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triamterene-hydrochlorothiazide 37.5-25 mg tb generic maxzide-25mg

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Triamterene is used in the management of edema associated with heart failure, cirrhosis of the liver, or the nephrotic syndrome, as well as in the management of steroid-induced edema, idiopathic edema, and edema caused by secondary hyperaldosteronism. Careful etiologic diagnosis should precede the use of any diuretic. Triamterene should not be used alone as initial therapy in severe heart failure since its maximum therapeutic effect may occur slowly. However, it may be used in combined initial therapy with more effective, rapidly acting diuretics such as thiazides, chlorthalidone, furosemide, or ethacrynic acid or after rapid initial diuresis has been achieved by other means. Triamterene may be particularly useful in patients excreting excessive amounts of potassium (especially those who cannot tolerate potassium supplements) and for those in whom potassium loss could be detrimental, such as digitalized patients or those with myasthenia gravis. Triamterene promotes increased diuresis when patients prove resistant or only partially responsive to thiazides or other diuretics because of secondary hyperaldosteronism. Unlike spironolactone, the effectiveness of triamterene is independent of aldosterone concentrations; therefore, triamterene may be effective in some patients unresponsive to spironolactone. Although triamterene is effective alone, its chief value lies in combined therapy with other diuretics that act at different sites in the nephron. Some patients resistant to triamterene alone may respond to combined therapy with a thiazide diuretic, furosemide, ethacrynic acid, or chlorthalidone. Triamterene decreases potassium excretion caused by kaliuretic diuretics.

Heart Failure

Triamterene generally is used concomitantly with other more effective, rapidly acting diuretics (e.g., thiazides, chlorthalidone, loop diuretics) in the management of edema associated with heart failure. Most experts state that all patients with symptomatic heart failure who have evidence for, or a history of, fluid retention generally should receive diuretic therapy in conjunction with moderate sodium restriction, an agent to inhibit the renin-angiotensin-aldosterone (RAA) system (e.g., angiotensin-converting enzyme [ACE] inhibitor, angiotensin II receptor antagonist, angiotensin receptor-neprilysin inhibitor [ARNI]), a β-adrenergic blocking agent (β-blocker) and in selected patients, an aldosterone antagonist. Some experts state that because of limited and inconsistent data, it is difficult to make precise recommendations regarding daily sodium intake and whether it should vary with respect to the type of heart failure (e.g., reduced versus preserved ejection fraction), disease severity (e.g., New York Heart Association [NYHA] class), heart failure-related comorbidities (e.g., renal dysfunction), or other patient characteristics (e.g., age, race). The American College of Cardiology Foundation (ACCF) and American Heart Association (AHA) state that limiting sodium intake to 1.5 g daily in patients with ACCF/AHA stage A or B heart failure may be reasonable. While data currently are lacking to support recommendation of a specific level of sodium intake in patients with ACCF/AHA stage C or D heart failure, ACCF and AHA state that limiting sodium intake to some degree (e.g., less than 3 g daily) in such patients may be considered for symptom improvement.

Diuretics play a key role in the management of heart failure because they produce symptomatic benefits more rapidly than any other drugs, relieving pulmonary and peripheral edema within hours or days compared with weeks or months for cardiac glycosides, ACE inhibitors, or β-blockers. However, since there are no long-term studies of diuretic therapy in patients with heart failure, the effects of diuretics on morbidity and mortality in such patients are not known. Although there are patients with heart failure who do not exhibit fluid retention in the absence of diuretic therapy and even may develop severe volume depletion with low doses of diuretics, such patients are rare and the unique pathophysiologic mechanisms regulating their fluid and electrolyte balance have not been elucidated.

Most experts state that loop diuretics (e.g., bumetanide, ethacrynic acid, furosemide, torsemide) are the diuretics of choice for most patients with heart failure. However, thiazides may be preferred in some patients with concomitant hypertension because of their sustained antihypertensive effects.


Triamterene has been used in the management of hypertension; however, other antihypertensive drugs (i.e., ACE inhibitors, angiotensin II receptor antagonists, calcium-channel blockers, thiazide diuretics) generally are preferred because of their established clinical benefits (e.g., reductions in overall mortality and in adverse cardiovascular, cerebrovascular, and renal outcomes). Triamterene alone has little if any hypotensive effect; however, it may be used with another diuretic (e.g., hydrochlorothiazide) or a hypotensive agent in the management of mild to moderate hypertension. In the management of hypertension, triamterene is used principally in patients with diuretic-induced hypokalemia or to prevent hypokalemia in patients receiving diuretics and at risk of this adverse effect. Potassium-sparing diuretics should be avoided in patients with renal insufficiency and in those with hyperkalemia (e.g., serum potassium concentrations exceeding 5 mEq/L while not receiving drug therapy).

