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Published on: May 31, 2016
Alpha 2-Heremans-Schmid glycoprotein gene polymorphism (rs4918) is associated with coronary artery calcification in
Shuqi Dai1, Yun Chen1, Da Shang1
1Department of Nephrology, Huashan Hospital, Fudan University, Shanghai, China.
Insights
The AHSG gene polymorphism rs4918 is linked to coronary artery calcification (CAC) progression in peritoneal dialysis (PD) patients. This genetic variant influences serum fetuin-A levels, a key calcification inhibitor.
Area of Science:
- Nephrology
- Genetics
- Cardiovascular Disease
Background:
- Coronary artery calcification (CAC) is a severe complication in peritoneal dialysis (PD) patients.
- Fetuin-A, a serum calcification inhibitor, is encoded by the alpha 2-Heremans-Schmid glycoprotein (AHSG) gene.
Purpose of the Study:
- To investigate the association between AHSG gene polymorphism rs4918 and CAC in PD patients.
- To examine the role of rs4918 in the progression of CAC among PD patients.
Main Methods:
- Prospective study of 202 incident PD patients followed for 2 years.
- CAC measurements at baseline and 2-year follow-up.
- Analysis of AHSG gene polymorphism rs4918, serum fetuin-A, and clinical data using binary logistic regression.
Main Results:
- Genotype GG of AHSG rs4918 was an independent risk factor for CAC (OR=2.153) and CAC progression (OR=2.482).
- Serum fetuin-A levels showed a dose-dependent effect influenced by the number of G alleles in rs4918.
Conclusions:
- AHSG gene polymorphism rs4918 impacts serum fetuin-A levels.
- rs4918 is significantly associated with the presence and progression of CAC in PD patients.
Aim:
Coronary artery calcification (CAC) is a common and severe complication in peritoneal dialysis (PD) patients, and it progresses in a majority of patients. Fetuin-A, encoded by the alpha 2-Heremans-Schmid glycoprotein (AHSG) gene, is a serum calcification inhibitor. The study aimed to examine the role of AHSG gene polymorphism rs4918 in CAC and CAC progression of PD patients.
Methods:
Incident PD patients at Huashan Hospital Fudan University in China from August 2007 to July 2018 were recruited in this prospective study and followed up for 2 years. Patients underwent CAC measurements at recruitment and 2 years later. AHSG gene polymorphism rs4918 and serum fetuin-A were determined at baseline. The demographic characteristics, clinical data, and laboratory data were collected during the follow-up period. Binary logistic regression was performed to explore the association between rs4918 with CAC and CAC progression.
Results:
A total of 202 PD patients (112 men, 55.4%) were recruited, with a mean age of 54 ± 16 years. The multivariate logistic regression identified genotype GG as an independent risk factor that correlates to CAC (odds ratio [OR] = 2.153; 95% CI: 1.182-3.925; p = .012) and CAC progression (OR = 2.482; 95% CI: 1.422-4.330; p = .001). The serum fetuin-A level was influenced by the rs4918 variants of AHSG, with a dose-dependent effect depending on the number of the G allele.
Conclusion:
AHSG gene polymorphism rs4918 affects serum fetuin-A levels and is significantly associated with both CAC and CAC progression in a cohort of patients receiving PD.
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