Soluble tumor necrosis factor-like weak inducer of apoptosis plasma levels as a novel biomarker of endothelial function in prevalent orthotopic heart transplant recipients.

[1]  J. Carrero,et al.  Soluble TWEAK and PTX3 in nondialysis CKD patients: impact on endothelial dysfunction and cardiovascular outcomes. , 2011, Clinical journal of the American Society of Nephrology : CJASN.

[2]  J. Małyszko,et al.  Prevalence of chronic kidney disease in orthotopic heart transplant recipients and kidney allograft recipients using the new Chronic Kidney Disease Epidemiology Collaboration formula. , 2010, Transplantation proceedings.

[3]  J. Małyszko Mechanism of endothelial dysfunction in chronic kidney disease. , 2010, Clinica chimica acta; international journal of clinical chemistry.

[4]  H. Katus,et al.  Soluble TWEAK is markedly upregulated in patients with ST-elevation myocardial infarction and related to an adverse short-term outcome. , 2010, Atherosclerosis.

[5]  J. Carrero,et al.  Combined therapy with renin-angiotensin system and calcium channel blockers in type 2 diabetic hypertensive patients with proteinuria: effects on soluble TWEAK, PTX3, and flow-mediated dilation. , 2010, Clinical journal of the American Society of Nephrology : CJASN.

[6]  J. Carrero,et al.  Soluble TWEAK plasma levels as a novel biomarker of endothelial function in patients with chronic kidney disease. , 2009, Clinical journal of the American Society of Nephrology : CJASN.

[7]  H. Katus,et al.  Decreased soluble TWEAK levels predict an adverse prognosis in patients with chronic stable heart failure , 2009, European journal of heart failure.

[8]  N. Banner,et al.  Chronic kidney disease after heart transplantation. , 2009, Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association.

[9]  Mohit M. Jain,et al.  A Novel Role for Tumor Necrosis Factor–Like Weak Inducer of Apoptosis (TWEAK) in the Development of Cardiac Dysfunction and Failure , 2009, Circulation.

[10]  M. Fasshauer,et al.  Serum levels of the atherosclerosis biomarker sTWEAK are decreased in type 2 diabetes and end-stage renal disease. , 2008, Atherosclerosis.

[11]  J. Winkles The TWEAK–Fn14 cytokine–receptor axis: discovery, biology and therapeutic targeting , 2008, Nature Reviews Drug Discovery.

[12]  P. Reese,et al.  Chronic kidney disease after nonrenal solid-organ transplantation. , 2007, Journal of the American Society of Nephrology : JASN.

[13]  M. Girgenrath,et al.  TWEAK, via its receptor Fn14, is a novel regulator of mesenchymal progenitor cells and skeletal muscle regeneration , 2006, The EMBO journal.

[14]  J. Kirklin,et al.  Increasing referral for renal transplant evaluation in recipients of nonrenal solid-organ transplants: a single-center experience. , 2006, Clinical journal of the American Society of Nephrology : CJASN.

[15]  R. Henning,et al.  Endothelial dysfunction in chronic kidney disease: determinant of susceptibility to end-organ damage and therapeutic response. , 2006, Journal of nephrology.

[16]  C. Putterman,et al.  Proinflammatory Effects of Tweak/Fn14 Interactions in Glomerular Mesangial Cells1 , 2006, The Journal of Immunology.

[17]  K. Borch-Johnsen,et al.  Preventive cardiology: abstractVery low levels of microalbuminuria are associated with increased risk of coronary heart disease and death independently of renal function, hypertension, and diabetes☆ , 2004 .

[18]  R. Wolfe,et al.  Chronic renal failure after transplantation of a nonrenal organ. , 2003, The New England journal of medicine.

[19]  C. Jurkovitz,et al.  Anemia and renal insufficiency are independent risk factors for death among patients with congestive heart failure admitted to community hospitals: a population-based study. , 2002, Journal of the American Society of Nephrology : JASN.

[20]  Ethan M Balk,et al.  K/DOQI clinical practice guidelines for chronic kidney disease: evaluation, classification, and stratification. , 2002, American journal of kidney diseases : the official journal of the National Kidney Foundation.

[21]  Y. Hsu,et al.  TWEAK, a New Secreted Ligand in the Tumor Necrosis Factor Family That Weakly Induces Apoptosis* , 1997, The Journal of Biological Chemistry.

[22]  A. Haeberli,et al.  Anticoagulant Properties of the Vascular Endothelium , 1997, Thrombosis and Haemostasis.

[23]  A. Levey,et al.  Creatinine filtration, secretion and excretion during progressive renal disease. Modification of Diet in Renal Disease (MDRD) Study Group. , 1989, Kidney international. Supplement.

[24]  J. Carrero,et al.  Additive effects of soluble TWEAK and inflammation on mortality in hemodialysis patients. , 2009, Clinical journal of the American Society of Nephrology : CJASN.

[25]  B. Miller Chronic kidney disease in solid-organ transplantation. , 2006, Advances in chronic kidney disease.

[26]  Kdoqi Disclaimer K/DOQI clinical practice guidelines for chronic kidney disease: evaluation, classification, and stratification. , 2002, American journal of kidney diseases : the official journal of the National Kidney Foundation.