ACE inhibition or angiotensin receptor blockade: Impact on potassium in renal failure

Background Inhibition of the renin-angiotensin system is known to raise ser um potassium [K+] levels in patients with renal insufficiency or diabetes. No study has evaluated the comparative effects of an angiotensin-converting enzyme (ACE) inhibitor versus an angiotensin receptor blocker (ARB) on the changes in serum [K+] in people with renal insufficiency. Methods. The study was a multicenter, randomized, double crossover design, with each period lasting one month. A total of 35 people (21 males and 14 f emales, 19 African Americans and 16 Caucasian) participated, with the mean age being 56 +/- 2 years. Mean baseline serum [K+] was 4.4 +/- 0.1 mEq/L. T he glomerular filtration rate (GFR) was 65 +/- 5 mLmin/1.73 m(2), and blood pressure was 150 +/- 2/88 +/- 1 mm Hg. The main outcome measure was the di fference from baseline in the level of serum [K+], plasma aldosterone, and GFR following the initial and crossover periods. Results. For the total group, serum [K+] changes were not significantly dif ferent between the lisinopril or valsartan treatments. The subgroup with GF R values of less than or equal to 60 mL/min/1.73 m(2) who received lisinopr il demonstrated significant increases in serum [K+] of 0.28 mEq/L above the mean baseline of 4.6 mEq/L (P = 0.04). This increase in serum [K+] was als o accompanied by a decrease in plasma aldosterone (P = 0.003). Relative to the total group, the change in serum [K+] from baseline to post-treatment i n the lisinopril group was higher among those with GFR values of less than or equal to 60 mL/min/1.73 m2. The lower GFR group taking valsartan, howeve r, demonstrated a smaller rise in serum [K+], 0.12 mEq/L above baseline (P = 0.1), a 43% lower value when compared with the change in those who receiv ed lisinopril. This blunted rise in [K+] in people taking valsartan was not associated with a significant decrease in plasma aldosterone (P = 0.14). Conclusions. In the presence of renal insufficiency, the ARE valsartan did not raise serum [K+] to the same degree as the ACE inhibitor lisinopril. Th is differential effect on serum [K+] is related to a relatively smaller red uction in plasma aldosterone by the ARE and is not related to changes in GF R. This study provides evidence that increases in serum [K+] are less likel y with ARE therapy compared with BCE inhibitor therapy in people with renal insufficiency.