目的:心肾串扰被认为是心肾综合征。我们研究了慢性肾脏疾病(CKD)人群中心脏功能和结构与替代治疗(KFRT)肾衰竭风险的关系。
方法:前瞻性观察性队列研究。
方法:来自慢性肾功能不全队列研究的3,027名参与者。
方法:评估心脏结构和功能不同方面的五个预选变量:左心室质量指数(LVMI),低压音量,左心房(LA)面积,三尖瓣反流(TR)峰值速度,通过超声心动图评估左心室射血分数(EF)。
结果:事件KFRT(主要结果),和年度估计肾小球滤过率(eGFR)斜率(次要结果)。
方法:多变量Cox模型和混合效应模型。
结果:参与者的平均年龄为59±11SD岁,54%是男性,平均eGFR为43±17mL/min/1.73mL。2003年至2018年(中位随访,9.9年),883名参与者开发了KFRT。更高的LVMI,低压音量,洛杉矶地区,峰值TR速度,和较低的EF均与KFRT风险增加有统计学意义,最高四分位数与最低四分位数(EF最低与最高)的相应HR为1.70(95%CI,1.27-2.26),1.50(95%CI,1.19-1.90),1.43(95%CI,1.11-1.84),1.45(95%CI,1.06-1.96),和1.26(95%CI,1.03-1.56),分别。对于次要结果,最高四分位数与最低四分位数(EF最低与最高)的参与者eGFR下降速度在统计学上显著加快,除洛杉矶地区外(每年的ΔeGFR坡度,LVMI为-0.57[95%CI,-0.68至-0.46]mL/min/1.73m2,左心室容积-0.25[95%CI,-0.35至-0.15]mL/min/1.73m2,LA面积-0.01[95%CI,-0.12至-0.01]mL/min/1.73m2,峰值TR速度-0.42[95%CI,-0.56至-0.28]mL/min/1.73m2,EF为-0.11[95%CI,-0.20至-0.01]mL/min/1.73m2,分别)。
结论:残留混杂的可能性。
结论:心脏结构和功能的多个方面与KFRT的风险有统计学意义。这些发现表明,心脏异常和KFRT的发生率可能与高血压之间的相互作用有关。心力衰竭,和冠状动脉疾病。
Heart-kidney crosstalk is recognized as the cardiorenal syndrome. We examined the association of cardiac function and structure with the risk of kidney failure with replacement therapy (KFRT) in a chronic kidney disease (CKD) population.
Prospective observational cohort study.
3,027 participants from the Chronic Renal Insufficiency Cohort Study.
Five preselected variables that assess different aspects of cardiac structure and function: left ventricular mass index (LVMI), LV volume, left atrial (LA) area, peak tricuspid regurgitation (TR) velocity, and left ventricular ejection fraction (EF) as assessed by echocardiography.
Incident KFRT (primary outcome), and annual estimated glomerular filtration rate (eGFR) slope (secondary outcome).
Multivariable Cox models and mixed-effects models.
The mean age of the participants was 59±11 SD years, 54% were men, and mean eGFR was 43±17mL/min/1.73m2. Between 2003 and 2018 (median follow-up, 9.9 years), 883 participants developed KFRT. Higher LVMI, LV volume, LA area, peak TR velocity, and lower EF were each statistically significantly associated with an increased risk of KFRT, with corresponding HRs for the highest versus lowest quartiles (lowest vs highest for EF) of 1.70 (95% CI, 1.27-2.26), 1.50 (95% CI, 1.19-1.90), 1.43 (95% CI, 1.11-1.84), 1.45 (95% CI, 1.06-1.96), and 1.26 (95% CI, 1.03-1.56), respectively. For the secondary outcome, participants in the highest versus lowest quartiles (lowest vs highest for EF) had a statistically significantly faster eGFR decline, except for LA area (ΔeGFR slope per year, -0.57 [95% CI, -0.68 to-0.46] mL/min/1.73m2 for LVMI, -0.25 [95% CI, -0.35 to-0.15] mL/min/1.73m2 for LV volume, -0.01 [95% CI, -0.12 to-0.01] mL/min/1.73m2 for LA area, -0.42 [95% CI, -0.56 to-0.28] mL/min/1.73m2 for peak TR velocity, and -0.11 [95% CI, -0.20 to-0.01] mL/min/1.73m2 for EF, respectively).
The possibility of residual confounding.
Multiple aspects of cardiac structure and function were statistically significantly associated with the risk of KFRT. These findings suggest that cardiac abnormalities and incidence of KFRT are potentially on the same causal pathway related to the interaction between hypertension, heart failure, and coronary artery diseases.
Heart disease and kidney disease are known to interact with each other. In this study, we examined whether cardiac abnormalities, as assessed by echocardiography, were linked to the subsequent progression of kidney disease among people living with chronic kidney disease (CKD). We found that people with abnormalities in heart structure and function had a greater risk of progression to advanced CKD that required kidney replacement therapy and had a faster rate of decline in kidney function. Our study indicates the potential role of abnormal heart structure and function in the progression of kidney disease among people living with CKD.