Lucove Jaime, Vupputuri Suma, Heiss Gerardo, North Kari, Russell Marie
Department of Epidemiology, University of North Carolina-Chapel Hill, NC, USA.
Am J Kidney Dis. 2008 Jan;51(1):21-8. doi: 10.1053/j.ajkd.2007.09.014.
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.
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.
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).
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% CI, 1.0 to 1.9) and 1.3 (95% CI, 1.0 to 1.6), respectively. The relationship between metabolic syndrome and kidney outcomes was stronger in those who developed diabetes during follow-up.
Intraindividual variability in serum creatinine and ACR measures may have resulted in some misclassification of participants by outcome status.
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.
2型糖尿病之前的代谢障碍，如代谢综合征，可能会促使慢性肾脏病（CKD）的发生。本研究记录了在“强心研究”中无糖尿病的美国印第安人中CKD的患病率和发病率，以及代谢综合征与CKD之间的前瞻性关联。
前瞻性队列研究。
利用部落记录招募了来自3个地理区域的45至74岁美国印第安人，并在1989年至1999年期间每3年进行一次评估，作为“强心研究”的一部分。排除在基线检查时患有2型糖尿病、接受透析治疗或接受肾移植的参与者。
采用成人治疗小组III标准定义的代谢综合征。
通过使用估计肾小球滤过率（eGFR）和尿白蛋白肌酐比值（ACR），并在传统临界值处进行二分法测量CKD。使用多变量Cox比例风险模型和二项回归评估代谢综合征与新发CKD之间的关联，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。
基线时，896名参与者（37.7%）存在代谢综合征，1484名参与者（62.3%）不存在代谢综合征。基线检查时ACR≥30 mg/g的患病率为12.1%，有290例新病例，发病率为233/10000人年。eGFR<60 mL/min/1.73 m²的患病率为7.8%，有189例新病例，发病率为138/10000人年。CKD的患病率为17.8%，有388例新病例，发病率为342/10000人年。与代谢综合征相关的CKD调整后风险比为1.3（95%置信区间[CI]，1.1至1.6）。ACR>30 mg/g和eGFR<60 mL/min/1.73 m²的等效风险比分别为1.4（95%CI，1.0至1.9）和1.3（95%CI，1.0至1.6）。在随访期间发生糖尿病的患者中，代谢综合征与肾脏结局之间的关系更强。
血清肌酐和ACR测量的个体内变异性可能导致部分参与者结局状态的错误分类。
代谢综合征与无糖尿病的美国印第安人发生CKD的风险增加相关。代谢综合征在该人群中可能导致CKD的机制可能是糖尿病的发生。
