Orth S R, Stöckmann A, Conradt C, Ritz E, Ferro M, Kreusser W, Piccoli G, Rambausek M, Roccatello D, Schäfer K, Sieberth H G, Wanner C, Watschinger B, Zucchelli P
Department of Internal Medicine and Institute for Medical Biometry, Ruperto Carola University Heidelberg, Germany.
Kidney Int. 1998 Sep;54(3):926-31. doi: 10.1046/j.1523-1755.1998.00067.x.
It is not known whether smoking increases the risk of end-stage renal failure (ESRF) in patients with primary renal disease.
We performed a retrospective multicenter case-control study including 582 patients from nine centers in Germany, Italy and Austria. The diseases investigated were IgA glomerulonephritis (IgA-GN) as a model of inflammatory renal disease and autosomal dominant polycystic kidney disease (ADPKD) as a model of non-inflammatory renal disease. Cases were patients who had progressed to ESRF and controls were patients who were not in ESRF, that is, whose serum-creatinine failed to progress to >3 mg/dl during the observation period and who did not require renal replacement therapy. Matching for renal disease (IgA-GN, ADPKD), gender, age at renal death and region of residence resulted in 102 individually matched pairs (IgA-GN N = 54, ADPKD N = 48). Multiple conditional logistic regression was used to estimate adjusted odds ratios for independent tobacco effects.
In men (matched pairs: IgA-GN N = 44, ADPKD N = 28), a significant dose-dependent increase of the risk to progress to ESRF was found (non-adjusted). The baseline risk was defined as <5 pack-years (PY): (i) 5 to 15 PY, odds ratio 3.5 (95% CI 1.3 to 9.6), P = 0.017; (ii) >15 PY = 5.8 (2.0 to 17), P = 0.001. Systolic blood pressure, ACE inhibitor treatment and age at diagnosis emerged as potential confounders. After adjustment, the risk for ESRF in men with >5 PY was highly increased for patients without ACE inhibitor treatment [10.1 (2.3 to 45), P = 0.002] but not with ACE inhibitor treatment [1.4 (0.3 to 7.1), P = 0.65].
Smoking increases the risk of ESRF in men with inflammatory and non-inflammatory renal disease.
原发性肾病患者中,吸烟是否会增加终末期肾衰竭(ESRF)的风险尚不清楚。
我们进行了一项回顾性多中心病例对照研究,纳入了来自德国、意大利和奥地利九个中心的582例患者。所研究的疾病包括作为炎性肾病模型的IgA肾小球肾炎(IgA-GN)和作为非炎性肾病模型的常染色体显性遗传性多囊肾病(ADPKD)。病例为进展至终末期肾衰竭的患者,对照为未发生终末期肾衰竭的患者,即在观察期内血清肌酐未进展至>3mg/dl且不需要肾脏替代治疗的患者。根据肾病类型(IgA-GN、ADPKD)、性别、肾脏疾病死亡时年龄和居住地区进行匹配,得到102对个体匹配对(IgA-GN 54对,ADPKD 48对)。采用多条件逻辑回归估计独立烟草效应的调整优势比。
在男性中(匹配对:IgA-GN 44对,ADPKD 28对),发现进展至终末期肾衰竭的风险存在显著的剂量依赖性增加(未调整)。基线风险定义为<5包年(PY):(i)5至15 PY,优势比3.5(95%CI 1.3至9.6),P = 0.017;(ii)>15 PY = 5.8(2.0至17),P = 0.001。收缩压、ACE抑制剂治疗和诊断时年龄成为潜在混杂因素。调整后,吸烟量>5 PY的男性中,未接受ACE抑制剂治疗的患者发生终末期肾衰竭的风险显著增加[10.1(2.3至45),P = 0.002],而接受ACE抑制剂治疗的患者则未增加[1.4(0.3至7.1),P = 0.65]。
吸烟会增加患有炎性和非炎性肾病男性发生终末期肾衰竭的风险。