ECTS2014 Poster Presentations Other diseases of bone and mineral metabolism (44 abstracts)
1Division of Endocrinology and Metabolism, Department of Internal Medicine, Medical University of Graz, Graz, Austria; 2Institute of Pathology, Medical University of Graz, Graz, Austria; 3Division of Transplantation Surgery, Department of Surgery, Medical University of Graz, Graz, Austria; 4Joanneum Research Health, Graz, Austria.
Background: Pathophysiological calcification in the vasculature is a risk factor for cardiovascular disease (CVD). CVD are among the most common causes of death in patients with chronic kidney disease and crucial for kidney transplantation (RTX) outcomes.
Aim: The aim of this study is to identify differences in the pattern and the onset of expression of regulators of calcification (RC) in atherosclerosis (AS) and media sclerosis (MS).
Methods
We investigated the expression of RCin the arteria iliaca externa in 26 donors (D) and 25 recipients (R) of RTX.
Gene expression of RC was performed using TaqMan gene expression assays with a LC480 system. Determination of calcification type in donors (AS) was done histologically and in recipients (MS) via computed tomography (CT) by applying a score ranging from 0 to 3 in 0.5 intervals. Classification of stages in donors and recipients: 0 (unaffected vessels), 1 (AS: intima thickening, MS: CT score 0.5), 2 (AS: intima calcification, MS: CT scores 13).
Results: Gene expression of OPG, OPN, RANKL, SMAD6, RunX2 and BSP was significantly higher in donors than in recipients (P=0.004, P=0.001, P=0.004, P=0.026, P=0.027 and P=0.068 respectively).
Gene expression did not significantly differ in vessels of D and R at stage 0. In stage one of AS, OPG expression increased, whereas expression in stage one of MS was unchanged. In progressive calcification (stage 2), expression of OPG, OPN and SMAD6 was significantly higher (P=0.048, P=0.024, P=0.048 respectively) in D (AS) than in R (MS); RANKL and RunX2 (P=0.089, P=0.085 respectively) were only slightly higher. AS and MS were compared separately.
Conclusion: We demonstrate a different gene expression pattern in a clinical model of AS and MS and a different onset of calcification. These data might lead to a more comprehensive insight in the mechanisms of calcification.