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Amiodarone induced thyrotoxicosis (AIT) is a form of hyperthyroidism due to treatment with antiarrhythmic drug, amiodarone. Amiodarone induced thyroid dysfunction more commonly results in hypothyroidism , estimated to occur in 6-32% of patients, whereas hyperthyroidism from amiodarone use is estimated at 1-12%. [ 1 ]
This can occur both through damage of cardiac muscle as well as through alteration of the ion currents of cardiomyocytes. [1] Two distinct drug classes in which cardiotoxicity can occur are in anti-cancer and antiarrhythmic drugs. Anti-cancer drug classes that cause cardiotoxicity include anthracyclines, monoclonal antibodies, and antimetabolites.
Amiodarone has been used both in the treatment of acute life-threatening arrhythmias as well as the long-term suppression of arrhythmias. [13] Amiodarone is commonly used to treat different types of abnormal heart rhythms, such as atrial arrhythmias (supraventricular arrhythmias) and ventricular arrhythmias.
Drug-induced glomerular disease is not common but there are a few drugs that have been implicated. Glomerular lesions occur primarily through immune-mediated pathways rather than through direct drug toxicity. Heroin and Pamidronate are known to cause focal segmental glomerulosclerosis; Gold salts therapy can cause membranous nephropathy [4 ...
A small proportion of individuals with analgesic nephropathy may develop end-stage kidney disease. Analgesic nephropathy was once a common cause of kidney injury and end-stage kidney disease in parts of Europe, Australia, and the United States. In most areas, its incidence has declined sharply since the use of phenacetin fell in the 1970s and ...
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]