Effect of Heavy Cigarette Smoking on Renal and Myocardial Arterioles

Black, Henry R.; Zeevi, Gary R.; Silten, Robert M.; Smith, Greg T.

doi:10.1159/000183005

Cited by 62 publications

(29 citation statements)

References 22 publications

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“…This hypothesis is supported by autopsy studies (31,32) demonstrating morphopathologic changes in the renal microvasculature in cigarette smokers. In addition, glomerular hyperfiltration has been demonstrated to be a predictor of GBM thickening in adolescents with type 1 diabetes (33).…”

Section: Discussionmentioning

confidence: 68%

Effects of Cigarette Smoking on Glomerular Structure and Function in Type 2 Diabetic Patients

Baggio

Budakovic

Vestra

et al. 2002

Journal of the American Society of Nephrology

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Abstract. Prospective studies have established smoking as an independent risk factor for diabetic nephropathy, suggesting an adverse effect of smoking on glomerular structure and function. To test this hypothesis, this study evaluated GFR, metabolic profile, and smoking habits in 96 patients with type 2 diabetes and abnormal albumin excretion rate (AER). All patients underwent percutaneous kidney biopsy: mesangial fractional volume [Vv (mes/glom)] and glomerular basement membrane (GBM) width were estimated by electron microscopic morphometric analysis; interstitial fibrosis was estimated semiquantitatively by light microscopy. Forty-eight patients were smokers. Compared with nonsmokers, smokers had higher values of HbA 1c (P ϭ 0.002), AER (P ϭ 0.026), GFR (P ϭ 0.004), and GBM width (P ϭ 0.002); moreover, GFR was higher in current smokers than in former smokers (P ϭ 0.001), and GBM width was related to heavy smoking (F ϭ 5.4; P ϭ 0.006). Multiple linear regression analyses revealed that HbA 1c was associated with fasting blood glucose (␤ coef ϭ 0.52; P Ͻ 0.001), smoking habit (␤ coef ϭ 0.31; P Ͻ 0.001), insulin therapy (␤ coef ϭ 0.22; P ϭ 0.012), and male gender (␤ coef ϭ Ϫ0.20; P ϭ 0.020); AER was related to Vv (mes/glom) (␤ coef ϭ 0.32; P ϭ 0.003), GBM width (␤ coef ϭ 0.28; P ϭ 0.016), and interaction between smoking habit and HbA 1c (␤ coef ϭ 0.24; P ϭ 0.040). GFR was negatively correlated with Vv (mes/glom) (␤ coef ϭ Ϫ0.57; P Ͻ 0.001) and age (␤ coef ϭ Ϫ0.29; P ϭ 0.001) and positively correlated with GBM width (␤ coef ϭ 0.27; P ϭ 0.012), heavy current smoking (␤ coef ϭ 0.24; P ϭ 0.028), and HbA 1c (␤ coef ϭ 0.28; P ϭ 0.040); GBM width was explained by Vv (mes/ glom) (␤ coef ϭ 0.53; P Ͻ 0.001), interaction between heavy smoking and HbA 1c levels (␤ coef ϭ 0.25; P ϭ 0.003), and diabetes duration (␤ coef ϭ 0.23; P ϭ 0.010). Smoking habit did not affect the index of interstitial fibrosis. In conclusion, cigarette smoking affects glomerular structure and function in type 2 diabetes and may be an important factor for the onset and progression of diabetic nephropathy.Several observations suggest that the kidney, in addition to other peripheral vascular beds, is another target organ of smoking. Acute and chronic smoking has been documented to be associated with renal functional impairment, probably mediated by smoking-induced changes in vasoactive hormones (1-3). Cross-sectional and longitudinal studies have shown that smoking has an adverse effect on renal outcome in essential hypertension, primary and secondary nephropathies, and on graft and patient survival in renal transplant recipients (4 -9). In diabetic renal disease, smoking emerged as an independent risk factor for the onset of microalbuminuria, the acceleration in the rate of progression from microalbuminuria to proteinuria, and subsequent renal failure both in type 1 and type 2 diabetes (10,11).The presence of microalbuminuria is the earliest clinical marker of renal injury in diabetic nephropathy; it is therefore conceivable that the documented associati...

