MO962: C-Peptide and Epicardial Adipose Tissue in Chronic Kidney Disease

Abstract

Abstract BACKGROUND AND AIMS Recent studies suggest that C-peptide (CP) may exhibit characteristics of a hormone and show physiological functions in various tissues. Moreover, it has been proposed that CP could be involved in the regulation of lipolysis, adiponectin release and function of mesenchymal stem cells in adipose tissue. However, there is a certain controversy regarding reported effects of the CP. Its beneficial effects have been demonstrated in long-term complication in type 1 diabetes mellitus (T1DM). Substitution of CP in T1DM improves glomerular hyperfiltration, hypertrophy and proteinuria. In contrast to this, CP in T2DM shows proinflammatory and proatherogenic effects. The aim of this study was to find the association between CP, epicardial adipose tissue (EAT) and vascular calcifications in diabetic subjects under insulin treatment on dialysis. METHOD This is a retrospective study of 62 consecutive chronic kidney disease (CKD) stages 5D patients awaiting kidney transplantation referred for risk stratification. Computer tomography (CT) was used to assess quantify coronary artery calcium (CAC) and to measure EAT volume. CAC was considered present if a minimum of three contiguous pixels with an attenuation of ≥130 Hounsfield Units (HU) were detected along the course of a coronary artery. CAC scores were calculated using the method described by Agatston. EAT was identified as a hypodense area surrounding the myocardium and limited by pericardium. The pericardium was traced manually from the mid-left atrium to the left ventricular apex interpolating slices of 10 mm thickness; the application of an attenuation threshold in the range of -250 to -30 HU effectively excluded myocardium, coronary arteries, coronary calcium, aorta and blood pool, leaving in evidence the EAT alone. Demographic and anthropometrics data were collected on all patients through record review. RESULTS Demographic, clinical and laboratorial characteristics of patients enrolled in the study are resume in the Table 1. Young women and smoking were more prevalent; none of the analytical parameters were correlated with CP. Subjects with higher BMI exhibited higher levels of CP (P 0.03). EAT was strongly correlated with higher levels of CP (P 0.03). EAT was significantly correlated with severity of CAC scores (P 0.01). No correlation was found between CP and CAC. CONCLUSION As a marker of insulin reserve, CP can be used to evaluate insulin needs and overdose in dialysis patients and to avoid its lipogenic effects. New and novel hypoglycemic therapies may help in this issue. While EAT was correlated to CP, this was not associated with vascular calcification (CAC); this final observation may be related to the lower levels of vascular damage observed in CKD patients from kidney transplantation waiting list. More studies are needed to explore this association and utility.