<p>The <i>Aldehyde dehydrogenase 2</i> (<i>ALDH2</i>) rs671 polymorphism, a common variant that impairs aldehyde detoxification, has been linked to cardiovascular disease, but its role in chronic kidney disease (CKD) remains unclear. This study examined the association between the <i>ALDH2</i> rs671 polymorphism and incident CKD in a population-based cohort, and whether alcohol consumption modifies this relationship. We analyzed 5,369 Korean adults aged 40–69 years without CKD at baseline from the community-based Korean Genome and Epidemiology Stud<b>y</b>, followed biennially for up to 18 years. The main exposures were <i>ALDH2</i> genotype (GG vs. GA/AA) and categorized alcohol consumption (none, low, moderate, high). Incident CKD was defined as an estimated glomerular filtration rate (eGFR) &lt; 60 mL/min/1.73&#xa0;m² or new-onset proteinuria (≥ 1 + on dipstick). Cox proportional hazards models estimated adjusted hazard ratios (HRs). During a mean 11.7-year follow-up, 1,396 participants (26.0%) developed CKD. CKD risk did not differ significantly between genotypes, and alcohol intake was not associated with CKD incidence. These associations were consistent across genotype or sex. Overall, <i>ALDH2</i> rs671 and alcohol intake showed limited relevance to CKD onset, suggesting that <i>ALDH2</i>-related biological effects may be more pertinent to disease progression rather than initiation in the general population.</p>

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Association of ALDH2 rs671 Polymorphism with chronic kidney disease incidence in a population-based Korean cohort

  • Hyun Jin Lee,
  • Jaekyung Noh,
  • Seunghwan Jeong,
  • Heeyeon Lee,
  • Haekyung Lee,
  • Hyoungnae Kim,
  • Jin Seok Jeon,
  • Hyunjin Noh,
  • Soon Hyo Kwon

摘要

The Aldehyde dehydrogenase 2 (ALDH2) rs671 polymorphism, a common variant that impairs aldehyde detoxification, has been linked to cardiovascular disease, but its role in chronic kidney disease (CKD) remains unclear. This study examined the association between the ALDH2 rs671 polymorphism and incident CKD in a population-based cohort, and whether alcohol consumption modifies this relationship. We analyzed 5,369 Korean adults aged 40–69 years without CKD at baseline from the community-based Korean Genome and Epidemiology Study, followed biennially for up to 18 years. The main exposures were ALDH2 genotype (GG vs. GA/AA) and categorized alcohol consumption (none, low, moderate, high). Incident CKD was defined as an estimated glomerular filtration rate (eGFR) < 60 mL/min/1.73 m² or new-onset proteinuria (≥ 1 + on dipstick). Cox proportional hazards models estimated adjusted hazard ratios (HRs). During a mean 11.7-year follow-up, 1,396 participants (26.0%) developed CKD. CKD risk did not differ significantly between genotypes, and alcohol intake was not associated with CKD incidence. These associations were consistent across genotype or sex. Overall, ALDH2 rs671 and alcohol intake showed limited relevance to CKD onset, suggesting that ALDH2-related biological effects may be more pertinent to disease progression rather than initiation in the general population.