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(Circulation. 2008;118:1609-1611.)
© 2008 American Heart Association, Inc.

Editorial

Hyperkalemia Associated With Inhibitors of the Renin-Angiotensin-Aldosterone System

Balancing Risk and Benefit

Akshay Desai, MD, MPH

From the Cardiovascular Division, Brigham and Women’s Hospital, Boston, Mass.

Correspondence to Akshay Desai, MD, MPH, Cardiovascular Division, Brigham and Women’s Hospital, 75 Francis St, Boston, MA 02115. E-mail adesai@partners.org

Key Words: Editorials • aldosterone • drugs • heart failure • myocardial infarction • potassium

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Maintenance of normal potassium homeostasis is increasingly an important limiting factor in the therapy of cardiovascular disease. Many pharmacological agents that reduce morbidity and mortality in patients with complicated myocardial infarction and chronic heart failure, including β-blockers, angiotensin-converting enzyme inhibitors, angiotensin-receptor blockers (ARBs), and aldosterone receptor antagonists, are also known to raise serum potassium and augment the risk of life-threatening hyperkalemia. Conversely, loop diuretics, a mainstay of heart failure treatment, tend to enhance the risk of hypokalemia and ventricular arrhythmias, which may in part account for their consistent dose-related association with increased mortality in observational studies. Because combination drug therapy may simultaneously improve clinical outcomes and enhance the risk of potassium-related adverse events, an appropriate balance of benefit and risk depends heavily on careful patient selection and adequate surveillance of serum potassium and renal function.

Article p 1643

The ability of the kidney to maintain potassium homeostasis even as the glomerular filtration rate declines depends critically on adequate sodium delivery to the distal nephron, normal production of aldosterone, and adequate sodium/potassium exchange in the cortical collecting duct.¹ Reduction in the filtered sodium load (as a consequence of decreased renal perfusion or reduced cardiac output), diminished aldosterone production, or impaired potassium secretion by the cortical collecting duct (related, for example, to tubulointerstitial disease or use of potassium-sparing diuretics) may attenuate tubular compensatory mechanisms and precipitate hyperkalemia in the vulnerable patient. Aldosterone production is decreased in the elderly, in diabetic patients, and in those receiving drugs that block the production or action . . . [Full Text of this Article]