European Journal of Molecular & Clinical Medicine

Abstract

Introduction: Neutralization of a key Wnt inhibitor elevated in the circulation in CKD, Dkk1, and inhibited CKD induced vascular dedifferentiation, vascular calcification, and renal osteodystrophy. This effect was surprising since Wnt signalling in the vascular smooth muscle is implicated in stimulating osteoblastic transition and vascular calcification. However, recent studies demonstrate that Dkk1 mediated inhibition of aortic Wnt7b stimulates smad mediated aortic endothelial-mesenchymal transition (EndMT) and vascular calcificatio. EndMT is a developmental physiologic process involved in the development of the cardiac valves, the cardiac septum and the aortic root, and it may or may not contribute to cardiac fibrosis in various adult disease states.
Methodology: This is an observational study with no interventions carried out on any subject. Furthermore, all the CKD individuals were divided in to two groups based on the dialysis. Finally, the statistical analyses were performed between the predialysis, dialysis and control population to find the possible or potential diagnostic marker for CKD-MBD. Results: A total 68 individuals were genotyped for this study which includes 19 control subjects, 25 Non Dialysis patients and 24 Dialysis patients. The distribution of OPG gene polymorphisms among the control, Non dialysis and dialysis group were documented. Of the 19 studied control subjects 17 (85%) TT, 2 (10% TC) and 1 (5%) TC genotypes were observed.
Conclusion: Among the 25 non dialysis patients the observed genotypes are 15 (60%) TT, 6 (24%) and 4 (16%)TC. The Dialysis group 11 TT (45.8%), 8 TC (33.3%) and 5 TC (20.8%) genotypes were observed.