Medico-legal Update, April-June 2020, Vol. 20, No. 2 339 Serum Vitronectin and Related Molecules in Chronic Kidney Disease Ekhlas Abdallah Hassan 1 , Fayhaa M. Khaleel 2 1 Lecturer, 2 Assistant Professor, Chemistry Dept. College of Science for Women, Baghdad University, Baghdad, Iraq Abstract One in eight people are reported to have chronic kidney disease (CKD). The renal function slowly deteriorates when nephrons become impaired by inflammatory and fibrotic processes. In this study, the relationships between vitronectin (VTN), plasminogen activator inhibitor-1 (PAI-1) and growth factor translation β1 (TGF-β1) are studied in CKD to assess the role as predict about progression stages of diseases. 105 patients with early stages (1 to 3) of CKD and 35-69 age matched healthy controls were included in the study. The VTN, PAI-1, TGF-Bate levels of all participants were examined by Enzyme linked immune sorbent assay, creatinine, and urea by enzymatic method . Early morning urine sample was collected to be used for determination albumin creatinine ratio in patient with early stages of CKD. The renal function tests were significantly elevated in CKD group compared with healthy controls. The serum concentration of VTN increase in early stages(1-2) of CKD and decrease significantly with progression of disease (stage 3). Serum PAI-1 antigen level increased significantly. With the development of CKD, the effective role of TFG-β became more severe,the correlation among VTN, TGF-β and PAI-1 was positive. Conclusions: These results indicate that VTN is important indicator for predict of CKD progression and both VTN, PAI-1 are connected to TGF-β’s active form and can be used as a prediction for progression of CKD. Keywords: CKD, Vitronectin, PAI-1, TGF-B. Introduction The role of VTN in the pathogenesis of chronic kidney injury is of particular interest due to its high binding affinity to the potent fibrosis-promoting molecule (PAI-1) (1) . VTN is known to be a cofactor in proteolytic inhibitory activities of PAI-1 [2] . Once PAI-1 is attached to VTN, it stabilizes its effective verification and raises its half-life nearly fourfold. [3] . when serine proteases become active, the VTN/PAI-1 complex effectively inhibits plasmin production and proteolytic responses induced by plasmine. Nevertheless, during kidney damage, plasmin has pleiotropic and even opposite consequences.Recent surveys promote the belief that plasmin is beneficial in acute glomerular disease but in chronic tubulointerstitial disease it induces fibrosis [4] . PAI-1 elevated expression is observed in mesangial cells endothelial cells glomeruli podocyte cells, interstitial narrow arteries,proximal tubular epithelial cells, and fibroblast cells.However, some primary renal fibrosis modulators induced PAI-1. The most prominent molecular characteristic of progression kidney diseases is over-expression of TGF-ß, a 28-kDa dimeric protein composed of two 14-kDa subunits produced by different cell types, including T cells and monocytes [5] . TGF-ß significantly increases the development of PAI-1 by cultivated glomeruli, mesangial cells and tubular cells andit is associated with increased expression of PAI-1 in disease [6] . All main components of the renin-angiotensin-aldosterone system; renin, ang II and aldosterone quickly and significantly enhance the production of PAI-1 via pathways that are independent of and dependent on TGF-ß [7] . Material and Method A total of 105 Patients most of them were early staged included in this study (54 female,65 male),age