The relationship between serum fetuin a levels and fetuin gene polymorphism in hemodialysis patients. Atila Altuntaş 1* , Ayşe Yiğit 2 , Efkan Uz 3 , Salih İnal 1 , Veysel Kidir 1 , BünyaminAydin 4 , Hasan Basri Savaş 3 , Mehmet Sert 5 , Mehmet Tuğrul Sezer 1 1 Department of Internal Medicine, Division of Nephrology, Süleyman Demirel University School of Medicine, Isparta, Turkey 2 Department of Medical Genetics, Süleyman Demirel University School of Medicine, Isparta, Turkey 3 Department of Medical Biochemistry, Süleyman Demirel University School of Medicine, Isparta, Turkey 4 Department of Internal Medicine, Division of Endocrinology and Metabolism, Süleyman Demirel University School of Medicine, Isparta, Turkey 5 Division of Nephrology, Isparta State Hospital, Isparta, Turkey Abstract Introduction: Fetuin A, also called Heramans Schmid alpha 2 glycoprotein (AHSG), is one of the important proteins that inhibit vascular calcification. In this study, we aimed to evaluate relationship between AHSG gene polymorphism and fetuin A levels. Materials and methods: 152 patients receiving regular hemodialysis treatment and 61 healthy controls were included to this cross-sectional study. Serum fetuin-A levels were assessed by ELISA method. Thr256Ser and Thr248Met gene polymorphisms are determined by PCR-RFLP. Results: Serum fetuin A level in hemodialysis patients (330.5 ± 171.2 mg/L) was significantly lower as compared to control group (382.9 ± 138.5 mg/L) (p=0.001). Significant negative correlation between fetuin-A and C-reactive protein (CRP) (r=-0.28, p<0.0001) was found. The distribution of Thr256Ser and Thr248Met gene polymorphisms in hemodialysis and control groups were similar. In hemodialysis group, serum fetiun A levels in the patients with genotype Thr/Thr (n=94, 366.9 ± 184.2 mg/L) were found to be singnificantly higher than in the patients with genotype Thr/Ser (n=52, 278.1 ± 132.7 mg/L) and Ser/Ser (n=6, 212.5 ± 63.3 mg/L) (respectively; p=0.005, p=0.022). Unlike Thr256Ser polymorphism, serum Fetuin-A levels did not differ between Thr248Met gene polymorphism genotypes. Conclusion: The current study showed that HD patients with altered polymorphism of the AHSG Thr256Ser gene appear to be a negative prognostic factor on serum Fetuin-A levels. In other words, it can be speculated that fetuin-A Thr256Ser gene polymorphism, particularly genotypes Thr/Ser and Ser/ Ser, may be an additional promoting risk factor for vascular ossification in HD patients. Keywords: Fetuin A, Genetic Polymorphism, Hemodialysis, Inflammation. Accepted on May 04, 2016 Introduction The mortality rate among dialysis patients is obviously more than that of the general population and cardiovascular diseases are the leading causes of mortality among dialysis patients [1,2]. This very high cardiovascular mortality rate in this population is only partially explained by the high prevalence of traditional risk factors which are classically related to atherosclerosis [3]. The vascular changes observed in chronic kidney disease (CKD) are not only based on atherosclerosis, but also arteriosclerosis is widely seen associated with pathological vascular calcification of both media and intima [4]. Eventually, arterial stiffening and the extent of calcification are reported to be strong prognostic markers of mortality rates in hemodialysis (HD) patients [5]. It is assumed that this may be partially related to a relative lack of calcification inhibitors or vascular protective factors like fetuin-A. Fetuin-A, also known as α2-Heremans-Schmid glycoprotein (AHSG), is a circulating negative acute-phase glycoprotein with 62-kDa molecular weight [6]. It is synthesized in liver and is a member of cystatin superfamily of cysteine proteases. Fetuin-A is involved in several biological processes including the inhibition of ectopic mineral calcification and decreased serum levels are reported during inflammation [7,8]. In vitro ISSN 0970-938X www.biomedres.info Biomed Res- India 2017 Volume 28 Issue 2 495 Biomedical Research 2017; 28 (2): 495-502