Key result
ACE I/D polymorphism had a significant direct positive effect on plasma ACE levels (path coefficient = 0.302, p=0.021), which indirectly increased ASCVD and cardiovascular mortality risk.
Why the study?
The association between ACE I/D polymorphisms and plasma ACE levels may allow optimization of preventive interventions to reduce cardiovascular morbidity and mortality in the CKD population, leading researchers to examine its association with cardiovascular mortality risk in non-hemodialyzed CKD patients.
Does ACE I/D polymorphism affect cardiovascular mortality risk in non-hemodialyzed CKD patients?
Cross-Sectional (n=70)
Does ACE I/D polymorphism affect cardiovascular mortality risk in non-hemodialyzed CKD patients?
Effect estimate: path coefficient 0.302
p-value: p=0.021
In Javanese patients with non-hemodialyzed CKD, the ACE I/D polymorphism indirectly increases the risk of ASCVD and cardiovascular mortality by elevating plasma ACE levels.
The association between angiotensin-converting enzyme insertion/deletion (ACE I/D) polymorphisms and plasma ACE levels may allow for the optimization of a preventive intervention to reduce cardiovascular morbidity and mortality in the chronic kidney disease (CKD) population. In this study, we aimed to analyze the association between ACE I/D polymorphism and cardiovascular mortality risk among non-hemodialyzed chronic kidney disease patients. This cross-sectional study examined 70 patients of Javanese ethnic origin with stable CKD who did not receive hemodialysis. ACE I/D polymorphisms, plasma ACE levels, atherosclerotic cardiovascular disease (ASCVD) risk, and cardiovascular mortality risk were investigated. As per our findings, the I allele was found to be more frequent (78.6) than the D allele (21.4), and the DD genotype was less frequent than the II genotype (4.3 vs. 61.4). The ACE I/D polymorphism had a significant direct positive effect on plasma ACE levels (path coefficient = 0.302, p = 0.021). Similarly, plasma ACE levels had a direct and significant positive effect on the risk of atherosclerotic cardiovascular disease (path coefficient = 0.410, p = 0.000). Moreover, atherosclerotic cardiovascular disease risk had a significant positive effect on cardiovascular mortality risk (path coefficient = 0.918, p = 0.000). The ACE I/D polymorphism had no direct effect on ASCVD and cardiovascular mortality risk. However, our findings show that the indirect effects of high plasma ACE levels may be a factor in the increased risk of ASCVD and cardiovascular mortality in Javanese CKD patients.
No takes yet. Share an insight, caveat, or question.
Susilo et al. (2022) conducted a cross-sectional in Non-hemodialyzed chronic kidney disease (n=70). ACE I/D polymorphism was evaluated on Plasma ACE levels (path coefficient 0.302, p=0.021). ACE I/D polymorphism had a significant direct positive effect on plasma ACE levels (path coefficient = 0.302, p=0.021), which indirectly increased ASCVD and cardiovascular mortality risk.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: