Division of Nephrology, Department of Medicine, University of Texas Southwestern Medical Center, Dallas, TX.
Division of Biostatistics, Department of Clinical Sciences, University of Texas Southwestern Medical Center, Dallas, TX.
J Am Heart Assoc. 2017 Jul 5;6(7):e005235. doi: 10.1161/JAHA.116.005235.
Cardiac troponin T and brain natriuretic peptide (BNP) are elevated in >50% of dialysis patients and are associated with poor outcomes. Few data investigated these associations in earlier chronic kidney disease (CKD).
We studied whether CKD modified associations of elevated BNP, N-terminal-pro-BNP, high-sensitivity cardiac troponin T, coronary artery calcification, and left ventricular hypertrophy with all-cause death and cardiovascular death/events in 3218 multiethnic individuals followed for 12.5 years, and whether biomarkers added prognostic information to traditional cardiovascular risk factors in CKD. Of the cohort, 279 (9%) had CKD. There were 296 deaths and 218 cardiovascular deaths/events. Of non-CKD individuals, 7% died and 6% had cardiovascular death/event versus 32% and 30% of CKD participants, <0.001 for both. The interaction between BNP and CKD on death was significant (=0.01): the adjusted hazard ratio in CKD was 2.05, 95% CI (1.34, 3.14), but not significant in non-CKD, 1.04 (0.76, 1.41). CKD modified the association of high-sensitivity cardiac troponin T with cardiovascular death/event, adjusted hazard ratio 3.34 (1.56, 7.18) in CKD versus 1.65 (1.16, 2.35) in non-CKD, interaction =0.09. There was an interaction between N-terminal-pro-BNP and CKD for death in those without prior cardiovascular disease. Addition of each biomarker to traditional risk factors improved risk prediction, except coronary artery calcification was not discriminatory for cardiovascular death/event in CKD.
Cardiac biomarkers, with the exception of coronary artery calcification, prognosticated outcomes in early-stage CKD as well as, if not better than, in non-CKD individuals, even after controlling for estimated glomerular filtration rate, and added to information obtained from traditional cardiovascular risk factors alone.
心脏肌钙蛋白 T 和脑利钠肽(BNP)在>50%的透析患者中升高,与不良结局相关。很少有数据研究这些在早期慢性肾脏病(CKD)中的关联。
我们研究了 CKD 是否改变了 BNP、N 末端脑利钠肽前体(NT-pro-BNP)、高敏心肌肌钙蛋白 T、冠状动脉钙化和左心室肥厚与全因死亡和心血管死亡/事件的相关性,以及生物标志物是否在 CKD 中为传统心血管危险因素提供了预后信息。在随访 12.5 年的 3218 名多民族个体中,有 279 名(9%)患有 CKD。有 296 人死亡,218 人发生心血管死亡/事件。非 CKD 患者中,有 7%死亡,6%发生心血管死亡/事件,而 CKD 患者分别为 32%和 30%,两者均<0.001。BNP 和 CKD 之间的死亡交互作用具有统计学意义(=0.01):CKD 患者的调整后危险比为 2.05,95%CI(1.34,3.14),而非 CKD 患者则无统计学意义,为 1.04(0.76,1.41)。CKD 改变了高敏心肌肌钙蛋白 T 与心血管死亡/事件的相关性,在 CKD 患者中调整后的危险比为 3.34(1.56,7.18),而非 CKD 患者为 1.65(1.16,2.35),交互作用=0.09。在没有心血管疾病既往史的患者中,NT-pro-BNP 和 CKD 之间存在死亡的交互作用。除了在 CKD 中对心血管死亡/事件没有判别能力外,将每个生物标志物添加到传统危险因素中均能改善风险预测。
除了冠状动脉钙化外,心脏生物标志物在早期 CKD 中的预后结果与非 CKD 个体一样好,如果不是更好的话,甚至在控制估计肾小球滤过率后也是如此,并且增加了仅从传统心血管危险因素获得的信息。