Sakuragi Satoru, Ichikawa Keishi, Yamada Keiji, Tanimoto Masafumi, Miki Takashi, Otsuka Hiroaki, Yamamoto Kazuhiko, Kawamoto Kenji, Katayama Yusuke, Tanakaya Machiko, Ito Hiroshi
Department of Cardiovascular Medicine, Iwakuni Clinical Center, Iwakuni, Japan.
Department of Cardiovascular Medicine, Iwakuni Clinical Center, Iwakuni, Japan.
Int J Cardiol. 2015;190:287-92. doi: 10.1016/j.ijcard.2015.04.189. Epub 2015 Apr 24.
Cystatin C is an endogenous marker of kidney function that overcomes the limitations of serum creatinine. High serum cystatin C levels have been associated with increased cardiovascular mortality and morbidity. In this cross-sectional study, we aimed to determine the associations between serum cystatin C levels and structural and functional cardiac changes in patients with stage 2 or 3 chronic kidney disease (CKD).
We enrolled 429 consecutive patients (aged 24-97 years) with CKD stage 2 or 3 and left ventricular (LV) ejection fraction (LVEF)>40%. Echocardiographic parameters, including LV mass index (LVMI), early diastolic mitral annulus velocity (e' velocity), left atrial volume index (LAVI), and N-terminal of the prohormone brain natriuretic peptide (NT-proBNP) were measured. Patients were categorized into quartiles according to serum cystatin C levels. Cystatin C was associated with LAVI (p=0.0055), LVEF (p=0.0432), LVMI (p=0.0409), e' (p=0.0051), E/e' (p=0.0027), and log-transformed NT-proBNP (p<0.0001) according to multivariate linear regression analysis, after adjustment for confounding factors including creatinine-based estimated glomerular filtration rate (eGFRcreat) and urinary albumin to creatinine ratio. Incidence of eccentric and concentric hypertrophy increased with increasing cystatin C (Q1, 38%; Q2 49%; Q3, 51%; Q4, 66%, p=0.0008), mainly because of increasing concentric hypertrophy (Q1, 30%; Q2, 39%; Q3, 39%; Q4, 51%, p=0.0187).
A high serum cystatin C is strongly associated with structural cardiac abnormalities such as LVH and left atrial enlargement, impaired LV relaxation, and an increased NT-proBNP, independently of eGFRcreat in patients with stage 2 or 3 CKD.
胱抑素C是一种肾功能的内源性标志物,克服了血清肌酐的局限性。血清胱抑素C水平升高与心血管死亡率和发病率增加相关。在这项横断面研究中,我们旨在确定2期或3期慢性肾脏病(CKD)患者血清胱抑素C水平与心脏结构和功能变化之间的关联。
我们纳入了429例连续的2期或3期CKD患者(年龄24 - 97岁),左心室(LV)射血分数(LVEF)>40%。测量了超声心动图参数,包括左心室质量指数(LVMI)、二尖瓣环舒张早期速度(e'速度)、左心房容积指数(LAVI)和脑钠肽前体N末端(NT-proBNP)。根据血清胱抑素C水平将患者分为四分位数。多因素线性回归分析显示,在校正包括基于肌酐的估计肾小球滤过率(eGFRcreat)和尿白蛋白与肌酐比值等混杂因素后,胱抑素C与LAVI(p = 0.0055)、LVEF(p = 0.0432)、LVMI(p = 0.04)、e'(p = 0.0051)、E/e'(p = 0.0027)和对数转换后的NT-proBNP(p < 0.0001)相关。离心性和向心性肥厚的发生率随胱抑素C升高而增加(Q1,38%;Q2,49%;Q3,51%;Q4,66%,p = 0.0008),主要是由于向心性肥厚增加(Q1,30%;Q2,39%;Q3,39%;Q4,51%,p = 0.0187)。
在2期或3期CKD患者中,高血清胱抑素C与心脏结构异常如左心室肥厚和左心房扩大、左心室舒张功能受损以及NT-proBNP升高密切相关,且独立于eGFRcreat。