BACKGROUND: Smoking is an important player in the pathogenesis of hypertensive nephropathy. To shed more light on this issue, we performed a case-control cross-sectional study and stratification analyses to evaluate the influence of smoking on surrogate markers of kidney injury and oxidative stress in patients supposed to have hypertensive nephropathy. The dependence of kidney lesions on the 'extent' of smoking was determined as well. METHODS: 82 patients with essential hypertension and micro- or macro-albuminuria were recruited. The control group consisted of 41 sex- and age-matched healthy individuals. Urine albumin creatinine ratio and plasma von Willebrand factor activity were analysed as markers of endothelial injury. N-acetyl-beta-D-glucosaminidase, transforming growth factor-beta1 and 15-isoprostane F2t urine excretions were regarded as markers of tubular dysfunction, renal fibrosis and oxidative stress, respectively. Patients' smoking habits were recorded and categorized on the basis of a self-administered questionnaire. RESULTS: In multivariate regression analysis, the independent associations between smoking and urine albumin (p < 0.05; beta = 0.27), von Willebrand factor activity (p < 0.05; beta = 0.29) and urine isoprostanes (p < 0.05; beta = 0.28) were found. When the smokers were stratified according to the number of cigarettes smoked per day and the time from which they started smoking, 'heavy smokers' and 'long-term smokers' presented with higher albumin excretion and higher von Willebrand factor activity than 'light smokers' and 'short-term smokers', respectively. The passive smokers had numerically higher albumin excretion and von Willebrand factor activity than nonsmokers. CONCLUSION: The study showed that smoking induces oxidative stress. Smoking was also found to be a strong predictor for the extent of endothelial injury in patients with hypertensive kidney injury. Subjects who smoke heavily and for a long time, as well as passive smokers, seem to be particularly exposed to endothelial damage. Copyright 2006 S. Karger AG, Basel
BACKGROUND: Smoking is an important player in the pathogenesis of hypertensive nephropathy. To shed more light on this issue, we performed a case-control cross-sectional study and stratification analyses to evaluate the influence of smoking on surrogate markers of kidney injury and oxidative stress in patients supposed to have hypertensive nephropathy. The dependence of kidney lesions on the 'extent' of smoking was determined as well. METHODS: 82 patients with essential hypertension and micro- or macro-albuminuria were recruited. The control group consisted of 41 sex- and age-matched healthy individuals. Urine albumin creatinine ratio and plasma von Willebrand factor activity were analysed as markers of endothelial injury. N-acetyl-beta-D-glucosaminidase, transforming growth factor-beta1 and 15-isoprostane F2t urine excretions were regarded as markers of tubular dysfunction, renal fibrosis and oxidative stress, respectively. Patients' smoking habits were recorded and categorized on the basis of a self-administered questionnaire. RESULTS: In multivariate regression analysis, the independent associations between smoking and urine albumin (p < 0.05; beta = 0.27), von Willebrand factor activity (p < 0.05; beta = 0.29) and urine isoprostanes (p < 0.05; beta = 0.28) were found. When the smokers were stratified according to the number of cigarettes smoked per day and the time from which they started smoking, 'heavy smokers' and 'long-term smokers' presented with higher albumin excretion and higher von Willebrand factor activity than 'light smokers' and 'short-term smokers', respectively. The passive smokers had numerically higher albumin excretion and von Willebrand factor activity than nonsmokers. CONCLUSION: The study showed that smoking induces oxidative stress. Smoking was also found to be a strong predictor for the extent of endothelial injury in patients with hypertensive kidney injury. Subjects who smoke heavily and for a long time, as well as passive smokers, seem to be particularly exposed to endothelial damage. Copyright 2006 S. Karger AG, Basel
Authors: Solange Bandiera; Rianne R Pulcinelli; Fernanda Huf; Felipe B Almeida; Graziele Halmenschlager; Paula E R Bitencourt; Eliane Dallegrave; Marilda C Fernandes; Rosane Gomez; Mauricio S Nin Journal: Toxicol Res Date: 2020-08-13