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

G. L. Bakris, M. Siomos, D. Richardson, I. Janssen, W. K. Bolton, L. Hebert, Rajiv Agarwal, D. Catanzaro

Research output: Contribution to journalArticle

195 Citations (Scopus)

Abstract

Background. Inhibition of the renin-angiotensin system is known to raise serum 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 females, 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. The glomerular filtration rate (GFR) was 65 ± 5 mL/min/1.73 m2, and blood pressure was 150 ± 2/88 ± 1 mm Hg. The main outcome measure was the difference 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 different between the lisinopril or valsartan treatments. The subgroup with GFR values of ≤60 mL/min/1.73 m2 who received lisinopril 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 also 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 in the lisinopril group was higher among those with GFR values of ≤60 mL/min/1.73 m2. The lower GFR group taking valsartan, however, 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 received 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 ARB valsartan did not raise serum [K+] to the same degree as the ACE inhibitor lisinopril. This differential effect on serum [K+] is related to a relatively smaller reduction in plasma aldosterone by the ARB and is not related to changes in GFR. This study provides evidence that increases in serum [K+] are less likely with ARB therapy compared with ACE inhibitor therapy in people with renal insufficiency.

Original languageEnglish (US)
Pages (from-to)2084-2092
Number of pages9
JournalKidney International
Volume58
Issue number5
DOIs
StatePublished - 2000

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Angiotensin Receptors
Peptidyl-Dipeptidase A
Renal Insufficiency
Potassium
Valsartan
Lisinopril
Serum
Glomerular Filtration Rate
Angiotensin Receptor Antagonists
Aldosterone
Angiotensin-Converting Enzyme Inhibitors
Enzyme Therapy
Mineralocorticoid Receptors
Renin-Angiotensin System
African Americans
Cross-Over Studies
Therapeutics
Outcome Assessment (Health Care)

Keywords

  • Diabetes
  • Hyperkalemia
  • Kidney disease
  • Lisinopril
  • Plasma aldosterone
  • Valsartan

ASJC Scopus subject areas

  • Nephrology

Cite this

Bakris, G. L., Siomos, M., Richardson, D., Janssen, I., Bolton, W. K., Hebert, L., ... Catanzaro, D. (2000). ACE inhibition or angiotensin receptor blockade: Impact on potassium in renal failure. Kidney International, 58(5), 2084-2092. https://doi.org/10.1046/j.1523-1755.2000.00381.x

ACE inhibition or angiotensin receptor blockade : Impact on potassium in renal failure. / Bakris, G. L.; Siomos, M.; Richardson, D.; Janssen, I.; Bolton, W. K.; Hebert, L.; Agarwal, Rajiv; Catanzaro, D.

In: Kidney International, Vol. 58, No. 5, 2000, p. 2084-2092.

Research output: Contribution to journalArticle

Bakris, GL, Siomos, M, Richardson, D, Janssen, I, Bolton, WK, Hebert, L, Agarwal, R & Catanzaro, D 2000, 'ACE inhibition or angiotensin receptor blockade: Impact on potassium in renal failure', Kidney International, vol. 58, no. 5, pp. 2084-2092. https://doi.org/10.1046/j.1523-1755.2000.00381.x
Bakris, G. L. ; Siomos, M. ; Richardson, D. ; Janssen, I. ; Bolton, W. K. ; Hebert, L. ; Agarwal, Rajiv ; Catanzaro, D. / ACE inhibition or angiotensin receptor blockade : Impact on potassium in renal failure. In: Kidney International. 2000 ; Vol. 58, No. 5. pp. 2084-2092.
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abstract = "Background. Inhibition of the renin-angiotensin system is known to raise serum 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 females, 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. The glomerular filtration rate (GFR) was 65 ± 5 mL/min/1.73 m2, and blood pressure was 150 ± 2/88 ± 1 mm Hg. The main outcome measure was the difference 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 different between the lisinopril or valsartan treatments. The subgroup with GFR values of ≤60 mL/min/1.73 m2 who received lisinopril 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 also 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 in the lisinopril group was higher among those with GFR values of ≤60 mL/min/1.73 m2. The lower GFR group taking valsartan, however, 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 received 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 ARB valsartan did not raise serum [K+] to the same degree as the ACE inhibitor lisinopril. This differential effect on serum [K+] is related to a relatively smaller reduction in plasma aldosterone by the ARB and is not related to changes in GFR. This study provides evidence that increases in serum [K+] are less likely with ARB therapy compared with ACE inhibitor therapy in people with renal insufficiency.",
keywords = "Diabetes, Hyperkalemia, Kidney disease, Lisinopril, Plasma aldosterone, Valsartan",
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T1 - ACE inhibition or angiotensin receptor blockade

T2 - Impact on potassium in renal failure

AU - Bakris, G. L.

AU - Siomos, M.

AU - Richardson, D.

AU - Janssen, I.

AU - Bolton, W. K.

AU - Hebert, L.

AU - Agarwal, Rajiv

AU - Catanzaro, D.

PY - 2000

Y1 - 2000

N2 - Background. Inhibition of the renin-angiotensin system is known to raise serum 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 females, 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. The glomerular filtration rate (GFR) was 65 ± 5 mL/min/1.73 m2, and blood pressure was 150 ± 2/88 ± 1 mm Hg. The main outcome measure was the difference 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 different between the lisinopril or valsartan treatments. The subgroup with GFR values of ≤60 mL/min/1.73 m2 who received lisinopril 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 also 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 in the lisinopril group was higher among those with GFR values of ≤60 mL/min/1.73 m2. The lower GFR group taking valsartan, however, 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 received 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 ARB valsartan did not raise serum [K+] to the same degree as the ACE inhibitor lisinopril. This differential effect on serum [K+] is related to a relatively smaller reduction in plasma aldosterone by the ARB and is not related to changes in GFR. This study provides evidence that increases in serum [K+] are less likely with ARB therapy compared with ACE inhibitor therapy in people with renal insufficiency.

AB - Background. Inhibition of the renin-angiotensin system is known to raise serum 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 females, 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. The glomerular filtration rate (GFR) was 65 ± 5 mL/min/1.73 m2, and blood pressure was 150 ± 2/88 ± 1 mm Hg. The main outcome measure was the difference 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 different between the lisinopril or valsartan treatments. The subgroup with GFR values of ≤60 mL/min/1.73 m2 who received lisinopril 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 also 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 in the lisinopril group was higher among those with GFR values of ≤60 mL/min/1.73 m2. The lower GFR group taking valsartan, however, 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 received 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 ARB valsartan did not raise serum [K+] to the same degree as the ACE inhibitor lisinopril. This differential effect on serum [K+] is related to a relatively smaller reduction in plasma aldosterone by the ARB and is not related to changes in GFR. This study provides evidence that increases in serum [K+] are less likely with ARB therapy compared with ACE inhibitor therapy in people with renal insufficiency.

KW - Diabetes

KW - Hyperkalemia

KW - Kidney disease

KW - Lisinopril

KW - Plasma aldosterone

KW - Valsartan

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