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Section: Discussionmentioning

confidence: 68%

Effects of Cigarette Smoking on Glomerular Structure and Function in Type 2 Diabetic Patients

Baggio

Budakovic

Vestra

et al. 2002

Journal of the American Society of Nephrology

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“…This is consistent with the literature that states that smoking has little effect on arteriolar diameter or causes only mild arteriolar narrowing rather than widening. 36,37 The strengths of the present investigation are the long observation period of 20 years and the unique homogeneity of the study population. Structural changes in the retinal vasculature are found both in hypertensive patients and in the normal ageing population.…”

Section: Discussionmentioning

confidence: 99%

Blood pressure development and hypertensive retinopathy: 20-year follow-up of middle-aged normotensive and hypertensive men

Gudmundsdottir¹,

Taarnhøj

Strand

et al. 2009

J Hum Hypertens

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Screening for hypertensive organ damage is important in assessing cardiovascular risk in hypertensive individuals. In a 20-year follow-up of normotensive and hypertensive men, signs of end-organ damage were examined, focusing on hypertensive retinopathy. In all, 56 of the original 79 men were reexamined for hypertensive organ damage, including by digital fundus photography. The diameters of the central retinal artery equivalent (CRAE) and vein were estimated and the artery-to-vein diameter ratio calculated. Components of metabolic syndrome were assessed. Fifty percent of the normotensive men developed hypertension during follow-up. Significant differences appeared in CRAE between the different blood pressure groups (P ¼ 0.025) while no differences were observed for other markers of hypertensive organ damage. There were significant relationships between CRAE and blood pressure at baseline (r ¼ -0.466, P ¼ 0.001) and at follow-up (r ¼ -0.508, Po0.001). A linear decrease in CRAE was observed with increasing number of components of the metabolic syndrome (b ¼ -3.947, R 2 ¼ 0.105, P ¼ 0.023). Retinal vascular diameters were closely linked to blood pressures and risk factors of the metabolic syndrome. The diversity in the development of hypertensive organ damage, with changes in retinal microvasculature preceding other signs of damage, should encourage more liberal use of fundus photography in assessing cardiovascular risk in hypertensive individuals.

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“…Evidence of thickening of the walls of the renal arterioles and small arteries after nicotine abuse has been found during autopsies of patients with renal disease 33 and subjects without known renal or vascular disease. 34 Moreover, animal experimental evidence indicates that cigarette smoking enhanced the permeability of the endothelial monolayers 35 and an elevation of intraglomerular capillary pressure, which is associated with an elevated GFR. It was reported that there is an association between an elevated GFR and a high-normal albuminuria in the nondiabetic population.…”

Section: Discussionmentioning

confidence: 99%

C-reactive protein is associated with cigarette smoking-induced hyperfiltration and proteinuria in an apparently healthy population

et al. 2010

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Although cigarette smoking is known to be an important risk factor for renal disease, the mechanism by which smoking induces progressive renal disease in a healthy population has not been established. We hypothesized that oxidative stress (measured as 8-iso-prostaglandin F 2a , 8-iso-PGF2a), inflammation (highly sensitive C-reactive protein (CRP), hs-CRP) and nitric oxide may be associated with an alteration in the estimated glomerular filtration rate (eGFR) and proteinuria in otherwise healthy smokers. A total of 649 eligible subjects were classified according to their smoking status. Plasma NOx was measured using ozone-based chemiluminescence, urinary 8-iso-PGF2a was measured using enzyme immunoassay and serum hs-CRP was measured using a latex aggregation nephelometry method. The levels of 8-iso-PGF2a and hs-CRP increased in current smokers (P¼0.001 and P¼0.029, respectively), although there was not an increase in the NOx level. The prevalence of a high eGFR increased in light smokers (odds ratio (OR) 1.15 (95% confidence interval (CI), 0.61-2.17)) and heavy smokers (OR 2.33 (95% CI, 1.06-5.10)) when compared with non-and past smokers (P for trend¼0.024). The multivariable-adjusted mean values of the eGFR in current smokers, reported from the lowest to the highest quintiles of hs-CRP levels, were 82.1, 85.1, 86.4 and 88.5 ml per min per 1.73 m 2 (P for trend¼0.027). The mean values of proteinuria were 28.6, 34.6, 37.2 and 39.5 mg g À1 creatinine (P for trend¼0.003). The correlation coefficient between hs-CRP and eGFR was increased significantly (P¼0.03) across non-(r¼0.03), past (r¼À0.17), light (r¼0.13) and heavy smokers (r¼0.31). In conclusion, cigarette smoking is a risk factor for renal function alteration in healthy smokers and is characterized by a high eGFR and a high urinary protein associated with an increase in the hs-CRP. This finding suggests that hs-CRP may help mediate the alteration of renal function in smokers.

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Effect of Heavy Cigarette Smoking on Renal and Myocardial Arterioles

Cited by 62 publications

References 22 publications

Effects of Cigarette Smoking on Glomerular Structure and Function in Type 2 Diabetic Patients

Effects of Cigarette Smoking on Glomerular Structure and Function in Type 2 Diabetic Patients

Blood pressure development and hypertensive retinopathy: 20-year follow-up of middle-aged normotensive and hypertensive men

C-reactive protein is associated with cigarette smoking-induced hyperfiltration and proteinuria in an apparently healthy population

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