Hyperkalemia angiotensin converting

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. 

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. 

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. 

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. 

Reardon LC, Macpherson DS. Hyperkalemia in outpatients using angiotensin-converting eiiZ5nne inhibitors. Arch Intern Med 1998 158 26-32. 

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

Angiotensin-converting Hypotension, cough (with ACEIs), hyperkalemia. BP every 2 hours x 3 for first dose then every 8 hours... 

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. 

Berry C, McMurray J. Life-threatening hyperkalemia during combined tiierapy with angiotensin-converting enz3nne inhibitors and spironolactone. Am JMed(2001) 111, 587. 

Stoltz ML, Andrews CE. Severe hyperkalemia during very-low-calorie diets and angiotensin converting enzyme use. JAMA (1990) 264, 2121-Z. 

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... 

In the generally healthy population with normal kidney function, a high potassium intake from foods poses no risk because excess potassium is readily excreted in the urine. In contrast, supplemental potassium can lead to acute toxicity in healthy individuals. Also, in individuals whose urinary potassium excretion is impaire a potassium intake less than 4.7g/day (120 mmol/day) is appropriate because of adverse cardiac effects (arrhythmias) from hyperkalemia. Drugs that commonly impair potassium excretion are angiotensin converting... 

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