Related Experiment Video

Updated: May 29, 2026

5/6 Nephrectomy Using Sharp Bipolectomy Via Midline Laparotomy in Rats
05:34

5/6 Nephrectomy Using Sharp Bipolectomy Via Midline Laparotomy in Rats

Published on: April 4, 2025

Effects of beta-adrenergic antagonists in patients with chronic kidney disease: a systematic review and meta-analysis

Sunil V Badve1, Matthew A Roberts, Carmel M Hawley

  • 1Australasian Kidney Trials Network, School of Medicine, The University of Queensland, Brisbane, Queensland, Australia. Sunil_Badve@health.qld.gov.au

Journal of the American College of Cardiology
|September 3, 2011
PubMed

Insights

Beta-blockers reduce mortality in chronic kidney disease (CKD) patients with heart failure, but increase risks of bradycardia and hypotension. Evidence is insufficient for CKD patients without heart failure.

Area of Science:

  • Nephrology
  • Cardiology
  • Clinical Pharmacology

Background:

  • Cardiovascular disease and mortality are elevated in patients with chronic kidney disease (CKD).
  • The role of beta-adrenergic antagonists (beta-blockers) in managing CKD patients, particularly those with heart failure, remains under investigation.
  • Uncertainty exists regarding the net benefit and risk profile of beta-blockers in this vulnerable population.

Purpose of the Study:

  • To systematically review the benefits and risks of beta-blocker therapy in patients diagnosed with chronic kidney disease (CKD).
  • To evaluate the impact of beta-blockers on mortality outcomes in CKD stages 3-5.
  • To assess adverse events associated with beta-blocker use in CKD patients.

Main Methods:

  • Systematic review of randomized controlled trials (RCTs) sourced from CENTRAL, Medline, and Embase databases.
  • Included trials required a minimum follow-up of 3 months and reported mortality outcomes in CKD stages 3-5.
  • Meta-analysis using a random effects model was employed for eligible studies.

Main Results:

  • Six placebo-controlled trials (5,972 participants) in CKD patients with systolic heart failure showed beta-blockers significantly reduced all-cause mortality (RR: 0.72, 95% CI: 0.64-0.80) and cardiovascular mortality (RR: 0.66, 95% CI: 0.49-0.89).
  • However, beta-blocker treatment in this group also increased the risk of bradycardia (RR: 4.92, 95% CI: 3.20-7.55) and hypotension (RR: 5.08, 95% CI: 3.48-7.41).
  • Two trials (977 participants) comparing beta-blockers to ACE inhibitors in CKD patients without known heart failure could not be meta-analyzed due to clinical heterogeneity and insufficient data.

Conclusions:

  • Beta-blocker therapy demonstrates a mortality benefit for patients with chronic kidney disease and chronic systolic heart failure.
  • The increased risks of bradycardia and hypotension necessitate careful monitoring in CKD patients with heart failure receiving beta-blockers.
  • Insufficient evidence currently supports or refutes the use of beta-blockers for mortality benefit in CKD patients without diagnosed heart failure.
Abstract

Related Concept Videos

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System01:26

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System

The activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS) contributes to cardiac remodeling, and inhibiting the RAAS is a pharmacological target in heart failure management. As a result, neurohumoral modulation is a crucial treatment principle for managing heart failure. This approach involves using medications like ACE inhibitors (ACEIs), angiotensin receptor blockers (ARBs), β-blockers, mineralocorticoid receptor antagonists (MRAs), and neutral...
Antihypertensive Drugs: Action of β1 Blockers01:17

Antihypertensive Drugs: Action of β1 Blockers

β1-receptors are primarily located in the heart and kidneys. In cardiac myocytes, these receptors interact with neurotransmitters released by the sympathetic nervous system during heightened activity or danger. As a result, β1-receptors get activated, initiating a series of biochemical processes. Excessive activation of beta receptors due to chronic stress can abnormally increase heart rate and contractility, resulting in high blood pressure or hypertension. To counteract this, β1-blockers...
Chronic Kidney Disease III: Interprofessional Care01:28

Chronic Kidney Disease III: Interprofessional Care

Chronic kidney disease (CKD) requires collaborative and comprehensive management. CKD progresses through stages and can lead to end-stage kidney disease (ESKD) if untreated. Interprofessional collaboration and patient education are crucial, enabling patients to manage their health and improve their quality of life.Diagnostic approach for chronic kidney diseaseThe diagnosis of CKD primarily focuses on the glomerular filtration rate (GFR), which assesses kidney function by measuring how well...
Antihypertensive Drugs: Direct Renin Inhibitors01:25

Antihypertensive Drugs: Direct Renin Inhibitors

The renin-angiotensin-aldosterone system (RAAS) is an intricate physiological pathway involving numerous enzymes and hormones, including renin, angiotensin-converting enzyme (ACE), angiotensin I and II, and aldosterone. Imbalances within this system increase the production of angiotensin II and aldosterone. Increased angiotensin II levels promote vasoconstriction and blood pressure elevation. Concurrently, higher aldosterone levels stimulate sodium and water reabsorption in the kidneys,...
Heart Failure Drugs: β-Blockers01:22

Heart Failure Drugs: β-Blockers

β-adrenergic antagonists, commonly known as β-blockers, block the effects of sympathetic neurotransmitters such as noradrenaline (NA) and adrenaline (ADR). They have several beneficial effects in heart failure treatment. They reduce heart rate, the force of contraction, and cardiac muscle relaxation. They also slow the atrial-ventricular conduction rate and raise the threshold for arrhythmias. The concentration of β-blockers determines their effects on bronchodilation, vasodilation, and...
Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors01:30

Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors

Angiotensin-converting enzyme (ACE), a vital component of the renin-angiotensin-aldosterone system, is abundant in lung endothelial cells. ACE converts the inactive decapeptide, angiotensin I, into the active octapeptide, angiotensin II. This potent vasoconstrictor narrows blood vessels, increasing resistance to blood flow and elevating blood pressure. Angiotensin II also stimulates aldosterone production, encouraging kidney cells to reabsorb more sodium and water from urine, thereby increasing...