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Amiloride is a potassium-sparing diuretic that acts in the distal convoluted tubule independently of the action of aldosterone, inhibiting sodium channels. It is a relatively safe drug with few reported adverse effects.
Patients with congenital nephrogenic diabetes insipidus are often treated with a combination of a thiazide and a potassium-sparing diuretic, without consensus on the preferred potassium-sparing diuretic. A Japanese adult was systematically studied to determine the renal effects of hydrochlorothiazide plus amiloride and hydrochlorothiazide plus triamterene [ ]. The combination with amiloride was superior to that with triamterene in preventing excessive urinary potassium loss, hypokalemia, and metabolic alkalosis. These results suggest that amiloride is the preferred add-on therapy to hydrochlorothiazide in nephrogenic diabetes insipidus.
An isolated report [ ] suggests that amiloride may have prodysrhythmic potential in a small proportion of patients with inducible sustained ventricular tachycardia.
Amiloride has a specific effect on sodium flux in the renal tubules; severe hyponatremia has been reported with the combination of a thiazide diuretic and amiloride.
As a potassium-sparing diuretic, amiloride can cause hyperkalemia [ ], even in patients who are taking a potassium-wasting diuretic [ ]. This effect can be enhanced by concomitant therapy with ACE inhibitors or angiotensin-II receptor antagonists. In five patients with diabetes mellitus over 50 years of age who were taking an ACE inhibitor the serum potassium rose markedly 8–18 days after the addition of amiloride [ ]. All but one had some degree of renal impairment. In four cases potassium concentrations were between 9.4 and 11 mmol/l.
Rashes with diarrhea and eosinophilia have been reported [ ].
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