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.
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).