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Torasemide

A Review of its Pharmacological Properties and Therapeutic Potential

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Summary

Synopsis

Torasemide (torsemide) is a high-ceiling loop diuretic which acts on the thick ascending limb of the loop of Henle to promote rapid and marked excretion of water, sodium and chloride. Like furosemide (frusemide), its major site of action is from the luminal side of the cell. Torasemide is at least twice as potent as furosemide on a weight-for-weight basis, produces equivalent diuresis and natriuresis at lower urinary concentrations and has a longer duration of action, allowing once-daily administration without the paradoxical antidiuresis seen with furosemide. Torasemide also appears to promote excretion of potassium and calcium to a lesser extent than furosemide

In trials of up to 48 weeks’ duration in patients with mild to moderate essential hypertension, torasemide, administered as a single daily dose, has been shown to achieve adequate blood pressure control reaching steady-state within 8 to 12 weeks. Those patients not responding initially have generally responded to a doubling of the dose. Comparative trials of up to 6 months show torasemide is as effective as indapamide, hydrochlorothiazide or a combination of triamterene/hydrochlorothiazide in maintaining control of blood pressure

Torasemide has also been used successfully to treat oedematous states associated with chronic congestive heart failure, renal disease and hepatic cirrhosis. In short term trials control of blood pressure, bodyweight and residual oedema has been sustained. Torasemide appears to be a useful alternative to furosemide in these patients, providing potent and long-lasting diuresis while being relatively potassium and calcium sparing

In clinical trials to date torasemide has been well tolerated with adverse effects of a mild, transient nature reported by only small numbers of patients. Changes in biochemical parameters have been common, including decreases in plasma sodium and potassium levels and increases in plasma creatinine and uric acid levels. These changes are typical of loop diuretics. No changes were clinically significant nor were clinically relevant changes noted in glucose metabolism, cholesterol or triglyceride levels or in haematological values

Thus, torasemide is an interesting new loop diuretic with potential use in the treatment of mild to moderate essential hypertension and of oedematous states in which diuretic therapy is warranted. Preliminary studies suggest it to be as efficacious as other diuretics in common use and to have some advantage over furosemide in duration of action and in effects on potassium and calcium. However, further long term trials in larger groups of patients are needed to delineate the place of torasemide in therapy fully, both as a single agent and in combination with other currently accepted drug regimens

Pharmacodynamic Properties

Torasemide is a potent loop diuretic of the furosemide type, which acts via blockade of active sodium and chloride reabsorption in the thick ascending limb of the loop of Henle, producing a rapid and pronounced diuresis and saluresis. Urinary volume and the excretion of sodium and chloride increase linearly with increasing dose, the pattern being similar to that found with an equipotent dose of furosemide. However, the duration of action with torasemide is longer and there is generally a smaller effect on the excretion of potassium. Secondary antidiuresis after torasemide may be less prominent than with other shorter-acting high-ceiling loop diuretics. Over-all a dose of 10 to 20mg torasemide is considered equivalent in diuretic potency to furosemide 40mg, bumetanide 1mg or piretanide 12mg

Adequate diuresis can be produced with torasemide in patients with chronic heart failure or advanced renal disease. In patients with cirrhotic liver disease the acute diuretic effect of torasemide is more pronounced and prolonged than that of furosemide, while the excretion of potassium, calcium and magnesium ions appears to be less

Single doses of torasemide 2.5 to 10mg administered to patients with mild to moderate essential hypertension produced α fall in mean diastolic blood pressure of 24 to 29mm Hg. In a multicentre study in patients with hypertension, torasemide treatment for 24 weeks did not affect serum potassium levels

Single doses of torasemide produce the increases in plasma renin activity, in angiotensin II and aldosterone levels, and in the urinary excretion of renal prostaglandin E and dopamine characteristic of loop diuretics, but no statistically significant effects have been reported in multiple-dose studies. No consistent effect on glomerular filtration rate has been observed

Pharmacokinetic Properties

Torasemide is rapidly absorbed following an oral dose; peak plasma concentration is achieved in the first hour. The pharmacokinetics of torasemide can be described by a 2-compartment open model. Both the plasma concentration of torasemide and the area under the plasma concentration-time curve (AUC) are linearly related to dose. The systemic availability of torasemide is in the range of 76 to 92%

The volume of distribution after a single intravenous dose of torasemide ranges from 0.14 to 0.19 L/kg, which approximates extracellular fluid volume. Plasma protein binding is estimated at 97 to 99%

The metabolism and elimination of torasemide involves hepatic biotransformation followed by both renal and nonrenal excretion of metabolites. Three main metabolites have been identified in humans: the M1 metabolite is about one-tenth as potent as torasemide, the M3 metabolite is equivalent in potency, and the M5 metabolite is inactive. Time to peak plasma concentration and elimination half-life of the metabolites are similar to those of the parent compound. However, the plasma concentration and urinary recovery of the two active metabolites are low and thus they are not of clinical importance in patients with normal renal and hepatic function

After a single oral dose of torasemide, the cumulative urinary excretion is comprised of 21% parent compound, 12% metabolite M1, 2% metabolite M3 and 34% inactive metabolite M5. The elimination half-life of torasemide and metabolites is in the range of 2 to 4 hours

Alterations in the pharmacokinetics of torasemide have not been demonstrated in elderly patients with normal renal and hepatic function or in patients with advanced renal disease

A linear correlation between torasemide dose and diuretic effect has been demonstrated over the range from 5 to 100mg with a flattening of the dose-response curve at higher doses. Urinary volume and the excretion of sodium and chloride are linearly related to dose