Dosage and Administration


Triamterene is administered orally. Triamterene has been administered IV, but the poor solubility of the drug and acidity of the solutions make administration by this route extremely difficult and a parenteral dosage form currently is not available in the US.


Dosage of triamterene should be individualized according to the patient's requirements and response. It has been theorized that abrupt withdrawal of triamterene may result in rebound kaliuresis; therefore, the drug should be withdrawn gradually. Experts state that diuretics should be administered at a dosage sufficient to achieve optimal volume status and relieve congestion without inducing an excessively rapid reduction in intravascular volume, which could result in hypotension, renal dysfunction, or both.

Triamterene Therapy


The usual initial adult dosage of triamterene in the management of edema is 100 mg twice daily after meals. Once edema is controlled, most patients can be maintained on 100 mg daily or every other day. Dosage should not exceed 300 mg daily. When triamterene is used in combination with other diuretics, the initial dosage of each drug should be lowered and adjusted to individual requirements and tolerance.

For the management of fluid retention (e.g., edema) associated with heart failure, some experts recommend initiating triamterene at a low dosage (e.g., 50-75 mg twice daily) and increasing the dosage (maximum of 200 mg daily) until urine output increases and weight decreases, generally by 0.5-1 kg daily.


When triamterene is used in the management of hypertension in adults (usually in combination with a kaliuretic diuretic), an initial dosage of 25 mg once daily has been recommended; however, an appropriate formulation for administering this dosage is no longer commercially available in the US. A usual dosage of 50-100 mg daily (given as a single dose or in 2 divided doses) has been recommended.

Triamterene/Hydrochlorothiazide Fixed-combination Therapy

Commercially available preparations containing triamterene and hydrochlorothiazide in fixed combination generally should not be used as initial therapy, except in patients in whom the clinical consequences of potential thiazide-induced hypokalemia represent an important risk (e.g., patients receiving cardiac glycosides or patients with cardiac arrhythmias).

When Dyazide, Maxzide or Maxzide-25 mg, or therapeutically equivalent formulations of the combination are used, the manufacturers state that the usual adult dosage in terms of triamterene is 37.5-75 mg once daily with appropriate monitoring of serum potassium concentrations. Patients who become hypokalemic while receiving hydrochlorothiazide 25 or 50 mg daily may be switched to a fixed-combination preparation containing triamterene in combination with the equivalent hydrochlorothiazide dosage. In patients who require hydrochlorothiazide and in whom hypokalemia cannot be risked, therapy with the fixed combination may be initiated at a triamterene dosage of 37.5 mg daily (with hydrochlorothiazide 25 mg daily). The manufacturers state that clinical experience with the fixed-combination tablets suggests that the risk of electrolyte imbalance and renal dysfunction may be increased when triamterene 75 mg daily (with hydrochlorothiazide 50 mg daily) is administered in 2 divided doses rather than as a single daily dose. The manufacturers also state that there is no clinical experience to date with dosages of these more bioavailable formulations exceeding 75 mg of triamterene and 50 mg of hydrochlorothiazide daily. (See Pharmacokinetics: Absorption.)

Pediatric Dosage

The safety and efficacy of triamterene in children have not been established; however, some clinicians suggest an initial dosage of 4 mg/kg daily or 115 mg/m daily, given in two divided doses after meals. If necessary, dosage may be increased to 6 mg/kg daily; however, pediatric dosage should not exceed 300 mg daily. Dosage should be reduced if triamterene is used with other diuretics.

If triamterene is used for the management of hypertension in children, some experts recommend an initial triamterene dosage of 1-2 mg/kg daily given in 2 divided doses. Dosage may be increased as necessary up to 3-4 mg/kg (maximum 300 mg) daily given in 2 divided doses.


