The CTGF gene ？945？G/C polymorphism is not associated with cardiac or kidney complications in subjects with type 2 diabetes

The CTGF ？945？G/C polymorphism (rs6918698) was examined in 495 Caucasian subjects with type 2 diabetes. Cardiac structure and function were assessed by transthoracic echocardiography. Kidney function was assessed using estimated glomerular filtration rate (eGFR) and albuminuria, and CKD defined as the presence of kidney damage (decreased kidney function (eGFR <60？ml/min/1.73？m2) or albuminuria).The mean age？±？SD of the cohort was 62？±？14？years, with a body mass index (BMI) of 31？±？6？kg/m2 and median diabetes duration of 11？years [25th, 75th interquartile range; 5, 18]. An abnormal echocardiogram was present in 73% of subjects; of these, 8% had LVH alone, 74% had diastolic dysfunction and 18% had systolic？±？diastolic dysfunction. CKD was present in 42% of subjects. There were no significant associations between the CTGF ？945？G/C polymorphism and echocardiographic parameters of LV mass or cardiac function, or kidney function both before and after adjustment for covariates of age, gender, BMI, blood pressure and hypertension. CTGF ？945 genotypes were not associated with the cardiac complications of LVH, diastolic or systolic dysfunction, nor with CKD.In Caucasians with type 2 diabetes, genetic variation in the CTGF ？945？G/C polymorphism is not associated with cardiac or kidney complications.Connective tissue growth factor (CTGF) also known as CCN-2, is a cysteine rich secreted protein that mediates tissue fibrosis in multiple organs including the heart and kidney [1-3]. In the heart, CTGF is expressed in myocytes and fibroblasts [4] and can induce hypertrophy [5], and extracellular matrix production [6]. In man, CTGF gene expression is increased in ischaemic cardiac tissue [4], and both CTGF gene and protein expression are up-regulated in experimental models of cardiac injury and diabetes, and associated with ongoing cardiac fibrosis [5,7-10]. Cardiac fibrosis increases the mechanical stiffness of the heart, which impairs myocardial contractility and contributes to lef