: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy
Nitroprusside: Blood Pressure Lowering Agents may enhance the hypotensive effect of Nitroprusside. Risk C: Monitor therapy
Nonsteroidal Anti-Inflammatory Agents: May diminish the diuretic effect of Loop Diuretics. Loop Diuretics may enhance the nephrotoxic effect of Nonsteroidal Anti-Inflammatory Agents. Management: Monitor for evidence of kidney injury or decreased therapeutic effects of loop diuretics with concurrent use of an NSAID. Consider avoiding concurrent use in CHF or cirrhosis. Concomitant use of bumetanide with indomethacin is not recommended. Risk D: Consider therapy modification
Nonsteroidal Anti-Inflammatory Agents (Topical): May diminish the therapeutic effect of Loop Diuretics. Risk C: Monitor therapy
Obinutuzumab: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Management: Consider temporarily withholding blood pressure lowering medications beginning 12 hours prior to obinutuzumab infusion and continuing until 1 hour after the end of the infusion. Risk D: Consider therapy modification
Opioid Agonists: May enhance the adverse/toxic effect of Diuretics. Opioid Agonists may diminish the therapeutic effect of Diuretics. Risk C: Monitor therapy
Pentoxifylline: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy
Phenytoin: May diminish the diuretic effect of Loop Diuretics. Risk C: Monitor therapy
Pholcodine: Blood Pressure Lowering Agents may enhance the hypotensive effect of Pholcodine. Risk C: Monitor therapy
Phosphodiesterase 5 Inhibitors: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy
Probenecid: May enhance the adverse/toxic effect of Loop Diuretics. Probenecid may diminish the diuretic effect of Loop Diuretics. Probenecid may increase the serum concentration of Loop Diuretics. Management: Monitor for decreased diuretic effects or increased adverse effects of loop diuretics with concomitant use of probenecid. Bumetanide prescribing information recommends against concomitant use of probenecid. Risk C: Monitor therapy
Promazine: Loop Diuretics may enhance the QTc-prolonging effect of Promazine. Risk X: Avoid combination
Prostacyclin Analogues: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy
Quinagolide: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy
Reboxetine: May enhance the hypokalemic effect of Loop Diuretics. Risk C: Monitor therapy
RisperiDONE: Loop Diuretics may enhance the adverse/toxic effect of RisperiDONE. Risk C: Monitor therapy
Salicylates: May diminish the diuretic effect of Loop Diuretics. Loop Diuretics may increase the serum concentration of Salicylates. Risk C: Monitor therapy
Sodium Phosphates: Diuretics may enhance the nephrotoxic effect of Sodium Phosphates. Specifically, the risk of acute phosphate nephropathy may be enhanced. Management: Consider avoiding this combination by temporarily suspending treatment with diuretics, or seeking alternatives to oral sodium phosphate bowel preparation. If the combination cannot be avoided, hydrate adequately and monitor fluid and renal status. Risk D: Consider therapy modification
Tobramycin (Oral Inhalation): Loop Diuretics may enhance the nephrotoxic effect of Tobramycin (Oral Inhalation). Loop Diuretics may enhance the ototoxic effect of Tobramycin (Oral Inhalation). Risk C: Monitor therapy
Topiramate: Loop Diuretics may enhance the hypokalemic effect of Topiramate. Risk C: Monitor therapy
Warfarin: Torsemide may increase the serum concentration of Warfarin. Risk C: Monitor therapy
Xipamide: May enhance the adverse/toxic effect of Loop Diuretics. Specifically, the risk of hypovolemia, electrolyte disturbances, and prerenal azotemia may be increased. Risk C: Monitor therapy
Zoledronic Acid: Loop Diuretics may enhance the hypocalcemic effect of Zoledronic Acid. Risk C: Monitor therapy
Adverse events have been observed in animal reproduction studies.
It is not known if torsemide is present in breast milk. Diuretics can suppress lactation.
May cause potassium loss; potassium supplement or dietary changes may be required.
Periodically monitor renal function, serum electrolytes (eg, hypokalemia, hyponatremia, hypomagnesemia, hypocalcemia, hypochloremic alkalosis), serum glucose, volume status, BP, and diuretic effect; close medical supervision of aggressive diuresis required.
Inhibits reabsorption of sodium and chloride in the ascending loop of Henle and distal renal tubule, interfering with the chloride-binding cotransport system, thus causing increased excretion of water, sodium, chloride, magnesium, and calcium; does not alter GFR, renal plasma flow, or acid-base balance
Onset of action: Diuresis: Within 1 hour
Peak effect: Diuresis: 1 to 2 hours; Antihypertensive: 4 to 6 weeks (up to 12 weeks)
Duration: Diuresis: ~6 to 8 hours
Distribution: Vd: 12 to 15 L; Cirrhosis: ~24 to 30 L
Protein binding: >99%
Metabolism: Hepatic (~80%) via CYP2C9 and to a minor extent, CYP2C8 and CYP2C18
Bioavailability: ~80%
Half-life elimination: ~3.5 hours
Time to peak, plasma: Within 1 hour; delayed ~30 minutes when administered with food
Excretion: Urine (21%)
Renal function impairment: Renal clearance is markedly decreased in renal failure; a smaller fraction of the administered dose is delivered to the intraluminal site of action, and the natriuretic action is reduced.
Hepatic function impairment: Volume of distribution, plasma half-life, and renal clearance are increased in patients with cirrhosis.
Heart failure: Hepatic and renal clearance are decreased. Total clearance is ~50% of that seen in healthy volunteers, and the plasma half-life and AUC are correspondingly increased.
Tablets (Soaanz Oral)
20 mg (per each): $9.56
40 mg (per each): $9.76
60 mg (per each): $9.96
Tablets (Torsemide Oral)
5 mg (per each): $0.63
10 mg (per each): $0.70
20 mg (per each): $0.82
100 mg (per each): $3.04
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