Adverse Effects

In general, adverse effects of triamterene are mild and respond to withdrawal of the drug. The most serious adverse effect of triamterene therapy is electrolyte imbalance, mainly hyperkalemia (serum potassium concentrations may exceed 5.5 mEq/L), especially in patients with renal insufficiency or diabetes, geriatric or severely ill patients, or those receiving prolonged therapy with large doses. Hyperkalemia may be associated with cardiac irregularities. At least 3 fatal cases of hyperkalemia have been reported in patients receiving triamterene and a thiazide diuretic; however, 2 of these patients were also receiving spironolactone which may have contributed to the hyperkalemia.

Potassium loss has been reported during triamterene therapy in some patients with hepatic cirrhosis and may result in signs and symptoms of hepatic coma or precoma. Serum potassium concentrations should be closely monitored in patients with hepatic cirrhosis and potassium supplementation administered if required.

Diuretics increase urinary sodium excretion and decrease physical signs of fluid retention in patients with heart failure. Results of short-term studies in patients with heart failure indicate that diuretic therapy is associated with a reduction in jugular venous pressures, pulmonary congestion, ascites, peripheral edema, and body weight within a few days of initiating such therapy. In addition, diuretics may improve cardiac function, symptoms, and exercise tolerance in these patients. However, since there are no long-term studies of diuretic therapy in patients with heart failure, the effects of diuretics on morbidity and mortality are not known. Nevertheless, most long-term studies of therapeutic interventions for heart failure have been in patients receiving diuretic therapy. Diuretics should not be used as monotherapy in patients with heart failure even if symptoms of fluid overload (e.g., peripheral edema, pulmonary congestion) are well controlled, because diuretics alone do not prevent progression of heart failure.

Depending on the dosage employed, diuretics may alter the efficacy and safety of concomitantly used drugs in heart failure, and therefore diuretic dosage should be selected carefully. Excessive diuretic dosages may lead to volume depletion, which can increase the risk of hypotension in patients receiving angiotensin-converting enzyme (ACE) inhibitors or vasodilators and renal insufficiency in patients receiving ACE inhibitors or angiotensin II receptor antagonists. Inadequate diuretic dosages may lead to fluid retention, which can decrease the response to ACE inhibitors and increase the risk of β-adrenergic blocking agent (β-blocker) therapy. Patients with mild heart failure may respond favorably to low doses of diuretics, since absorption of diuretics from the GI tract is rapid and the drugs are distributed rapidly to the renal tubules in such patients; however, as heart failure advances, absorption of the drugs may be delayed because of bowel edema or intestinal hypoperfusion, and distribution may be impaired because of decreases in renal perfusion and function. Therefore, dosage of diuretics usually needs to be increased with progression of heart failure; eventually, patients may become resistant to even high dosages of diuretic therapy. If resistance to diuretics occurs, IV administration of a diuretic or concomitant use of 2 or more diuretics (e.g., a loop diuretic and metolazone, a loop diuretic and a thiazide diuretic) may be necessary, or alternatively, short-term administration of a drug that increases blood flow (e.g., a positive inotropic agent such as dopamine) may be necessary. ACCF and AHA state that IV loop diuretics should be administered promptly to all hospitalized heart failure patients with substantial fluid overload to reduce morbidity. ACCF and AHA state that low-dose dopamine infusions may be considered in combination with loop diuretics to augment diuresis and preserve renal function and renal blood flow in patients with acute decompensated heart failure, although data are conflicting and additional study and experience are needed.

Most experts state that the diuretics of choice for most patients with heart failure usually are loop diuretics (e.g., bumetanide, ethacrynic acid, furosemide, torsemide), especially in those with renal impairment or substantial fluid retention, since loop diuretics increase sodium excretion to 20-25% of the filtered load of sodium, enhance free water clearance, and maintain their efficacy unless renal function is severely impaired (e.g., creatinine clearance less than 5 mL/minute). In contrast, thiazide diuretics increase fractional sodium excretion to only 5-10% of the filtered load, tend to decrease free water clearance, and lose their efficacy in patients with moderate renal impairment (e.g., creatinine clearance less than 30 mL/minute). Thiazides may be preferred in some patients with concomitant hypertension because of their sustained effects. If electrolyte imbalance(s) occurs during diuretic therapy for heart failure, the patient should be treated aggressively (preferably with low doses of a potassium-sparing diuretic instead of potassium or magnesium supplements) and diuresis should be continued. In patients who develop azotemia or hypotension before therapeutic goals are achieved, consideration to decreasing the rate of diuresis may be made, but diuretic therapy should continue until fluid retention is eliminated, provided that decreases in blood pressure remain asymptomatic; excessive concern about hypotension and azotemia may result in suboptimal diuretic therapy leading to refractory edema.

