Serum Troponin T Concentration as a Predictor of Mortality in Hemodialysis and Peritoneal Dialysis Patients Bas Havekes, MD, Jeannette G. van Manen, PhD, Raymond T. Krediet, MD, PhD, Elisabeth W. Boeschoten, MD, PhD, Jan P. Vandenbroucke, MD, PhD, and Friedo W. Dekker, PhD, for the NECOSAD Study Group ● Background: Troponin T is a good predictor of all-cause and cardiovascular mortality in cardiac patients. Although it is known that troponin T is an independent risk factor in dialysis patients as well, its prognostic value when measured routinely in clinical practice, particularly in addition to other risk indicators, is unclear. Methods: A cohort of 847 patients who started dialysis therapy between 1997 and 2001 and participated in a multicenter follow-up study was examined. Clinical data were determined 3 months after the start of dialysis therapy. Patients were followed up until date of death or censoring in November 2003. Results: For patients with troponin T values of 0.05 to 0.10 g/L, hazard ratio for all-cause mortality was 2.2 (95% confidence interval [CI], 1.7 to 2.8) compared with patients with values less than 0.05 g/L. For patients with values greater than 0.10 g/L (11%), hazard ratio was 3.3 (95% CI, 2.5 to 4.5). A survival model with clinical and laboratory risk indicators yielded an area under the curve of 0.81, which did not increase when troponin T level was added to the model. The area under the curve for troponin T level alone was 0.67. No important differences were found between patients on hemodialysis or peritoneal dialysis therapy and between patients with high and low residual renal function. Conclusion: Although troponin T level is an independent risk factor for mortality in dialysis patients, it has limited added predictive power as a routine screening test over other clinical risk factors in dialysis patients. Am J Kidney Dis 47:823-829. © 2006 by the National Kidney Foundation, Inc. INDEX WORDS: Mortality; kidney (disease); prognosis (troponin). C ARDIAC TROPONINS, especially tropo- nin T, have emerged as useful clinical parameters in establishing a diagnosis and prog- nosis in patients with suspected acute coronary syndromes. 1 Troponin T also might be an impor- tant prognostic factor for patients with end-stage renal disease (ESRD) because cardiovascular events are very frequent in these patients. 2 Although it was suggested that an elevated troponin T level might be caused by retention of proteolytic degradation products of troponin T, 3 an increasing number of articles suggest that whatever the effect of renal clearance, elevated troponin T levels must be the result of small areas of clinically silent myocar- dial necrosis 4 or left ventricular hypertrophy. One study showed that prediction of prognosis by troponin levels is irrespective of creatinine clearance. 5 Recent evidence suggests that troponin T level is a predictor of long-term all-cause and cardio- vascular mortality in patients with ESRD. 6-22 Although these studies showed that troponin T level is an independent risk factor for mortality, this does not necessarily imply that it is able to accurately distinguish between patients with a good or poor prognosis. In some studies, this discriminative ability of troponin T was calcu- lated by means of receiver operating characteris- tic (ROC) analysis and was considered moderate to good. 11,13,14,22 A recent meta-analysis by Khan From the Departments of Internal Medicine and Clini- cal Epidemiology, Leiden University Medical Center, Lei- den; Department of Nephrology, Academic Medical Cen- ter–University of Amsterdam; and Hans Mak Institute, Naarden, The Netherlands. Received August 18, 2005; accepted in revised form January 23, 2006. Originally published online as doi:10.1053/j.ajkd.2006.01.019 on March 29, 2006. For the Netherlands Cooperative Study on the Adequacy of Dialysis (NECOSAD) Study Group: A.J. Apperloo, J.N.M. Barendregt, R.J. Birnie, M. Boekhout, W.H. Boer, E.F.H. van Bommel, H.R. Büller, F.Th. de Charro, C.J. Dorp, W.T. van Doorenbos, A. van Es, W.J. Fagel, G.W. Feith, C.F.M. Franssen, L.A.M. Frenken, J.A.C.A. van Geelen, W. Geer- lings, P.G.G. Gerlag, J.P.M.C. Gorgels, W. Grave, R.M. Huisman, K.J. Jager, M.A. Jansen, K. Jie, W.A.H. Koning- Mulder, M.I. Koolen, T.K. Kremer Hovinga, A.T.J. Lavrijs- sen, A.W. Mulder, K.J. Parlevliet, J.B. Rosman, J.L.C.M. van Saase, M.J.M. Schonk, M.M.J. Schuurmans, P. Stevens, J.G.P. Tijssen, R.M. Valentijn, G. Vastenburg, C.A. Verburg, V.M.C. Verstappen, H.H. Vincent, and P. Vos. Support: The study was supported by grants from the Dutch Kidney Foundation and the Dutch National Health Insurance Board. Potential conflicts of interest: None. Address reprint requests to Friedo W. Dekker, PhD, De- partment of Clinical Epidemiology, Leiden University Medi- cal Center, Albinusdreef 2, PO Box 9600, 2300 RC Leiden, The Netherlands. E-mail: f.w.dekker@lumc.nl © 2006 by the National Kidney Foundation, Inc. 0272-6386/06/4705-0012$32.00/0 doi:10.1053/j.ajkd.2006.01.019 American Journal of Kidney Diseases, Vol 47, No 5 (May), 2006: pp 823-829 823