Inflammation, oxidative stress, glomerular filtration rate, and albuminuria in elderly men: a cross-sectional study.

Inflammation, oxidative stress, glomerular filtration rate, and albuminuria in elderly men: a cross-sectional study.
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DOI:
10.1186/1756-0500-5-537
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发表时间:
2012-09-27
期刊:
影响因子:
1.8
通讯作者:
Arnlöv J
Arnlöv J
中科院分区:
其他
文献类型:
--
作者:
Nerpin E;Helmersson-Karlqvist J;Risérus U;Sundström J;Larsson A;Jobs E;Basu S;Ingelsson E;Arnlöv J

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炎症和氧化应激在老年人轻度肾损害中的作用尚未得到很好的研究。因此,我们旨在调查社区老年男性队列中估计的肾小球滤过率(EGFR)、白蛋白/肌酐比值(ACR)以及不同炎症途径的标志物与氧化应激之间的关系。在Uppsala成年男性纵向研究(n = 647,平均年龄77 )中,评估了基于胱抑素C的肾小球滤过率、血管紧张素转换酶和细胞因子介导的炎症的生物标志物(白介素6、高敏C反应蛋白、血清淀粉样蛋白A)、环氧合酶介导的炎症(尿前列腺素F2α[PGF2α])和氧化应激(尿F2异前列腺素)。在调整了年龄、体重指数、吸烟、血压、低密度脂蛋白、高密度脂蛋白、甘油三酯以及他汀类药物、血管紧张素转换酶抑制剂、阿司匹林和抗炎药治疗的线性回归模型中,表皮生长因子受体与C反应蛋白、白介素6和唾液酸呈负相关(β系数−为0.13至−0.19,p < 均为0.001),与尿F2-异前列腺素呈正相关(β系数为0.09,p = 为0.02)。与此相一致,Acr与C反应蛋白、白介素6和唾液酸呈正相关(β系数为0.09~0.12,p < 均为0.02),与尿F2-异前列腺素呈负相关(β系数−为0.12,p = 为0.002)。除了F2-异前列腺素和SAA不再与表皮生长因子受体相关外,在表皮生长因子受体正常的子样本中,相关性相似,但回归系数较低(>60 m l/m in/1.73 m 2,n = 514)。我们的数据表明,细胞因子介导的炎症参与了老年人肾功能受损的早期阶段,但环氧合酶介导的炎症在这一阶段不起作用。更高的EGFR/更低的蛋白尿与尿中F2-异前列腺素增加之间的意外关联值得进一步研究。
The role of inflammation and oxidative stress in mild renal impairment in the elderly is not well studied. Accordingly, we aimed at investigating the associations between estimated glomerular filtration rate (eGFR), albumin/creatinine ratio (ACR), and markers of different inflammatory pathways and oxidative stress in a community based cohort of elderly men. Cystatin C-based GFR, ACR, and biomarkers of cytokine-mediated inflammation (interleukin-6, high-sensitivity C-reactive protein[CRP], serum amyloid A[SAA]), cyclooxygenase-mediated inflammation (urinary prostaglandin F2α [PGF2α]), and oxidative stress (urinary F2 isoprostanes) were assessed in the Uppsala Longitudinal Study of Adult Men(n = 647, mean age 77 years). In linear regression models adjusting for age, BMI, smoking, blood pressure, LDL-cholesterol, HDL-cholesterol, triglycerides, and treatment with statins, ACE-inhibitors, ASA, and anti-inflammatory agents, eGFR was inversely associated with CRP, interleukin-6, and SAA (β-coefficient −0.13 to −0.19, p < 0.001 for all), and positively associated with urinary F2-isoprostanes (β-coefficient 0.09, p = 0.02). In line with this, ACR was positively associated with CRP, interleukin-6, and SAA (β- coefficient 0.09-0.12, p < 0.02 for all), and negatively associated with urinary F2-isoprostanes (β-coefficient −0.12, p = 0.002). The associations were similar but with lower regression coefficients in a sub-sample with normal eGFR (>60 ml/min/1.73 m2, n = 514), with the exception that F2-isoprostane and SAA were no longer associated with eGFR. Our data indicate that cytokine-mediated inflammation is involved in the early stages of impaired kidney function in the elderly, but that cyclooxygenase-mediated inflammation does not play a role at this stage. The unexpected association between higher eGFR/lower albuminuria and increased F2-isoprostanes in urine merits further studies.