Hyperkalemia enzyme inhibitors

Medications can increase the risk of hyperkalemia in patients with CKD, including angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers, used for the treatment of proteinuria and hypertension. Potassium-sparing diuretics, used for the treatment of edema and chronic heart failure, can also exacerbate the development of hyperkalemia, and should be used with caution in patients with stage 3 CKD or higher. 

Treatment with angiotensin-converting enzyme inhibitors is also more likely to be associated with hyperkalemia in older individuals (69). Impaired angiotensin II formation limits this potent stimulus for aldosterone secretion, and this is superimposed on the already age-related decrease in activity of the renin-angiotensin-aldosterone axis. The same drug-induced hyporeninemic hypoaldosteronism is predicted for the angiotensin receptor blockers. However, to date this has not been documented clincally. 

Chiu TF, Bullard MJ, Chen JC, Liaw SJ, Ng CJ. Rapid life-threatening hyperkalemia after addition of amiloride HCl/ hydrochlorothiazide to angiotensin-converting enzyme inhibitor therapy. Ann Emerg Med 1997 30(5) 612-15. 

Angiotensin-converting enzyme inhibitor prototype used in HTN, diabetic nephropathy, and CHF. Tox hyperkalemia, fetal renal damage, cough ( sore throat ). Other prils benzepril, enalapril. lisinopril, quinapril. 

Additive pharmacodynamic effects. In the case when two or more drags exhibit similar pharmacodynamic effects it may produce an excessive manifestation of toxicity. It could be compounds whose combination may cause QT interval prolongation, leading to ventricular arrhythmia, as well as compounds that increase the concentration of potassium in blood and lead to hyperkalemia. An additive pharmacodynamic effect is also used for therapeutic purposes, so diuretics and angiotensin-converting enzyme inhibitors cause the blood pressure reduction... 

Hyperkalemia is an excess of potassium in the blood. Clinical symptoms are muscle weakness and cardiac arrhythmias. It is caused by, e.g., hyperaldosteronism and angiotensin-converting enzyme (ACE) inhibitors. 

The COX-2 enzyme is also produced normally in the kidney thus COX-2 inhibitors exert renal effects similar to those of conventional NSAIDs. Both drug classes may increase sodium reabsorption and fluid retention and can provoke renal insufficiency and hyperkalemia. COX-2 inhibitors should be used with caution in patients with heart failure or hypertension. 

Because indomethacin may increase serum potassium concentrations, indomethacin and spironolactone should be administered concomitantly with caution. Potassium-sparing diuretics should be used with caution, and serum potassium should be determined frequently in patients receiving an angiotensin-converting enzyme (ACE) inhibitor (e.g., captopril). Concomitant administration with an ACE inhibitor may increase the risk of hyperkalemia. The dosage of spironolactone should be reduced, or the drug discontinued, as necessary. Patients with renal impairment may be at increased risk of hyperkalemia [65]. 

ACE inhibitors prevent the formation of angiotensin II by angiotensin-converting enzyme (ACE) and thereby reduce peripheral vascular resistance and blood pressure. In addition, ACE inhibitors prevent the effect of angiotensin II on protein synthesis in myocardial and vascular muscle cells, and thus diminish ventricular hypertrophy. As adverse effects, ACE inhibitors may provoke dry cough, impaired renal function, and hyperkalemia. When ACE inhibitors are poorly tolerated, an ATq-receptor antagonist can be given. 

Angiotensin-converting enzyme (ACE) inhibitors Group toxicitv hyperkalemia, acute renal failure, anaioedema, rash, couah anemia, and liver toxicitv ... 

Renal papillary necrosis and other renal injury with long-term use. Most of the unwanted renal side effects of the class of NSAIDs are related to the inhibi-ton of prostanoid synthesis. The COX-2 enzyme has been implicated as a mediator of renal blood flow, renin release and sodium excretion. As a result, COX-2 inhibitors may lead to an alteration of renal homeostasis resulting in decreases in glomerular filtration rate, renal blood flow, sodium and water retention, and hyperkalemia [1]. 

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