Cigarette smoking and vascular pathology in renal biopsies

In recent years cigarette smoking has been identified as a progression factor in chronic nephropathies such as glomerulonephritis or diabetic nephropathy. The exact pathomechanism of nicotine-induced renal damage is, however, unknown. Autopsy studies and functional investigations suggest that the renal vasculature is primarily affected by smoking.

Renal vascular pathology, that is, glomerulosclerosis, hyalinosis of arterioles and myointimal hyperplasia of small arteries, was determined in 135 biopsies of patients over thirty years of age. A questionnaire about smoking habits was returned by 107 of the patients. For glomerular sclerosis the percentage of sclerotic glomeruli was determined, whereas arteriolar hyalinosis and myointimal hyperplasia of small arteries were described as present or absent without further quantification. A univariate analysis was performed for existence of vascular changes and ever-smoking status. In addition, a multivariate analysis for glomerular sclerosis and logistic regression analysis for arteriolar hyalinosis and myointimal hyperplasia and the variables ever-smoking, age, body mass index, creatinine clearance, blood pressure and lipids were performed.

Creatinine clearance was comparable for nonsmokers, ex-smokers and smokers. Frequency of myointimal hyperplasia of small arteries was twice as high in ever-smokers as compared to nonsmokers (50% vs. 25.5%, P < 0.01). Arteriolar hyalinosis was detected in 23.5% of nonsmokers and in 35.7% of smokers, showing a trend toward hyalinosis in ever-smokers (P=0.20). Glomerular sclerosis was found in 62.7% of nonsmokers and in 69.6% of ever-smokers. Logistic regression analysis confirmed an association between ever-smoking and myointimal hyperplasia (P < 0.01). This association also was present in males and patients over fifty years of age, but not in younger patients and females.

In patients with renal, especially glomerular disease, cigarette smoking exhibits its deleterious effect on the kidneys primarily through damage of small interlobular arteries.