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Previous Volume 351:585-592 August 5, 2004 Number 6 Next

	Since this article has no abstract, we have provided an extract of the first 100 words of the full text and any section headings.

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Angiotensin-converting–enzyme (ACE) inhibitors and angiotensin-receptor blockers are used commonly in clinical practice to treat hypertension and decrease cardiovascular events in high-risk patients. A side effect of such therapy is the development of hyperkalemia. Hyperkalemia has been attributed to the use of ACE inhibitors in 10 to 38 percent of hospitalized patients with this complication.^1,2,3,4 Hyperkalemia develops in approximately 10 percent of outpatients within a year after these drugs are prescribed.⁵ Patients at greatest risk for hyperkalemia include those with diabetes and those with impaired renal function in whom a defect in the excretion of renal potassium may already exist.

Hyperkalemia . . . [Full Text of this Article]

Normal Handling of Potassium in the Kidney

Induction of Hyperkalemia

Decreased Distal Delivery of Sodium

Decreased Aldosterone Activity

Abnormal Functioning of the Cortical Collecting Tubule

Minimizing the Risk of Hyperkalemia

Source Information

From the Department of Medicine, Division of Nephrology, University of Texas Southwestern Medical School, Dallas.

Address reprint requests to Dr. Palmer at the Department of Medicine, University of Texas Southwestern Medical School, 5323 Harry Hines Blvd., Dallas, TX 75390-8856, or at biff.palmer@utsouthwestern.edu.

Related Letters:

Hyperkalemia and Inhibitors of the Renin–Angiotensin–Aldosterone System
Segal A., Palmer B. F.
Extract | Full Text | PDF  
N Engl J Med 2004; 351:2450-2451, Dec 2, 2004. Correspondence

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