Therapeutic Use

In a small number of double-blind parallel trials in patients with mild to moderate essential hypertension, torasemide in daily doses of 2.5 to 5mg over 12 to 24 weeks was as effective as indapamide 2.5 to 5mg, hydrochlorothiazide 25mg or fixed combinations of triamterene/hydrochlorothiazide 50/25mg or amiloride/hydrochlorothiazide 5/50mg in achieving and maintaining blood pressure control. Tolerability was good in all studies. The efficacy of torasemide has also been demonstrated in several noncomparative clinical trials with durations up to 48 weeks. Torasemide was administered as monotherapy usually in a single daily dose of 2.5 to 5mg. A reduction in diastolic blood pressure to ≤ 90mm Hg was achieved in 71 to 95% of patients with a dose of 2.5 or 5mg; in nonresponders, doubling of the dose produced a reduction to target blood pressure in 70 to 80% of patients. Tolerance to the antihypertensive effect of torasemide was not apparent

A beneficial effect of torasemide 10mg daily on pulmonary and cardiac haemodynamics in patients with previously untreated chronic heart failure has been demonstrated in a study over 4 weeks. Parameters of both preload and afterload were reduced. Torasemide 5 to 20mg daily, administered to patients with congestive heart failure who had been pretreated for 4 weeks with furosemide, was shown to reduce body weight significantly and to conserve the status of patients initially free of oedema throughout the 48-week study. Of patients who had residual oedema after furosemide pretreatment, 82% were free of oedema at the end of the trial. In controlled comparative trials, torasemide 5 to 10mg daily has been as effective as furosemide 40mg daily in improving clinical symptoms in patients with chronic congestive heart failure with oedema, while a daily dose of torasemide 20mg provided greater efficacy. A starting dose of torasemide 5mg was suggested from these trials

A number of short term trials have compared torasemide in daily doses of 100 to 400mg with furosemide 250 to 1000mg for the diuretic management of patients with advanced chronic renal failure. Torasemide was as effective as furosemide in promoting diuresis and preventing weight gain without adversely affecting neurological status

Finally, the combination of torasemide with spironolactone has been shown to be as effective as furosemide/spironolactone and more effective than spironolactone monotherapy in the diuretic management of patients with hydropically decompensated liver failure. Oedema and ascites tended to resolve with an associated improvement in liver enzyme values and neurological status

Further comparative studies in larger groups of patients over prolonged periods may be necessary to delineate fully the clinical profile of torasemide, alone and in combination, relative to other diuretics in common use for the treatment of hypertension and chronic cardiac, renal or hepatic disease

Adverse Effects

Adverse effects of torasemide are mild and transient in nature, occurring in only small numbers of patients and rarely necessitating treatment withdrawal. They include orthostatic hypotension, gastrointestinal disturbance, muscle cramps, dizziness, fatigue, headache and skin rash. Although potentially ototoxic as a high-ceiling loop diuretic, torasemide did not produce hearing loss when administered in daily doses of up to 400mg over a 4-week period to patients with renal disease

Drug Interactions

Nonsteroidal anti-inflammatory drugs (NSAIDs) have been shown to decrease the diuretic and natriuretic response to loop diuretics. Indomethacin pretreatment has been shown to reduce the excretion of water and sodium caused by single doses of torasemide, essentially under conditions of sodium restriction. Although the effect of long term treatment with torasemide in combination with probenecid or NSAIDs is unknown, the possibility of reduced diuresis should be considered, especially in patients requiring dietary sodium restriction

Dosage and Administration

In patients with mild to moderate essential hypertension a daily dose of torasemide of between 2.5 and 5mg (in some cases up to 10mg) may be used. Incremental blood pressure reduction may continue for up to 8 weeks. In the treatment of patients with chronic congestive heart failure a suitable starting dose is 5mg daily with increments to 10 or 20mg as needed. In patients with advanced chronic renal failure a daily dose of torasemide 100 to 200mg has been used successfully without adverse effects. Dosage adjustment is not necessary in patients undergoing haemodialysis or haemofiltration. In patients with cirrhotic liver disease, torasemide can be used in daily doses of 10 to 20mg, in combination with an aldosterone antagonist to promote diuresis

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    Heather A. Friedel & Micaela M.-T Buckley

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  1. Heather A. Friedel
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Various sections of the manuscript reviewed by: V.E. Andreucci, Department of Nephrology, Second Faculty of Medicine, University of Naples, Naples, Italy; D.C. Brater, Clinical Pharmacology Division, School of Medicine, Indiana University, Indianapolis, Indiana, USA; G. Brunner, Medizinische Hochschule Hannover, Hannover, Federal Republic of Germany; W. Clasen, Krankenhaus der Missionsschwestern, Münster Hiltrup, Federal Republic of Germany; A.G. Dupont, Faculteit Geneeskunde en Farmacie, Vrije Universiteit Brüssel, Brussels, Belgium; A. Ebihara, Department of Clinical Pharmacology, Jichi Medical School, Tochigi, Japan; R. Greger, Institut für Physiologie, Universität Freiburg, Freiburg, Federal Republic of Germany; A. Herchuelz, Faculté de Médecine, Université Libre de Bruxelles, Brussels, Belgium; W.F. Keane, Department of Medicine, University of Minnesota, Minneapolis, Minnesota, USA; A. Lant, Department of Clinical Pharmacology and Therapeutics, Charing Cross and Westminster Medical School, University of London, London, England; T.O. Morgan, Department of Physiology, University of Melbourne, Melbourne, Victoria, Australia

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Friedel, H.A., Buckley, M.MT. Torasemide. Drugs 41, 81–103 (1991). https://doi.org/10.2165/00003495-199141010-00008

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