Metabolic syndrome and the development of CKD in American Indians: The Strong Heart Study

Metabolic syndrome and the development of CKD in American Indians: The Strong Heart Study
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DOI:
10.1053/j.ajkd.2007.09.014
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发表时间:
2008-01-01
影响因子:
13.2
通讯作者:
Russell, Marie
Russell, Marie
中科院分区:
医学1区
文献类型:
--
作者:
Lucove, Jaime;Vupputuri, Suma;Russell, Marie

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背景:2型糖尿病前的代谢损伤,如代谢综合征,可能导致慢性肾脏疾病(CKD)的发生。这项研究记录了美国印第安人中没有糖尿病的CKD的患病率和发病率,以及代谢综合征和CKD之间的前瞻性关联。研究设计:前瞻性队列研究。背景和对象:来自3个地理区域的45岁至74岁的美国印第安人通过部落记录招募,作为强心研究的一部分,从1989年到1999年每3年进行一次评估。2型糖尿病、接受透析治疗或在基线检查时接受肾移植的参与者被排除在外。预测因素:代谢综合征,根据成人治疗委员会III标准定义。结果与测量:慢性肾脏病是通过使用估计的肾小球滤过率(EGFR)和尿白蛋白-肌酐比(ACR)进行测量的。使用多变量Cox比例风险模型和二项回归,并对混杂因素(年龄、性别、研究中心、教育程度和吸烟)进行统计调整,评估代谢综合征与CKD发病的相关性。结果:基线时有896人(37.7%)存在代谢综合征,1484人(62.3%)没有代谢综合征。基线检查时ACR大于或等于30 mg/g的患病率为12.1%,新增病例290例,发病率为233/10,000人年。EGFR<60mL/min/1.73m(2)的患病率为7.8%,新增病例189例,发病率138/万人年。慢性病患病率为17.8%,新发病例388例,发病率342/万人年。调整后的CKD与代谢综合征相关的危险比为1.3(95%可信区间为1.1至1.6)。ACR>30 mg/g和EGFR<60mL/min/1.73m(2)的等效危险比分别为1.4(95%CI,1.0~1.9)和1.3(95%CI,1.0~1.6)。在随访期间发生糖尿病的患者中,代谢综合征和肾脏结局之间的关系更强。限制:血清肌酐和ACR测量的个体内变异性可能导致参与者根据结局状态对参与者进行错误分类。结论:在没有糖尿病的美洲印第安人中,代谢综合征与发生CKD的风险增加有关。代谢综合征可能导致这一人群慢性肾脏病的机制可能是糖尿病的发展。
Background: Metabolic impairments that precede type 2 diabetes, such as metabolic syndrome, may contribute to the development of chronic kidney disease (CKD). This study documents the prevalence and incidence of CKD and the prospective association between metabolic syndrome and CKD in American Indians without diabetes in the Strong Heart Study.Study Design: Prospective cohort study.Setting & Participants: American Indians aged 45 to 74 years from 3 geographic regions were recruited by using tribal records and were assessed every 3 years from 1989 to 1999 as part of the Strong Heart Study. Participants with type 2 diabetes, on dialysis therapy, or who received a kidney transplant at baseline examination were excluded.Predictor: Metabolic syndrome, defined using Adult Treatment Panel III criteria.Outcomes & Measurements: CKD was measured by using estimated glomerular filtration rate (eGFR) and urinary albumin-creatinine ratio (ACR) dichotomized at conventional cutoff values. The association between metabolic syndrome and incident CKD was evaluated by using multivariable Cox proportional hazards models and binomial regression, with statistical adjustment for confounders (age, sex, study center, education, and smoking).Results: Metabolic syndrome was present in 896 (37.7%) and absent in 1,484 participants (62.3%) at baseline. The prevalence of ACR of 30 mg/g or greater at baseline examination was 12.1%, with 290 new cases and an incidence of 233/10,000 person-years. The prevalence of eGFR less than 60 mL/min/1.73 m(2) was 7.8%, with 189 new cases and an incidence of 138/10,000 person-years. The prevalence of CKD was 17.8%, with 388 new cases and an incidence of 342/10,000 person-years. The adjusted hazard ratio for CKD associated with metabolic syndrome was 1.3 (95% confidence interval [CI], 1.1 to 1.6). Equivalent hazard ratios for ACR greater than 30 mg/g and eGFR less than 60 mL/min/1.73 m(2) were 1.4 (95% Cl, 1.0 to 1.9) and 1.3 (95% Cl, 1.0 to 1.6), respectively. The relationship between metabolic syndrome and kidney outcomes was stronger in those who developed diabetes during follow-up.Limitations: Intraindividual variability in serum creatinine and ACR measures may have resulted in some misclassification of participants by outcome status.Conclusions: Metabolic syndrome is associated with an increased risk of developing CKD in American Indians without diabetes. The mechanism through which metabolic syndrome may cause CKD in this population likely is the development of diabetes.