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Because renal excretion contributes only minimally to the elimination of amiodarone, dose adjustment based on kidney function is generally not necessary. This is because most patients with normal renal function can adequately clear the drug through hepatic metabolism and biliary elimination pathways. [13]
She explains that there are two main types of kidney disease: short-term (called acute kidney injury or AKI), which is reversible with timely treatment; and long-term (called chronic kidney ...
Nephrotoxicity is toxicity in the kidneys. It is a poisonous effect of some substances, both toxic chemicals and medications, on kidney function. [1] There are various forms, [2] and some drugs may affect kidney function in more than one way. Nephrotoxins are substances displaying nephrotoxicity.
When the kidneys detect low blood pressure, the renin–angiotensin–aldosterone system (RAAS) is activated and eventually, aldosterone is secreted. Aldosterone binds to aldosterone receptors (mineralocorticoid receptors) increasing sodium reabsorption in an effort to increase blood pressure and improve fluid status in the body.
Amiodarone has both direct and indirect effects on thyroid function. The most notable indirect thyroid altering property is that the drug is approximately one-third iodine by weight. As a result, amiodarone therapy elevates free circulating iodine levels up to 40 times greater than the iodine intake from the average American diet. [2]
Amiodarone is also safe to use in individuals with cardiomyopathy and atrial fibrillation, to maintain normal sinus rhythm. Amiodarone prolongation of the action potential is uniform over a wide range of heart rates, so this drug does not have reverse use-dependent action. Amiodarone was the first agent described in this class. [4]