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Updated: Jun 7, 2025
Assessment of Vascular Function in Patients With Chronic Kidney Disease
Published on: June 16, 2014
Causal Links Between Renal Function and Cardiac Structure, Function, and Disease Risk
Xiaoqin Zhou1,2,3, Weiqiang Ruan1, Lijun Zhao4,5
1Department of Cardiovascular Surgery, West China Hospital, Sichuan University, Chengdu 610041, P.R. China.
Insights
Genetic susceptibility to impaired kidney function causally influences cardiovascular disease risk and cardiac structure. This study clarifies the links between renal markers like eGFR and CVD endpoints, revealing significant associations.
Area of Science:
- Cardiovascular Medicine
- Nephrology
- Genetics
Background:
- Chronic kidney disease (CKD) is a known risk factor for adverse cardiovascular outcomes.
- The precise causal pathways linking renal function to cardiovascular diseases (CVD) require further elucidation.
- Understanding these relationships is crucial for developing targeted preventative strategies.
Purpose of the Study:
- To investigate the causal relationships between genetic predisposition to impaired renal function and the risk of various cardiovascular disease (CVD) endpoints.
- To examine the impact of genetic factors related to renal function on cardiac structure and function, assessed via cardiac magnetic resonance imaging (CMR).
- To establish causal links using Mendelian randomization (MR) analyses.
Main Methods:
- Bidirectional Mendelian randomization (MR) analyses were performed using genome-wide association study summary data.
- Key exposures included blood urea nitrogen (BUN), estimated glomerular filtration rate (eGFR), urine albumin-to-creatinine ratio (UACR), and CKD.
- Outcomes comprised major cardiovascular events (e.g., atrial fibrillation, coronary artery disease, stroke) and detailed cardiac parameters from CMR.
Main Results:
- Elevated BUN showed a causal link to increased coronary artery disease (CAD) risk, though attenuated by cardiometabolic factors.
- Increased UACR was causally associated with higher risks of CAD, myocardial infarction, and stroke, with stroke association persisting after adjustment.
- Reduced eGFR was causally linked to diminished cardiac dimensions and volumes, including aorta and pulmonary artery diameters and ventricular volumes.
- CKD demonstrated a causal association with reduced pulmonary artery-to-aorta ratio and proximal pulmonary artery diameter.
Conclusions:
- This MR study provides robust evidence for the causal role of genetic susceptibility to impaired renal function in influencing cardiovascular outcomes.
- The findings highlight specific renal function markers (BUN, UACR, eGFR) as causally linked to distinct cardiovascular risks and structural changes.
- These results underscore the importance of considering renal health in the context of cardiovascular disease prevention and management.
Background:
Chronic kidney disease (CKD) increases the risk of adverse cardiovascular outcomes. However, the causal relationships between renal function and cardiovascular diseases (CVD) remain incompletely understood. This study aimed to determine the causal relationships between genetic susceptibility to impaired renal function and the risk of CVD endpoints, as well as cardiac structure and function detectable by cardiac magnetic resonance imaging (CMR).
Methods:
Bidirectional Mendelian randomization (MR) analyses were conducted using summary-level data from genome-wide association studies. The exposures were blood urea nitrogen (BUN), estimated glomerular filtration rate (eGFR), urine albumin-to-creatinine ratio (UACR), and CKD. The outcomes included atrial fibrillation, coronary artery disease (CAD), myocardial infarction, heart failure, stroke, and various CMR parameters. Sensitivity analyses, multivariable MR adjusting for cardiometabolic traits, and replication in the FinnGen cohort were performed.
Results:
Elevated BUN levels (OR 1.505; 95% CI 1.077 to 2.103; P = 0.017) were causally associated with increased CAD risk, but this relationship was attenuated after adjusting for cardiometabolic traits. Increased UACR was causally linked to higher risks of CAD (OR 1.260; 95% CI 1.042 to 1.523; P = 0.017), myocardial infarction (OR 1.424; 95% CI 1.137 to 1.783; P = 0.002), and stroke (OR 1.182; 95% CI 1.012 to 1.379; P = 0.035), with the association for stroke remaining significant after multivariable adjustment. Reduced eGFR was causally related to decreases in ascending aorta diameter, proximal pulmonary artery diameter, right atrial size, left ventricular stroke volume, and right ventricular volumes, even after accounting for potential confounders. CKD was causally associated with a reduced pulmonary artery-to-aorta ratio and proximal pulmonary artery diameter.
Conclusions:
This comprehensive MR study establishes causal roles of genetic susceptibility to impaired renal function influencing cardiovascular outcomes and cardiac structure.
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