Once fluid retention has resolved in patients with heart failure, diuretic therapy should be maintained to prevent recurrence of fluid retention. Ideally, diuretic therapy should be adjusted according to changes in body weight (as an indicator of fluid retention) rather than maintained at a fixed dose.

Sodium depletion may occur when triamterene is administered to markedly edematous patients whose sodium chloride intake is restricted. Magnesium depletion may also occur, especially if triamterene is used concomitantly with another diuretic such as a thiazide which also increases excretion of magnesium. Serum chloride may be increased and serum bicarbonate decreased during triamterene therapy, resulting in decreased alkali reserve with the possibility of metabolic acidosis. Slight alkalinization of the urine may occur.

Increased BUN concentration caused by decreased glomerular filtration rate has been reported during therapy with triamterene. However, a rise in BUN concentration seldom occurs with intermittent (every other day) therapy and is reversible upon withdrawal of the drug. Serum creatinine concentration may be moderately increased during administration of triamterene but returns to pretreatment levels in 7-14 days after the drug is discontinued. Serum uric acid concentrations may be increased, especially in patients with gouty arthritis.

Megaloblastic anemia has occurred in patients with alcoholic cirrhosis receiving triamterene.

Renal colic occurred in one patient receiving triamterene and hydrochlorothiazide who had a previously asymptomatic partial urinary tract obstruction. Triamterene has occasionally caused nephrolithiasis. Renal calculi have been composed of triamterene and/or its metabolites (i.e., 6-p-hydroxytriamterene and its sulfate) alone, but apparently in a protein matrix, or combined with other usual calculus components (e.g., calcium oxalate monohydrate and dihydrate, uric acid, hydroxylapatite). Triamterene usually appears as the nucleus of the calculus as a central amorphous deposit around which calcium oxalate monohydrate or dihydrate or uric acid is deposited. Triamterene has reportedly caused acute interstitial nephritis in one patient.

Other adverse effects of triamterene include nausea, vomiting, diarrhea, or other GI disturbances. Nausea may be minimized by giving the drug after meals; however, nausea and vomiting may also be symptoms of electrolyte imbalance. Dizziness, hypotension, weakness, headache, muscle cramps, dry mouth, anaphylaxis, photosensitivity, rash, and blood dyscrasias such as granulocytopenia and eosinophilia have also been attributed to use of the drug.

Precautions and Contraindications

When triamterene is used as a fixed-combination preparation that includes hydrochlorothiazide, the cautions, precautions, and contraindications associated with thiazide diuretics must be considered in addition to those associated with triamterene.

Patients receiving prolonged triamterene therapy should be monitored for signs of electrolyte imbalance, especially those with heart failure, renal disease, or cirrhosis of the liver. It is particularly important that serum potassium concentrations be checked periodically, especially in geriatric, cirrhotic, or diabetic patients; in patients with impaired renal function; or when there is a change in dosage of triamterene. If hyperkalemia occurs, the drug should be discontinued. Periodic BUN and serum creatinine determinations should be performed, especially in patients with suspected or confirmed renal insufficiency.

Potassium supplementation in the form of potassium salts, a high potassium diet, or salt substitutes should not be given to patients receiving triamterene alone. When triamterene is added to other diuretic therapy or when patients are switched to triamterene from other diuretics, potassium supplementation should be discontinued. Patients receiving triamterene concomitantly with a thiazide or other diuretic that promotes potassium excretion (kaliuretic diuretic) should receive dietary potassium supplements only if they develop hypokalemia or their dietary intake of potassium is markedly impaired. It has been theorized that abrupt withdrawal of triamterene after intense or prolonged therapy may result in a rebound kaliuresis; therefore, the drug should be discontinued gradually.

Although a causal relationship has not been established between the drug and megaloblastic anemia, triamterene should be used with caution in pregnant women and in patients with alcohol dependence since these patients may have reduced stores of folate. Periodic blood studies should be performed in cirrhotic patients with splenomegaly as they are subject to marked hematologic variations; such patients also should be observed for exacerbation of underlying hepatic disease.

