title: Normalization of endothelial dysfunction  following renal transplantation is  accompanied by a reduction of circulating  visfatin/NAMPT. A novel marker of  endothelial damage?
abstract: Endothelial dysfunction is strongly linked to cardiovascular disease and outcome of patients with chronic kidney disease. We hypothesized that decreased inflammatory activity and increased adiponectin following transplantation could be one mechanism for a better endothelial health. Fifty-eight living donor kidney transplant non-diabetic recipients, 31 (23 male, 29 +/- 5 yr) on cyclosporine A and 27 (10 male, 26 +/- 5 yr) on tacrolimus immunsupression, were studied longitudinally. Visfatin, adiponectin, high sensitive C-reactive protein (hsCRP) levels, brachial artery flow mediated dilatation (FMD) and nitroglycerine mediated dilatation were measured before transplantation and on the 30th and 90th day after transplantation. Pre-transplantation visfatin, adiponectin and FMD values of patients were significantly higher than those of the controls (p < 0.001 for all). All values decreased significantly 30 and 90 d post-transplantation. Plasma visfatin and adiponectin, correlated negatively with FMD levels 90 d both before and after kidney transplantation (p < 0.001 for both). Endothelial function improved during the first month after transplantation, and the degree of improvement correlated to reductions in circulating visfatin, adiponectin and hsCRP levels. Of interest, the intracellular enzyme visfatin was the strongest predictor of FMD both before and after kidney transplantation and may thus reflect endothelial cell damage directly.
authors.affiliation: Nephrology, Departments of Gülhane School of Medicine, Etlik-Ankara, Turkey. mahmutiyilmaz@yahoo.com
authors.forename: Mahmut Ilker
authors.initials: MI
authors.lastname: Yilmaz
authors.forename: Mutlu
authors.initials: M
authors.lastname: Saglam
authors.forename: Juan Jesus
authors.initials: JJ
authors.lastname: Carrero
authors.forename: Abdul R
authors.initials: AR
authors.lastname: Qureshi
authors.forename: Kayser
authors.initials: K
authors.lastname: Caglar
authors.forename: Tayfun
authors.initials: T
authors.lastname: Eyileten
authors.forename: Alper
authors.initials: A
authors.lastname: Sonmez
authors.forename: Yusuf
authors.initials: Y
authors.lastname: Oguz
authors.forename: Ismail
authors.initials: I
authors.lastname: Aslan
authors.forename: Abdulgaffar
authors.initials: A
authors.lastname: Vural
authors.forename: Mujdat
authors.initials: M
authors.lastname: Yenicesu
authors.forename: Peter
authors.initials: P
authors.lastname: Stenvinkel
authors.forename: Bengt
authors.initials: B
authors.lastname: Lindholm
authors.forename: Jonas
authors.initials: J
authors.lastname: Axelsson
mesh_terms: D052242:Adiponectin / Q000097:blood; D000328:Adult; D015415:Biomarkers / Q000097:blood*; D001783:Blood Flow Velocity; D001916:Brachial Artery / Q000473:pathology*; D002097:C-Reactive Protein / Q000378:metabolism; D004730:Endothelium, Vascular / Q000503:physiopathology*; D005260:Female; D005919:Glomerular Filtration Rate; D006801:Humans; D007166:Immunosuppressive Agents / Q000627:therapeutic use; D007674:Kidney Diseases / Q000097:blood* / Q000628:therapy; D016030:Kidney Transplantation; D008137:Longitudinal Studies; D008297:Male; D054409:Nicotinamide Phosphoribosyltransferase / Q000097:blood*; D014664:Vasodilation
chemical_list: D052242:Adiponectin; D015415:Biomarkers; D007166:Immunosuppressive Agents; D002097:C-Reactive Protein; D054409:Nicotinamide Phosphoribosyltransferase