Park Meyeon, Vittinghoff Eric, Shlipak Michael G, Mishra Rakesh, Whooley Mary, Bansal Nisha
University of California, San Francisco, Division of Nephrology, San Francisco, CA.
University of California, San Francisco, Department of Epidemiology and Biostatistics, San Francisco, CA.
Am Heart J. 2014 Dec;168(6):931-9.e2. doi: 10.1016/j.ahj.2014.09.008. Epub 2014 Oct 14.
Subclinical volume overload in the absence of diagnosed heart failure (HF) may be an underrecognized contributor to kidney function decline in coronary artery disease (CAD) patients. We evaluated associations of circulating N-terminal pro-B-type natriuretic peptide (NT-proBNP), a marker of ventricular stretch, with change in estimated glomerular filtration rate (eGFR).
We evaluated 535 patients with stable CAD and no history of HF, who were enrolled in the Heart and Soul Study and followed for 5 years. N-terminal pro-B-type natriuretic peptide was measured at baseline. We evaluated the associations of NT-proBNP with change in kidney function over 5 years: (a) annual percent change in eGFR, (b) rapid kidney function loss (> 3% per year for 5 years), and (c) incident eGFR < 60 mL/min per 1.73 m2. In multivariable models, we adjusted for demographics, comorbid conditions, echocardiographic parameters, medications, and baseline kidney function.
Among 535 participants, median NT-proBNP was 130.6 (interquartile range 61.8-280.9) pg/mL, and median B-type natriuretic peptide (BNP) was 32.5 (14.4-75.9) pg/mL. Individuals with NT-proBNP levels in the highest quartile (> 280.9 pg/mL) had a greater odds of rapid kidney function loss after full adjustment (odds ratio 2.95; 95% CI 1-8.65; P = .0492). Associations with incident eGFR < 60 mL/min per 1.73 m2 were also significant (adjusted odds ratio 4.23; 95% CI 1.05-16.98; P = .0422). Results were similar when analyzed using BNP as the predictor.
N-terminal pro-B-type natriuretic peptide and BNP are strongly and independently associated with accelerated kidney function loss, even in the absence of clinical HF. These findings suggest that subclinical cardiovascular dysfunction may contribute to elevated kidney disease risk in persons with CAD.
在未诊断为心力衰竭（HF）的情况下，亚临床容量超负荷可能是冠状动脉疾病（CAD）患者肾功能下降的一个未被充分认识的因素。我们评估了循环N末端B型利钠肽原（NT-proBNP）（一种心室扩张的标志物）与估计肾小球滤过率（eGFR）变化之间的关联。
我们评估了535例稳定CAD且无HF病史的患者，这些患者参加了“心灵研究”并随访了5年。在基线时测量N末端B型利钠肽原。我们评估了NT-proBNP与5年期间肾功能变化的关联：（a）eGFR的年度百分比变化，（b）快速肾功能丧失（5年内每年>3%），以及（c）eGFR<60 mL/min/1.73 m2的发生率。在多变量模型中，我们对人口统计学、合并症、超声心动图参数、药物治疗和基线肾功能进行了校正。
在535名参与者中，NT-proBNP的中位数为130.6（四分位间距61.8-280.9）pg/mL，B型利钠肽（BNP）的中位数为32.5（14.4-75.9）pg/mL。NT-proBNP水平处于最高四分位数（>280.9 pg/mL）的个体在完全校正后快速肾功能丧失的几率更高（比值比2.95；95%CI 1-8.65；P = 0.0492）。与eGFR<60 mL/min/1.73 m2发生率的关联也很显著（校正比值比4.23；95%CI 1.05-16.98；P = 0.0422）。以BNP作为预测指标进行分析时，结果相似。
即使在没有临床HF的情况下，N末端B型利钠肽原和BNP也与加速肾功能丧失密切且独立相关。这些发现表明，亚临床心血管功能障碍可能会增加CAD患者患肾病的风险。