Triamterene should be used with caution in patients with impaired hepatic function. Diuretic therapy in such patients should be initiated while the patient is hospitalized, because rapid alterations in fluid and electrolyte balance may precipitate hepatic coma. Patients receiving the drug should be observed for signs of liver damage, blood dyscrasias, or other idiosyncratic reactions. Triamterene should be administered cautiously to patients with impaired renal function. Although the manufacturer states that triamterene should be used with caution in patients with a history of renal calculi, some clinicians recommend that the drug not be used in these patients because of the risk of triamterene nephrolithiasis. If a patient passes a urinary calculus during triamterene therapy, the drug should be discontinued and the calculus analyzed for the presence of triamterene and/or its metabolites. (See Cautions: Adverse Effects.)

Triamterene should be administered with caution to patients with diabetes mellitus and should be given only to those diabetic patients whose blood glucose concentration is well controlled. The drug does not appear to be diabetogenic or to alter carbohydrate metabolism; however, diabetic patients appear to be more sensitive to changes in serum potassium concentrations than are nondiabetics. Elevations of serum potassium concentrations are exacerbated by administration of large quantities of glucose; therefore, comatose diabetic patients receiving triamterene therapy should not be tested for hypoglycemia by IV administration of dextrose.

Potassium-conserving therapy should generally be avoided in severely ill patients in whom respiratory or metabolic acidosis may occur; acidosis may result in rapid increases in serum potassium concentrations. If potassium-conserving therapy (e.g., triamterene) is used, frequent assessment of acid-base balance and serum electrolytes should be performed.

Triamterene is contraindicated in patients with severe or progressive kidney disease, severe hepatic disease, preexisting or drug-induced hyperkalemia, or hypersensitivity to the drug. Triamterene should also not be used in patients who develop hyperkalemia while receiving the drug.

Pediatric Precautions

Safety and efficacy of triamterene in children have not been established.

Mutagenicity and Carcinogenicity

Studies to determine the mutagenic and carcinogenic potentials of triamterene currently are not available.

Pregnancy, Fertility, and Lactation


There are no adequate and well-controlled studies using triamterene in pregnant women, and the drug should be used during pregnancy only when the potential benefits justify the possible risks (these include adverse effects reported in adults) to the fetus.


Reproduction studies in rats using triamterene doses up to 30 times the human dose have not revealed evidence of harm to the fetus or impaired fertility. The drug has been shown to cross the placental barrier and appear in the cord blood of ewes; similar distribution may occur in humans.


Since triamterene has been shown to distribute into milk in animals and may distribute into human milk, the drug should not be used in nursing women. If use of triamterene is deemed essential, nursing should be discontinued.

Drug Interactions

Potassium-sparing Agents

Triamterene should not be used concurrently with another potassium-sparing agent (e.g., amiloride, spironolactone), since concomitant therapy with these drugs may increase the risk of hyperkalemia compared with triamterene alone. At least 2 deaths have been reported in patients receiving triamterene and spironolactone concurrently; in one patient, recommended dosages were exceeded and, in the other patient, serum electrolytes were not closely monitored.

Potassium-sparing diuretics should be used with caution and serum potassium should be determined frequently in patients receiving an angiotensin-converting enzyme (ACE) inhibitor (e.g., captopril, enalapril), since concomitant administration with an ACE inhibitor may increase the risk of hyperkalemia. Dosage of triamterene should be reduced or the drug should be discontinued as necessary. Patients with renal impairment may be at increased risk of hyperkalemia.

Potassium-containing Preparations

Concurrent administration of triamterene with potassium supplements, potassium-containing medications (e.g., parenteral penicillin G potassium), or other substances containing potassium (e.g., salt substitutes, low-salt milk) may increase the risk of hyperkalemia as compared with triamterene alone, and such combined use is contraindicated.

Nonsteroidal Anti-inflammatory Agents

Concomitant use of triamterene and indomethacin has adversely affected renal function. In one study, concomitant administration of indomethacin and triamterene to 4 healthy adults resulted in a 60-70% decrease in creatinine clearance in 2 individuals; renal function returned to normal within 2 weeks after both drugs were discontinued. When the drugs were given separately, triamterene caused no consistent change in renal function; indomethacin induced an average 10% decrease in creatinine clearance. Acute anuric renal failure occurred within 2 days after concomitant use of indomethacin and triamterene in a 79-year-old woman with compensated heart failure. BUN and serum creatinine concentrations increased to 102 and 10.2 mg/dL, respectively, 5 days after discontinuance of the drugs in this woman, and subsequently returned toward normal over 2 months; anuria persisted for 11 days after discontinuance of the drugs. Although the mechanism of this interaction was not determined, it has been postulated that indomethacin may inhibit triamterene-stimulated synthesis of renal prostaglandins that mediate an adaptive mechanism for renal blood flow preservation in response to triamterene-mediated renal vasoconstriction. The manufacturer of indomethacin recommends that the combination of indomethacin and triamterene not be used. Triamterene should be used with caution in patients receiving other nonsteroidal anti-inflammatory agents.

