The epicardial fat layer originates from mesothelial cells and hence obtains its vascular supply from the coronary arteries. Much of the importance within the epicardial fat is its anatomical closeness to the myocardium and the fact that the two tissues share the same microcirculation. Epicardial fat is a metabolically active organ that secrets numerous bioactive substances, which may alter cardiac function. This small, visceral fat depot had been accepted as a rich source of free fatty acids and a number of bioactive molecules, such as adiponectin, resistin and inflammatory cytokines, which could lead to the coronary endothelial dysfunction. Furthermore, epicardial adipose mass might reflect intra-abdominal visceral fat. Epicardial adipose tissue is also clinically related to left ventricular mass and other features of the metabolic syndrome, such as concentrations of LDL cholesterol, fasting insulin and adiponectin, and arterial blood pressure. Epicardial fat thickness can be visualized and measured with two-dimensional (2D) echocardiography. Standard parasternal long-axis and short-axis views from 2D images permit the most accurate measurement of epicardial fat thickness on the right ventricle, with optimal cursor beam orientation in each view. Echocardiographically, epicardial fat is generally identified as the relatively echo-free space between the outer wall of the myocardium and the visceral layer of pericardium; its thickness is measured perpendicularly on the free wall of the right ventricle at end-systole in 3 cardiac cycles. Because it is compressed during diastole, epicardial fat thickness is best measured at end-systole at the point on the free wall of the right ventricle at which the ultrasound beam is oriented in a perpendicular manner, using the aortic annulus as an anatomic landmark. Epicardial fat thickness can be also appear as hyperechoic space, if in large amount (\>15 mm). Maximum epicardial fat thickness is measured from 2D parasternal long axis images at the point on the free wall of the right ventricle along the midline of the ultrasound beam, perpendicular to the aortic annulus, used as an anatomic landmark for this view. For midventricular parasternal short-axis assessment, maximum epicardial fat thickness is measured from 2D images on the right ventricular free wall along the midline of the ultrasound beam perpendicular to the interventricular septum at midchordal and tip of the papillary muscle level, as anatomic landmarks. The average value of 3 cardiac cycles from each echocardiographic view is determined. The majority of population based clinical studies have reported excellent interobserver and intraobserver agreement for epicardial fat thickness measurement. Echocardiographic epicardial fat measurement may have some advantages as an index of high cardiometabolic risk. It is a direct measure of visceral fat rather than an anthropometric measure, such as waist circumference, that includes muscle and skin layers. The echocardiographic measurement of epicardial fat provides a more sensitive and specific measure of true visceral fat content, avoiding the possible confounding effect of increased subcutaneous abdominal fat. It is an objective, noninvasive, readily available, and certainly less expensive measure of visceral fat than MRI or CT. Visceral cardiac fat can be quantified fairly precisely compared with ectopic fat deposition in organs such as the liver, which can be described only qualitatively unless expensive measurements are made, such as CT or MRI. Echocardiographic epicardial fat is a direct measure of ectopic fat deposition, whereas anthropometric measures can be associated only with ectopic fat deposition. It can be measured even from echocardiograms that were not specifically performed to optimize the measurement of epicardial fat. It can be quantified with other echocardiographic parameters, such left ventricular mass and ejection fraction, traditionally associated with cardiovascular risk. Echocardiographic epicardial fat could be a more reliable quantitative therapeutic marker during interventions modulating and reducing visceral adiposity. Diabetic nephropathy or diabetic kidney disease is a syndrome characterized by the presence of pathological quantities of urine albumin excretion, diabetic glomerular lesions, and loss of glomerular filtration rate (GFR) in diabetics. Incipient nephropathy is the initial presence of low but abnormal amounts of urine albumin, referred to as microalbuminuria (persistent albuminuria at level 30-299 mg/24 hours), while overt nephropathy or macroalbuminuria (persistent albuminuria at level 300 mg/24 hours).