Hogan Susan L, Vupputuri Suma, Guo Xuguang, Cai Jianwen, Colindres Romulo E, Heiss Gerardo, Coresh Josef
Division of Nephrology and Hypertension, Department of Medicine, University of North Carolina at Chapel Hill, North Carolina 27599-7155, USA.
Ren Fail. 2007;29(2):133-42. doi: 10.1080/08860220601098888.
The association of cigarette smoking with albuminuria has been reported but not examined in a representative U.S. population. No study has evaluated the association between serum cotinine (a biological marker for tobacco exposure) and kidney damage.
A cross-sectional analysis was conducted among 15,719 adult participants of the third National Health and Nutrition Examination Survey to assess the association between smoking exposure and kidney damage. Smoking was assessed by self-reported lifetime cigarette use and serum cotinine. Kidney damage was assessed by urine albumin-to-creatinine ratio (ACR), with albuminuria defined as ACR of > or =17 microg/mg in males and > or =25 microg/mg in females.
The analysis included 13,121 with normal albumin (mean ACR 6.3 microg/mg) and 2,414 with albuminuria (mean ACR 143 microg/mg); hypertension was prevalent in 27% and 59%, respectively. Former smoking was similar between groups (21%), while current smoking was more common in persons with albuminuria (26%) compared to normal ACR (21%). Adjusted for other risk factors, among hypertensives, current smokers were 1.85 (95% CI: 1.29, 2.64) times more likely to have albuminuria than never smokers. Current smokers with a > or =40 pack-year history were at highest risk for albuminuria. Among non-smoking hypertensives, those exposed to passive smoke (highest versus lowest quartile of serum cotinine) were 1.41 (95% CI: 1.04, 1.90) times more likely to have albuminuria. Former smoking with cessation of > or =1 year among hypertensives was not associated with albuminuria. Among non-hypertensives, smoking and albuminuria were not consistently associated.
Current and passive smoking, but not former smoking, were associated with the presence of albuminuria in the general U.S. population with hypertension, indicating a benefit to the kidney from smoking cessation.
吸烟与蛋白尿之间的关联已有报道,但尚未在具有代表性的美国人群中进行研究。尚无研究评估血清可替宁(烟草暴露的生物标志物)与肾脏损害之间的关联。
对第三次全国健康与营养检查调查的15719名成年参与者进行横断面分析,以评估吸烟暴露与肾脏损害之间的关联。吸烟情况通过自我报告的终生吸烟量和血清可替宁进行评估。肾脏损害通过尿白蛋白与肌酐比值(ACR)进行评估,男性蛋白尿定义为ACR≥17微克/毫克,女性为ACR≥25微克/毫克。
分析纳入了13121名白蛋白正常者(平均ACR为6.3微克/毫克)和2414名蛋白尿患者(平均ACR为143微克/毫克);高血压在两组中的患病率分别为27%和59%。两组之间的既往吸烟率相似(21%),而与正常ACR组(21%)相比,蛋白尿患者中当前吸烟者更为常见(26%)。在对其他危险因素进行校正后,在高血压患者中,当前吸烟者出现蛋白尿的可能性是从不吸烟者的1.85倍(95%置信区间:1.29,2.64)。吸烟史≥40包年的当前吸烟者出现蛋白尿的风险最高。在不吸烟的高血压患者中,暴露于被动吸烟的人群(血清可替宁最高四分位数与最低四分位数相比)出现蛋白尿的可能性是1.41倍(95%置信区间:1.04,1.90)。高血压患者中戒烟≥1年的既往吸烟者与蛋白尿无关。在非高血压患者中,吸烟与蛋白尿之间的关联并不一致。
在美国一般高血压人群中,当前吸烟和被动吸烟与蛋白尿的存在有关,而既往吸烟则无关,这表明戒烟对肾脏有益。