Inflammation and microalbuminuria in nondiabetic and type 2 diabetic subjects:: The Insulin Resistance Atherosclerosis Study
Inflammation and microalbuminuria in nondiabetic and type 2 diabetic subjects:: The Insulin Resistance Atherosclerosis Study
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DOI：
10.1046/j.1523-1755.2000.00331.x
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发表时间：
2000-10-01
影响因子：
19.6
通讯作者：
Haffner, SM
中科院分区：
文献类型：
--
作者：
Festa, A;D'Agostino, R;Haffner, SM
背景资料。微量白蛋白尿是心血管疾病的危险因素，但其潜在的发病机制仍然知之甚少。炎症的敏感标志物C反应蛋白(CRP)与动脉粥样硬化性疾病的关系最近已有报道。我们假设微量白蛋白尿可能与慢性炎症有关，并研究了胰岛素抵抗动脉粥样硬化研究(IRAS)中的大量三民族人群中，尿白蛋白排泄与两种炎症标志物(CRP和纤维蛋白原)的关系，尿白蛋白排泄是通过不定时的晨尿样本进行的。排除大量白蛋白尿的受试者后，共研究了1481名受试者。两种炎症标志物都与尿乙酰胆碱受体相关(C反应蛋白r=0.17，纤维蛋白原r=0.14，P=0.0001)，在调整人口统计变量、糖尿病状况、吸烟和血管紧张素转换酶抑制剂的使用后，这种相关性仍然显著(P<；0.01)。微量白蛋白尿组C反应蛋白和纤维蛋白原水平明显高于正常白蛋白尿组(P<0.0001)。在非糖尿病和2型糖尿病受试者中，以及IRA的三个民族(非西班牙裔白人、黑人和西班牙裔)之间的关联是一致的。在Logistic回归模型中，纤维蛋白原与微量白蛋白尿独立相关(P=0.047.0 5)，与高血压、女性、腰围、空腹血糖有关，而C反应蛋白与微量白蛋白尿无关(P=0.2 6)。我们已经证明，在2型糖尿病和非糖尿病患者中，在微量白蛋白尿范围内，CRP和纤维蛋白原与尿白蛋白排泄有关。因此，慢性炎症成为微量白蛋白尿和大血管疾病之间的潜在中介。
Background. Microalbuminuria is a risk factor for cardiovascular disease, but the underlying pathomechanisms are still poorly understood. A relationship between C-reactive protein (CRP), a sensitive marker of inflammation, and atherosclerotic disease has been reported recently.Methods. We hypothesized that microalbuminuria might be associated with chronic inflammation and investigated the relationship of urinary albumin excretion, as assessed from the albumin-to-creatinine ratio (ACR), in an untimed morning urine specimen, and two inflammatory markers (CRP and fibrinogen) in the large, triethnic population of the Insulin Resistance Atherosclerosis Study (IRAS). After exclusion of subjects with macroalbuminuria, 1481 subjects were studied.Results. Both inflammatory markers were related to urinary ACR (r = 0.17 for CRP and r = 0.14 for fibrinogen, both P = 0.0001), an association that remained significant after adjustment for demographic variables, diabetic status, smoking, and use of angiotensin-converting enzyme inhibitors (P < 0.01). Mean levels of CRP and fibrinogen were elevated in microalbuminuric (N = 262) versus normoalbuminuric (N = 1219) subjects (5.37 +/- 0.47 vs. 3.80 +/- 0.15 mg/L and 295.7 +/- 4.0 vs. 278.2 +/- 1.6 mg/dL, both P < 0.0001). The associations were consistent among nondiabetic and type 2 diabetic subjects and among the three ethnic groups of the IRAS (non-Hispanic whites, blacks, Hispanics). In a logistic regression model, fibrinogen was independently associated with microalbuminuria (P = 0.047), along with hypertension, female gender, waist circumference, and fasting blood glucose, while CRP was not independently related to microalbuminuria in this model (P = 0.26).Conclusion. We have shown an association of CRP and fibrinogen with urinary albumin excretion in the microalbuminuric range in type 2 diabetic and nondiabetic individuals. Chronic inflammation therefore emerges as a potential mediator between microalbuminuria and macrovascular disease.