Obesity and synergistic risk factors for chronic kidney disease in African American adults: the Jackson Heart Study

Obesity and synergistic risk factors for chronic kidney disease in African American adults: the Jackson Heart Study
复制标题

DOI:
10.1093/ndt/gfx230
复制
发表时间:
2018-06-01
影响因子:
6.1
通讯作者:
Scialla, Julia J.
Scialla, Julia J.
中科院分区:
医学1区
文献类型:
--
作者:
Olivo, Robert E.;Davenport, Clemontina A.;Scialla, Julia J.

文献摘要

被引文献

相似文献

背景资料。非洲裔美国人患慢性肾脏疾病(CKD)的风险很高。肥胖可能会加重代谢综合征的特征并促进肾小球高滤过,从而增加CKD的风险。其他影响这些途径的因素是否也可能放大或减轻肥胖与慢性肾脏病的关联还没有被调查。我们研究了参加杰克逊心脏研究的2043名没有基线肾病的非裔美国人肥胖与这些候选因素之间的相互作用。在一项中期研究访问中,我们将肥胖量化为体重指数(BMI)、性别归一化腰围和腹部计算机断层扫描测量的内脏脂肪体积。交互作用被假设为(I)代谢风险因素(饮食质量和体力活动,两者都根据美国心脏协会的指南进行量化)和(Ii)加剧或缓解高滤过的因素(饮食蛋白质摄入量、APOL1风险状态和肾素-血管紧张素系统阻断药物的使用)。使用多变量回归分析,我们评估了肥胖指标与随访期间发生的慢性肾脏病之间的关系,以及与代谢和高滤过因素之间的相互作用。经过中位数8年(范围6-11年)的评估,基线BMI和腰围与CKD的发生无关。较高的内脏脂肪体积与慢性肾脏病的发生率呈非线性相关(P=0.008),但这种影响仅限于饮食质量较低的人群(P=0.001;P交互作用=0.04)。在其他交互作用模型中,在低风险的APOL1基因携带者中,较高的腰围与发生CKD的风险较大(P=0.04),但与高危基因携带者无关(P-交互作用=0.02)。其他被提出的因素并没有改变肥胖与慢性肾脏病之间的联系。代谢活跃的内脏脂肪含量和与饮食质量相互作用的高风险表明,代谢因素可能是肥胖相关CKD风险的关键决定因素。在对非裔美国人的研究中,应该考虑肥胖和APOL1基因之间的相互作用。
Background. African Americans are at high risk for chronic kidney disease (CKD). Obesity may increase the risk for CKD by exacerbating features of the metabolic syndrome and promoting glomerular hyperfiltration. Whether other factors also affecting these pathways may amplify or mitigate obesity-CKD associations has not been investigated.Methods. We studied interactions between obesity and these candidate factors in 2043 African Americans without baseline kidney disease enrolled in the Jackson Heart Study. We quantified obesity as body mass index (BMI), sex-normalized waist circumference and visceral adipose volume measured by abdominal computed tomography at an interim study visit. Interactions were hypothesized with (i) metabolic risk factors (dietary quality and physical activity, both quantified by concordance with American Heart Association guidelines) and (ii) factors exacerbating or mitigating hyperfiltration (dietary protein intake, APOL1 risk status and use of renin-angiotensin system blocking medications). Using multivariable regression, we evaluated associations between obesity measures and incident CKD over the follow-up period, as well as interactions with metabolic and hyperfiltration factors.Results. Assessed after a median of 8 years (range 6-11 years), baseline BMI and waist circumference were not associated with incident CKD. Higher visceral adipose volume was independently associated with incident CKD (P = 0.008) in a nonlinear fashion, but this effect was limited to those with lower dietary quality (P = 0.001; P-interaction = 0.04). In additional interaction models, higher waist circumference was associated with greater risk of incident CKD among those with the low-risk APOL1 genotype (P = 0.04) but not those with a high-risk genotype (P-interaction = 0.02). Other proposed factors did not modify obesity-CKD associations.Conclusions. Higher risks associated with metabolically active visceral adipose volume and interactions with dietary quality suggest that metabolic factors may be key determinants of obesity-associated CKD risk. Interactions between obesity and APOL1 genotype should be considered in studies of African Americans.