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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...
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Related Experiment Video

Updated: Jun 28, 2025

A Modified Two Kidney One Clip Mouse Model of Renin Regulation in Renal Artery Stenosis
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Aortic Stenosis and Renal Function: A Bidirectional Mendelian Randomization Analysis.

Jonathan L Ciofani1,2,3, Daniel Han4,5,6, Usaid K Allahwala1,2

  • 1Faculty of Medicine and Health The University of Sydney Sydney NSW Australia.

Journal of the American Heart Association
|April 19, 2024
PubMed
Summary
This summary is machine-generated.

This study found no evidence that kidney function affects aortic stenosis risk. Further research is needed to understand the relationship between chronic kidney disease and aortic stenosis.

Keywords:
Mendelian randomizationaortic stenosisgeneticsrenal functionvalve disease

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Area of Science:

  • Cardiovascular Genetics
  • Nephrology
  • Epidemiology

Background:

  • Observational studies suggest an inverse association between renal function and aortic stenosis (AS) risk.
  • The causal nature of this relationship remains uncertain.
  • This study employed a bidirectional Mendelian randomization approach to investigate causality.

Purpose of the Study:

  • To determine if chronic kidney disease (CKD) causally influences the risk of developing aortic stenosis (AS).
  • To investigate if AS causally influences the risk of developing CKD.
  • To explore the genetic relationship between kidney function and AS.

Main Methods:

  • Utilized a bidirectional 2-sample Mendelian randomization design.
  • Analyzed genome-wide association study summary statistics from large cohorts (up to 1,004,040 participants).
  • Employed inverse-variance weighted analysis and multiple sensitivity analyses (weighted-median, MR-Egger).

Main Results:

  • No evidence of a causal effect of genetically predicted CKD liability on AS risk (OR, 0.94; P=0.26).
  • No robust evidence of a causal effect of genetically predicted AS liability on CKD risk (OR, 1.04; P=0.30).
  • Sensitivity analyses and analyses using various kidney function markers (eGFRcrea, eGFRcys, BUN) yielded neutral results.

Conclusions:

  • Genetically predicted renal impairment does not appear to substantially impact the risk of AS.
  • These findings suggest that the observed association may not be causal.
  • Implications for identifying prevention and treatment targets for both CKD and AS require re-evaluation.