Spironolactone and two of its metabolites (7a-thiomethyl-spironolactone) and canrenone are aldosterone antagonists that bind to cytoplasmic mineralocorticoid receptors in the distal tubules of the kidney and promote sodium and water excretion as well as potassium retention. Spironolactone, after oral tablet intake, reaches a maximum concentration in 2.6 hrs and an active metabolite (canrenone) reaches a maximum concentration in 4.3 hrs. When taken with food, its bioavailability increases to

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... . Spironolactone has a half-life of 1.6 hrs, while its metabolite, canrenone, has a half-life of 16.5 hrs, thus prolonging the biological effects of spironolactone. Spironolactone and eplerenone compete with aldosterone for binding to intracellular receptors, causing decreased gene expression and reduced synthesis of protein mediator that activates Na+ channels in the apical membrane and decreased the number of Na+ / K +ATPase pumps in basolateral membrane. Side effects of spironolactone can cause side effects, such as fluid and electrolyte imbalance (hyperkalemia, hyponatremia), mild acidosis, and transient elevation of serum urea nitrogen. Spironolactone used as diuresis in congestive heart failure, ascites, oedema, and nephritic syndrome reduction of hypokalemia induced by other diuretics or amphotericin; primary hyperaldosteronism. Coadministration of diuretics (spironolactone) with non-steroidal anti-inflammatory drugs escalated the pitfall of nephrotoxicity and non-steroidal anti-inflammatory drugs deescalate the hypotensive effect of diuretics.