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Potassium homeostasis and renin-angiotensin-aldosterone system inhibitors.
Clin J Am Soc Nephrol 2010; 5(3):531-48CJ

Abstract

Inhibition of the renin-angiotensin-aldosterone system (RAAS) is a key strategy in treating hypertension and cardiovascular and renal diseases. However, RAAS inhibitors (angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, aldosterone receptor antagonists, and direct renin inhibitors) increase the risk of hyperkalemia (serum potassium >5.5 mmol/L). This review evaluates the effects on serum potassium levels of RAAS inhibitors. Using PubMed, we searched for clinical trials published up to December 2008 assessing the effects on serum potassium levels of angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, aldosterone receptor antagonists, and direct renin inhibitors, alone and in combination, in patients with hypertension, heart failure (HF), or chronic kidney disease (CKD); 39 studies were identified. In patients with hypertension without risk factors for hyperkalemia, the incidence of hyperkalemia with RAAS inhibitor monotherapy is low (< or =2%), whereas rates are higher with dual RAAS inhibition (approximately 5%). The incidence of hyperkalemia is also increased in patients with HF or CKD (5% to 10%). However, increases in serum potassium levels are small (approximately 0.1 to 0.3 mmol/L), and rates of study discontinuation due to hyperkalemia are low, even in high-risk patient groups (1% to 5%). Patients with HF or CKD are at greater risk of hyperkalemia with RAAS inhibitors than those without these conditions. However, the absolute changes in serum potassium are generally small and unlikely to be clinically significant. Moreover, these patients are likely to derive benefit from RAAS inhibition. Rather than denying them an effective treatment, electrolyte levels should be closely monitored in these patients.

Authors+Show Affiliations

Division of Nephrology, Department of Medicine, University of Maryland School of Medicine, 22 South Greene Street, Room N3W143, Baltimore, MD 21201, USA. mweir@medicine.umaryland.eduNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Review

Language

eng

PubMed ID

20150448

Citation

Weir, Matthew R., and Mark Rolfe. "Potassium Homeostasis and Renin-angiotensin-aldosterone System Inhibitors." Clinical Journal of the American Society of Nephrology : CJASN, vol. 5, no. 3, 2010, pp. 531-48.
Weir MR, Rolfe M. Potassium homeostasis and renin-angiotensin-aldosterone system inhibitors. Clin J Am Soc Nephrol. 2010;5(3):531-48.
Weir, M. R., & Rolfe, M. (2010). Potassium homeostasis and renin-angiotensin-aldosterone system inhibitors. Clinical Journal of the American Society of Nephrology : CJASN, 5(3), pp. 531-48. doi:10.2215/CJN.07821109.
Weir MR, Rolfe M. Potassium Homeostasis and Renin-angiotensin-aldosterone System Inhibitors. Clin J Am Soc Nephrol. 2010;5(3):531-48. PubMed PMID: 20150448.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Potassium homeostasis and renin-angiotensin-aldosterone system inhibitors. AU - Weir,Matthew R, AU - Rolfe,Mark, Y1 - 2010/02/11/ PY - 2010/2/13/entrez PY - 2010/2/13/pubmed PY - 2010/5/29/medline SP - 531 EP - 48 JF - Clinical journal of the American Society of Nephrology : CJASN JO - Clin J Am Soc Nephrol VL - 5 IS - 3 N2 - Inhibition of the renin-angiotensin-aldosterone system (RAAS) is a key strategy in treating hypertension and cardiovascular and renal diseases. However, RAAS inhibitors (angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, aldosterone receptor antagonists, and direct renin inhibitors) increase the risk of hyperkalemia (serum potassium >5.5 mmol/L). This review evaluates the effects on serum potassium levels of RAAS inhibitors. Using PubMed, we searched for clinical trials published up to December 2008 assessing the effects on serum potassium levels of angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, aldosterone receptor antagonists, and direct renin inhibitors, alone and in combination, in patients with hypertension, heart failure (HF), or chronic kidney disease (CKD); 39 studies were identified. In patients with hypertension without risk factors for hyperkalemia, the incidence of hyperkalemia with RAAS inhibitor monotherapy is low (< or =2%), whereas rates are higher with dual RAAS inhibition (approximately 5%). The incidence of hyperkalemia is also increased in patients with HF or CKD (5% to 10%). However, increases in serum potassium levels are small (approximately 0.1 to 0.3 mmol/L), and rates of study discontinuation due to hyperkalemia are low, even in high-risk patient groups (1% to 5%). Patients with HF or CKD are at greater risk of hyperkalemia with RAAS inhibitors than those without these conditions. However, the absolute changes in serum potassium are generally small and unlikely to be clinically significant. Moreover, these patients are likely to derive benefit from RAAS inhibition. Rather than denying them an effective treatment, electrolyte levels should be closely monitored in these patients. SN - 1555-905X UR - https://www.unboundmedicine.com/medline/citation/20150448/Potassium_homeostasis_and_renin_angiotensin_aldosterone_system_inhibitors_ L2 - http://cjasn.asnjournals.org/cgi/pmidlookup?view=long&amp;pmid=20150448 DB - PRIME DP - Unbound Medicine ER -