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Inflammation, kidney function and albuminuria in the Framingham Offspring cohort.

机译:弗雷明汉后代队列中的炎症,肾脏功能和蛋白尿。

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摘要

BACKGROUND: Inflammation and chronic kidney disease (CKD) are both associated with cardiovascular disease (CVD). Whether inflammatory biomarkers are associated with kidney function and albuminuria after accounting for traditional CVD risk factors is not completely understood. METHODS: The sample comprised Framingham Offspring cohort participants (n = 3294, mean age 61, 53% women) who attended the seventh examination cycle (1998-2001). Inflammatory biomarkers [C-reactive protein (CRP), tumour necrosis factor (TNF)-alpha, interleukin-6, TNF receptor 2 (TNFR2), intercellular adhesion molecule-1 (ICAM-1), monocyte chemoattractant protein-1 (MCP-1), P-selectin, CD-40 ligand, osteoprotegerin, urinary isoprostanes, myeloperoxidase and fibrinogen] were measured on fasting blood samples. Serum creatinine-based estimated glomerular filtration rate (eGFR) and serum cystatin C concentration were used to assess kidney function. Urinary albumin-to-creatinine ratio (UACR) was used to assess albuminuria. Linear or logistic regression was used to test associations between biomarkers and kidney measures. RESULTS: Chronic kidney disease (CKD), defined as eGFR < 59/64 mL/min/1.73 m(2) in women/men, was present in 8.8% (n = 291) of participants. TNF-alpha, interleukin-6, TNFR2, MCP-1, osteoprotegerin, myeloperoxidase and fibrinogen were higher among individuals with CKD; all biomarkers except for urinary isoprostanes were elevated in higher cystatin C quartiles; and TNF-alpha, interleukin-6, TNFR2, ICAM-1 and osteoprotegerin were elevated in higher UACR quartiles-all assessed after multivariable adjustment. Almost 6% and 17% of variability in TNFR2 were explained by CKD status and higher cystatin C quartiles, respectively. CONCLUSIONS: Biomarkers of inflammation are associated with kidney function and albuminuria. In particular, substantial variability in soluble TNFR2 is explained by CKD and cystatin C.
机译:背景:炎症和慢性肾脏疾病(CKD)均与心血管疾病(CVD)相关。考虑到传统的CVD危险因素后,炎症生物标志物是否与肾功能和蛋白尿有关。方法:该样本包括参加第七次检查周期(1998-2001年)的弗雷明汉后代队列参与者(n = 3294,平均年龄61,女性53%)。炎症生物标志物[C反应蛋白(CRP),肿瘤坏死因子(TNF)-α,白介素6,TNF受体2(TNFR2),细胞间粘附分子1(ICAM-1),单核细胞趋化蛋白1(MCP- 1)在空腹血液样本中测量P-选择素,CD-40配体,骨保护素,尿异前列腺素,髓过氧化物酶和纤维蛋白原]。基于血清肌酐的估计肾小球滤过率(eGFR)和血清胱抑素C浓度用于评估肾功能。尿白蛋白/肌酐比值(UACR)用于评估白蛋白尿。线性或逻辑回归用于检验生物标志物与肾脏指标之间的关联。结果:慢性肾脏病(CKD)定义为eGFR <59/64 mL / min / 1.73 m(2),在男性/女性中存在8.8%(n = 291)的参与者。 CKD患者的TNF-α,白介素-6,TNFR2,MCP-1,骨保护素,髓过氧化物酶和纤维蛋白原较高;在较高的半胱氨酸蛋白酶抑制剂C四分位数中,除尿异前列腺素外,所有生物标志物均升高;在较高的UACR四分位数中,TNF-α,白细胞介素6,TNFR2,ICAM-1和骨保护素升高-所有这些均在多变量调整后评估。 TNFR2变异的近6%和17%分别由CKD状态和较高的胱抑素C四分位数解释。结论:炎症的生物标志物与肾功能和蛋白尿有关。特别是,CKD和胱抑素C解释了可溶性TNFR2的显着变异性。

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