renin-angiotensin-aldosterone system inhibitor (RAAS inhibitor)
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Introduction
Includes:
Indications
- treatment of hypertension
- benefit in patients with heart failure
- renal protective in patients with diabetes mellitus
- RAAS inhibitors that cross the blood-brain barrier* may be linked to less memory decline
- treatment of heart failure
- mineralocorticoid receptor antagonists improve outcomes in heart failure with preserved (HFpEF), reduced (HFrEF), & mildly reduced ejection fraction[7]
* ACE inhibitors that cross the blood-brain barrier
* ARBs that cross the blood-brain barrier
Adverse effects
- increases in serum creatinine after start of a RAAS inhibitor associated with adverse cardiorenal outcomes, even below guideline recommended threshold of a 30% increase for stopping treatment[3]
- concentric hypertrophy of renal arterioles possible leading to renal vascular damage[4]
- drug adverse effects of renin-angiotensin-aldosterone system inhibitors (RAAS inhibitors)
- drug adverse effects of antihypertensive agents
Laboratory
- serum creatinine & serum potassium
- within 120 days prior to therapy initation*
- at least twice within 10 days after therapy initiation*
- at least three times days 11-90 after therapy initiation*
* recommendations for patients with heart failure[2]
Mechanism of action
- pharmaceutical agents that inhibit the renin-angiotensin-aldosterone axis.
Notes
- among patients with mean eGFR of 12 mL/min/1.73 m2 continuation vs discontinuation of RAS inhibitor made little difference in eGFR[6]
More general terms
More specific terms
- aldosterone receptor antagonist (aldosterone antagonist)
- angiotensin II receptor antagonist (ARB)
- angiotensin II receptor type 2 & 4-inhibiting antihypertensive
- angiotensin II receptor type 2 & 4-stimulating antihypertensive
- angiotensin-converting enzyme (ACE) inhibitor
- finerenone (Kerendia)
- renin inhibitor
Additional terms
References
- ↑ Weir MR, Rolfe M. Potassium homeostasis and renin-angiotensin-aldosterone system inhibitors. Clin J Am Soc Nephrol. 2010 Mar;5(3):531-48. PMID: https://www.ncbi.nlm.nih.gov/pubmed/20150448
- ↑ 2.0 2.1 Cooper LB et al. Consistency of laboratory monitoring during initiation of mineralocorticoid receptor antagonist therapy in patients with heart failure. JAMA 2015 Nov 10; 314:1973 PMID: https://www.ncbi.nlm.nih.gov/pubmed/26547470
- ↑ 3.0 3.1 Schmidt M et al. Serum creatinine elevation after renin-angiotensin system blockade and long term cardiorenal risks: Cohort study. BMJ 2017 Mar 9; 356:j791 <PubMed> PMID: https://www.ncbi.nlm.nih.gov/pubmed/28279964 Free full text <Internet> http://www.bmj.com/content/356/bmj.j791
- ↑ 4.0 4.1 Pass W Memory benefit seen with antihypertensives crossing blood-brain barrier. Internal Medicine News. 2021. June 21. https://www.mdedge.com/internalmedicine/article/241878/neurology/memory-benefit-seen-antihypertensives-crossing-blood-brain
- ↑ Zoler ML ACE Inhibitors, ARBs Link With Kidney Damage in Small Study. Medscape. Feb 4, 2022 https://www.medscape.com/viewarticle/967898
Watanabe H, Martini AG, Brown EA et al Inhibition of the renin-angiotensin system causes concentric hypertrophy of renal arterioles in mice and humans. JCI Insight. 2021;6(24):e154337 https://insight.jci.org/articles/view/154337 - ↑ 6.0 6.1 Bhandari S, Mehta S, Khwaja A Renin-Angiotensin System Inhibition in Advanced Chronic Kidney Disease. N Engl J Med. 2022. Nov 3. PMID: https://www.ncbi.nlm.nih.gov/pubmed/36326117 https://www.nejm.org/doi/full/10.1056/NEJMoa2210639
- ↑ 7.0 7.1 Jhund PS, Talebi A, Henderson AD et al Mineralocorticoid receptor antagonists in heart failure: an individual patient level meta-analysis. Lancet. 2024 Aug 30:S0140-6736(24)01733-1. PMID: https://www.ncbi.nlm.nih.gov/pubmed/39232490 https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(24)01733-1/fulltext