PMID- 21693297
OWN - NLM
STAT- MEDLINE
DCOM- 20111014
LR  - 20171116
IS  - 1873-2623 (Electronic)
IS  - 0041-1345 (Linking)
VI  - 43
IP  - 5
DP  - 2011 Jun
TI  - Soluble tumor necrosis factor-like weak inducer of apoptosis plasma levels as a 
      novel biomarker of endothelial function in prevalent orthotopic heart transplant 
      recipients.
PG  - 1900-3
LID - 10.1016/j.transproceed.2011.03.040 [doi]
AB  - BACKGROUND: Nonrenal 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 
      METHODS: The 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). 
      RESULTS: Heart 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. CONCLUSION: TWEAK level is 
      dependent on kidney and heart function. It might also represent a surrogate 
      marker of endothelial dysfunction and atherosclerosis.
CI  - Copyright (c) 2011 Elsevier Inc. All rights reserved.
FAU - Przybylowski, P
AU  - Przybylowski P
AD  - Department of Cardiovascular Surgery and Transplantology, Collegium Medicum, 
      Jagiellonian University, John Paul II Hospital Cracow, Poland. piotrus@aol.com
FAU - Malyszko, J S
AU  - Malyszko JS
FAU - Malyszko, J
AU  - Malyszko J
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Transplant Proc
JT  - Transplantation proceedings
JID - 0243532
RN  - 0 (Biomarkers)
RN  - 0 (Cytokine TWEAK)
RN  - 0 (TNFSF12 protein, human)
RN  - 0 (Tumor Necrosis Factors)
SB  - IM
MH  - Adult
MH  - *Apoptosis
MH  - Biomarkers/*blood
MH  - Cytokine TWEAK
MH  - Endothelium, Vascular/*pathology
MH  - *Heart Transplantation
MH  - Humans
MH  - Middle Aged
MH  - Tumor Necrosis Factors/*blood
EDAT- 2011/06/23 06:00
MHDA- 2011/10/15 06:00
CRDT- 2011/06/23 06:00
PHST- 2011/02/28 00:00 [received]
PHST- 2011/03/09 00:00 [accepted]
PHST- 2011/06/23 06:00 [entrez]
PHST- 2011/06/23 06:00 [pubmed]
PHST- 2011/10/15 06:00 [medline]
AID - S0041-1345(11)00474-X [pii]
AID - 10.1016/j.transproceed.2011.03.040 [doi]
PST - ppublish
SO  - Transplant Proc. 2011 Jun;43(5):1900-3. doi: 10.1016/j.transproceed.2011.03.040.