Visfatin and apelin, new adipocytokines, and their relation to endothelial function in patients with chronic renal failure

Purpose: Visfatin and apelin are novel adipocytokines that have recently generated much interest. The aim of the study was to assess visfatin and apelin in correlation with markers of endothelial cell injury and inflammation in 22 patients with chronic kidney disease-CKD and 22 age- and sex-matched healthy volunteers. Methods: We assessed visfatin, apelin, markers of coagulation: TAT (thrombin-antithrombin complexes), prothrombin fragments 1+2; fibrinolysis: tPA (tissue plasminogen activator), PAI-1 (plasminogen activator inhibitor), PAP (plasmin-antiplasmin complexes); endothelial function/injury: vWF (von Willebrand factor), thrombomodulin, ICAM (intracellular adhesion molecule), VCAM (vascular cell adhesion molecule), CD146, CD40L, CD44, E-selectin, inflammation: hsCRP. Results: Triglycerides, hsCRP, creatinine, vWF, prothrombin fragments 1+2, TAT, thrombomodulin, ICAM, VCAM, CD146, CD44, CD40L, PAI-1, PAP, visfatin and E-selectin were elevated in chronic kidney disease patients when compared with the control group. Visfatin correlated significantly in patients with chronic kidney disease, in univariate analysis, with CD40L (r=-0.27, p<0.05), apelin (r=0.27, p<0.05), ICAM (r=0.26, p<0.05), VCAM (r=0.31, p<0.05) and tended to correlate with CD146 (r=0.21, p=0.10). Apelin correlated significantly with E-selectin (r=0.31, p<0.05) and VCAM (r=0.31, p<0.05). In the healthy volunteers visfatin correlated significantly with ICAM (r=-0.37, p<0.05) and serum creatinine (0.38, p<0.05). Conclusions: Elevated visfatin in CKD patients may be due to renal failure and/or inflammation. Adipocytokines related to adhesion molecules might support the importance of inflammation/endothelial cell injury in the pathogenesis of atherosclerosis and its consequences in CKD.