TY - JOUR
T1 - Prognostic value of cardiac troponin T is independent of inflammation, residual renal function, and cardiac hypertrophy and dysfunction in peritoneal dialysis patients
AU - Wang, AY
AU - Lam, CW
AU - Wang, M
AU - Chan, IH
AU - Goggins, WB
AU - Yu, CM
AU - Lui, SF
AU - Sanderson, John
PY - 2007/3/29
Y1 - 2007/3/29
N2 - BACKGROUND: We investigated whether cardiac troponin T (cTnT) independently predicted outcome and added prognostic value over other clinical risk predictors in chronic peritoneal dialysis (PD) with end-stage renal disease. METHODS: Baseline cTnT, echocardiography, indices of dialysis adequacy, and biochemical characteristics were assessed in 238 chronic PD patients who were followed prospectively for 3 years or until death. RESULTS: Using multivariable Cox regression analysis, cTnT remained predictive of all-cause mortality [hazard ratio 4.43, 95% CI 1.87-10.45, P = 0.001], cardiovascular death (4.12, 1.29-13.17, P = 0.017), noncardiovascular death (8.06, 1.86-35.03, P = 0.005), and fatal and nonfatal cardiovascular events (CVEs) (3.59, 1.48-8.70, P = 0.005) independent of background coronary artery disease, inflammation, residual renal function, left ventricular hypertrophy, and systolic dysfunction. cTnT alone had better predictive value than C-reactive protein (CRP) alone for mortality [area under the ROC curve (AUC) 0.774 vs 0.691; P = 0.089] and first CVE (AUC 0.711 vs 0.593; P = 0.009) at 3 years. Survival models including age, sex, and clinical, biochemical, and echocardiographic characteristics yielded AUCs of 0.813 (95% CI, 0.748-0.877), 0.800 (95% CI, 0.726-0.874), and 0.769 (95% CI, 0.708-0.830), respectively, in relation to all-cause mortality, cardiovascular death, and fatal and nonfatal cardiovascular events. After addition of cTnT, AUCs of the above models increased significantly to 0.832 (95% CI, 0.669-0.894; P = 0.0037), 0.810 (95% CI, 0.739-0.883; P = 0.0036), and 0.780 (95% CI, 0.720-0.840; P = 0.0002), respectively; no AUCs increased when CRP was added. CONCLUSIONS: cTnT is an independent predictor of long-term mortality, cardiovascular death and events, and noncardiovascular death in PD patients.
AB - BACKGROUND: We investigated whether cardiac troponin T (cTnT) independently predicted outcome and added prognostic value over other clinical risk predictors in chronic peritoneal dialysis (PD) with end-stage renal disease. METHODS: Baseline cTnT, echocardiography, indices of dialysis adequacy, and biochemical characteristics were assessed in 238 chronic PD patients who were followed prospectively for 3 years or until death. RESULTS: Using multivariable Cox regression analysis, cTnT remained predictive of all-cause mortality [hazard ratio 4.43, 95% CI 1.87-10.45, P = 0.001], cardiovascular death (4.12, 1.29-13.17, P = 0.017), noncardiovascular death (8.06, 1.86-35.03, P = 0.005), and fatal and nonfatal cardiovascular events (CVEs) (3.59, 1.48-8.70, P = 0.005) independent of background coronary artery disease, inflammation, residual renal function, left ventricular hypertrophy, and systolic dysfunction. cTnT alone had better predictive value than C-reactive protein (CRP) alone for mortality [area under the ROC curve (AUC) 0.774 vs 0.691; P = 0.089] and first CVE (AUC 0.711 vs 0.593; P = 0.009) at 3 years. Survival models including age, sex, and clinical, biochemical, and echocardiographic characteristics yielded AUCs of 0.813 (95% CI, 0.748-0.877), 0.800 (95% CI, 0.726-0.874), and 0.769 (95% CI, 0.708-0.830), respectively, in relation to all-cause mortality, cardiovascular death, and fatal and nonfatal cardiovascular events. After addition of cTnT, AUCs of the above models increased significantly to 0.832 (95% CI, 0.669-0.894; P = 0.0037), 0.810 (95% CI, 0.739-0.883; P = 0.0036), and 0.780 (95% CI, 0.720-0.840; P = 0.0002), respectively; no AUCs increased when CRP was added. CONCLUSIONS: cTnT is an independent predictor of long-term mortality, cardiovascular death and events, and noncardiovascular death in PD patients.
U2 - 10.1373/clinchem.2006.078378
DO - 10.1373/clinchem.2006.078378
M3 - Article
C2 - 17395709
SN - 0009-9147
VL - 53
SP - 882
EP - 889
JO - Clinical Chemistry
JF - Clinical Chemistry
IS - 5
ER -