Angiotensin-converting Enzyme Inhibitors

Potassium-sparing diuretics (e.g., triamterene) should be used with caution and serum potassium should be determined frequently in patients receiving an ACE inhibitor (e.g., enalapril), since hyperkalemia may occur. Potassium-sparing diuretics should be used with great caution, if at all, in patients receiving an ACE inhibitor (e.g., enalapril) for heart failure. Potassium-sparing diuretics should be discontinued or their dosage reduced as necessary in patients receiving an ACE inhibitor. ()

Other Drugs

Although triamterene alone does not consistently cause hypotension, lowering of blood pressure may occur, especially when it is used with hypotensive agents.

Diuretics including triamterene, generally should not be used concurrently with lithium since diuretics reduce renal lithium clearance and may increase the risk of lithium toxicity.



Triamterene is rapidly absorbed from the GI tract; however, the degree of absorption varies in different individuals. Diuresis usually occurs within 2-4 hours and diminishes in approximately 7-9 hours after oral administration of the drug, although the total duration of action may be 24 hours or longer. The maximum therapeutic effect may not occur until after several days of therapy. Peak plasma concentrations of 0.05-0.28 mcg/mL are achieved within 2-4 hours following administration of a 100- to 200-mg single oral dose.

Oral bioavailability of hydrochlorothiazide from the original formulation (no longer commercially available) of Dyazide capsules was about 50-65% that from Maxzide tablets or single-entity tablets or solutions of the drug. In one crossover study in a limited number of healthy adults receiving single doses of the drug, the mean hydrochlorothiazide dose recovered in urine within 72 hours was about 30% for the original formulation of Dyazide capsules and about 60% for Maxzide or single-entity tablets of the drug. In 1995, Dyazide capsules were reformulated to improve the oral bioavailability of triamterene and hydrochlorothiazide. The oral bioavailabilities of triamterene and hydrochlorothiazide from the reformulated Dyazide capsules now are comparable to those of aqueous suspensions of the individual drugs, averaging 85 and 82%, respectively, for the new formulation and 100 and 100%, respectively, for the suspensions. In addition, intraindividual variation in bioavailability from the reformulated Dyazide capsules was reduced by about 40% compared with the original formulation. The manufacturer states that the reformulated Dyazide capsules also are bioequivalent to single-entity 25-mg hydrochlorothiazide tablets and 37.5-mg triamterene capsules. Administration of reformulated Dyazide with a high-fat meal in healthy adults increased the average bioavailabilities of triamterene by about 67%, 6-p-hydroxytriamterene by about 50%, and hydrochlorothiazide by about 17% and the peak concentrations of triamterene and its p-hydroxy metabolite and delayed the absorption of the active drugs by up to 2 hours.


In animals, triamterene has been detected in the brain, heart, ocular fluid, fat, liver, and skeletal muscles. The drug is distributed into bile. Approximately 67% of the drug in the plasma is bound to proteins. Triamterene crosses the placenta in animals. No human data are available indicating whether triamterene appears in the milk of nursing women; however, animal studies have demonstrated the presence of very small amounts of the drug in breast milk.


The plasma half-life of triamterene is 100-150 minutes. The metabolic and excretory fate of triamterene has not been fully determined. The drug is reportedly metabolized to 6-p-hydroxytriamterene and its sulfate conjugate. Triamterene is excreted in urine as unchanged drug and metabolites. In one study in healthy males, the urinary excretion of 6-p-hydroxytriamterene was up to 3 times that of unchanged drug. Limited data indicate that the renal clearances of triamterene, hydroxytriamterene sulfate, and hydrochlorothiazide are reduced in geriatric patients receiving combined triamterene and hydrochlorothiazide therapy, principally as a result of age-related reductions in renal function.

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