Smoking as a Risk Factor for Renal Injury in Essential Hypertension

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Abstract

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-β- D-glucosaminidase, transforming growth factor-β1 and 15-isoprostane F<sub>2t</sub> 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; β = 0.27), von Willebrand factor activity (p < 0.05; β = 0.29) and urine isoprostanes (p < 0.05; β = 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.

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Most cited references 26

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Blood pressure and end-stage renal disease in men.

M J Klag, P K Whelton, B L Randall … (1996)

End-stage renal disease in the United States creates a large burden for both individuals and society as a whole. Efforts to prevent the condition require an understanding of modifiable risk factors. We assessed the development of end-stage renal disease through 1990 in 332,544 men, 35 to 57 years of age, who were screened between 1973 and 1975 for entry into the Multiple Risk Factor Intervention Trial (MRFIT). We used data from the national registry for treated end-stage renal disease of the Health Care Financing Administration and from records on death from renal disease from the National Death Index and the Social Security Administration. During an average of 16 years of follow-up, 814 subjects either died of end-stage renal disease or were treated for that condition (15.6 cases per 100,000 person-years of observation). A strong, graded relation between both systolic and diastolic blood pressure and end-stage renal disease was identified, independent of associations between the disease and age, race, income, use of medication for diabetes mellitus, history of myocardial infarction, serum cholesterol concentration, and cigarette smoking. As compared with men with an optimal level of blood pressure (systolic pressure or = 210 mm Hg or diastolic pressure > or = 120 mm Hg) was 22.1 (P < 0.001). These relations were not due to end-stage renal disease that occurred soon after screening and, in the 12,866 screened men who entered the MRFIT study, were not changed by taking into account the base-line serum creatinine concentration and urinary protein excretion. The estimated risk of end-stage renal disease associated with elevations of systolic pressure was greater than that linked with elevations of diastolic pressure when both variables were considered together. Elevations of blood pressure are a strong independent risk factor for end-stage renal disease; interventions to prevent the disease need to emphasize the prevention and control of both high-normal and high blood pressure.

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Increase in circulating products of lipid peroxidation (F2-isoprostanes) in smokers. Smoking as a cause of oxidative damage.

J Morrow, B Frei, A Longmire … (1995)

It has been hypothesized that the pathogenesis of diseases induced by cigarette smoking involves oxidative damage by free radicals. However, definitive evidence that smoking causes the oxidative modification of target molecules in vivo is lacking. We conducted a study to determine whether the production of F2-isoprostanes, which are novel products of lipid peroxidation, is enhanced in persons who smoke. We measured the levels of free F2-isoprostanes in plasma, the levels of F2-isoprostanes esterified to plasma lipids, and the urinary excretion of metabolites of F2-isoprostanes in 10 smokers and 10 nonsmokers matched for age and sex. The short-term effects of smoking (three cigarettes smoked over 30 minutes) and the effects of two weeks of abstinence from smoking on levels of F2-isoprostanes in the circulation were also determined in the smokers. Plasma levels of free and esterified F2-isoprostanes were significantly higher in the smokers (242 +/- 147 and 574 +/- 217 pmol per liter, respectively) than in the nonsmokers (103 +/- 19 and 345 +/- 65 pmol per liter; P = 0.02 for free F2-isoprostanes and P = 0.03 for esterified F2-isoprostanes). Smoking had no short-term effects on the circulating levels of F2-isoprostanes. However, the levels of free and esterified F2-isoprostanes fell significantly after two weeks of abstinence from smoking (250 +/- 156 and 624 +/- 214 pmol per liter, respectively, before the cessation of smoking, as compared with 156 +/- 67 and 469 +/- 108 pmol per liter after two weeks' cessation; P = 0.03 for free F2-isoprostanes and P = 0.02 for esterified F2-isoprostanes). The increased levels of F2-isoprostanes in the circulation of persons who smoke support the hypothesis that smoking can cause the oxidative modification of important biologic molecules in vivo.

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Passive smoking and impaired endothelium-dependent arterial dilatation in healthy young adults.

Gavin Robinson, J Deanfield, M R E McCredie … (1996)

Passive smoking has been linked to an increased risk of dying from atherosclerotic heart disease. Since endothelial dysfunction is an early feature of atherogenesis and occurs in young adults who actively smoke cigarettes, we hypothesized that passive smoking might also be associated with endothelial damage in healthy young-adult nonsmokers. We studied 78 healthy subjects (39 men and 39 women) 15 to 30 years of age (mean +/- SD, 22 +/- 4): 26 control subjects who had never smoked or had regular exposure to environmental tobacco smoke, 26 who had never smoked but had been exposed to environmental tobacco smoke for at least one hour daily for three or more years, and 26 active smokers. Using ultrasonography, we measured the brachial-artery diameter under base-line conditions, during reactive hyperemia (with flow increase causing endothelium-dependent dilatation), and after sublingual administration of nitroglycerin (an endothelium-independent dilator). Flow-mediated dilatation was observed in all control subjects (8.2 +/- 3.1 percent; range, 2.1 to 16.7) but was significantly impaired in the passive smokers (3.1 +/- 2.7 percent; range, 0 to 9; P < 0.001 for the comparison with the controls) and in the active smokers (4.4 +/- 3.1 percent; range, 0 to 10; P < 0.001 for the comparison with the controls; P = 0.48 for the comparison with the passive smokers). In the passive smokers, there was an inverse relation between the intensity of exposure to tobacco smoke and flow-mediated dilatation (r = -0.67, P < 0.001). In contrast, dilatation induced by nitroglycerin was similar in all groups. Passive smoking is associated with dose-related impairment of endothelium-dependent dilatation in healthy young adults, suggesting early arterial damage.

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Author and article information

Journal

Journal ID (publisher-id): NEC

Journal ID (nlm-ta): Nephron Clin Pract

Journal ID (doi): 10.1159/issn.1660-2110

Title: Nephron Clinical Practice

Publisher: S. Karger AG

ISSN (Electronic): 1660-2110

Publication date Subscription-year: 2006

Publication date (Print): July 2006

Publication date (Electronic): 24 April 2006

Volume: 103

Issue: 4

Pages: c121-c128

Affiliations

^aDepartment of Nephrology Transplantology and Internal Medicine, Medical University, Gdańsk, Poland; ^bDivision of Nephrology and Dialysis, Department of Medicine III, University Hospital, Vienna, Austria

Article

Publisher ID: 92908 Other ID: Nephron Clin Pract 2006;103:c121–c128

DOI: 10.1159/000092908

PubMed ID: 16636579

SO-VID: 9417a73c-67fd-4b52-a647-3b43f3ff7d31

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Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

History

Date received : 05 April 2005

Date accepted : 30 August 2005

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Tables: 6, References: 35, Pages: 1

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Smoking as a Risk Factor for Renal Injury in Essential Hypertension

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Abstract

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Karger: Nephrology

Most cited references 26

Blood pressure and end-stage renal disease in men.

Increase in circulating products of lipid peroxidation (F2-isoprostanes) in smokers. Smoking as a cause of oxidative damage.

Passive smoking and impaired endothelium-dependent arterial dilatation in healthy young adults.

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