| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 6249371 | Transplantation Proceedings | 2011 | 4 Pages |
BackgroundNonrenal solid organ transplantation is now an established method of therapy with significantly improved outcome over the last years; however, an increasingly prevalent complication in this population is chronic kidney disease. Endothelial dysfunction is highly prevalent in both cardiovascular disease and chronic kidney disease. Tumor necrosis factor (TNF)-like weak inducer of apoptosis (TWEAK) is a member of the TNF superfamily of cytokines.Materials and MethodsThe aim of the study was to assess TWEAK concentration in 134 prevalent heart transplant recipients in relation to kidney function. Complete blood count, urea, serum lipids, fasting glucose, creatinine, NT-proBNP were studied. Soluble TWEAK was assayed using commercially available kits from Bender MedSystems (VIenna, Austria). High-sensitivity C-reactive protein was assayed using commercially available kits from American Diagnostica (Greenwich, Conn, USA).ResultsHeart transplant recipients had significantly higher serum creatinine, urea, cholesterol, triglycerides, fasting glucose, white blood cell count, lower TWEAK levels and lower estimated glomerular filtration rate (eGFR) than the control group. Serum TWEAK levels fell together with New York Heart Association (NYHA) class and rise in GFR. Serum TWEAK was related to kidney function, NYHA class, NT-proBNP, and triglycerides. Kidney function and NYHA class turn out to be predictors of TWEAK in heart transplant recipients.ConclusionTWEAK level is dependent on kidney and heart function. It might also represent a surrogate marker of endothelial dysfunction and atherosclerosis.
