renal damage). Current smokers also had significantly abnormal glomerular filtration rates (increased or decreased) compared to nonsmokers. Former smokers had a risk for both events that fell between that of current smokers and nonsmokers, suggesting some degree of reversibility of the effects of smoking. Another large population-based, cross-sectional study (Halimi et al., 2000) of subjects without known renal disease showed that current and former smokers, even after adjusting for diagnoses of diabetes and hypertension, had greater risks for proteinuria by dipstick testing compared to nonsmokers (RR=2–3). Current male smokers in this study also had a higher creatinine clearance than nonsmokers, suggesting a degree of glomerular hyperfiltration.

Many mechanisms of smoking-attributable nephrotoxicity have been postulated including increased sympathetic nervous system activity, transient blood pressure elevation, endothelial cell damage and dysfunction of renal vasculature, direct toxic effects on tublar cells, and oxidative stress (Orth, 2000; Pinto-Sietsma et al., 2000).


It has been reported that up to 80% of patients with schizophrenia smoke cigarettes (McCreadie and Kelly, 2000; Simpson et al., 1999). The rate of smoking among schizophrenics is also higher than rates among other mentally ill patients (Leonard et al., 2000; Tidey et al., 1999). Many different reasons for the high rate of smoking among schizophrenics have been postulated including “self-medication” of the symptoms of schizophrenia, attenuation of the adverse effects of antipsychotic medication, social factors of schizophrenic patients that predispose them to smoke, or genetic vulnerability for both conditions (reviewed in Levin and Rezvani, 2000; Tidey et al., 1999). Nicotine may attenuate the negative symptoms of schizophrenia by stimulating the release of dopamine and glutamate (Dursun and Kutcher, 1999). Nicotine has also been found to stabilize sensory deficits found in schizophrenia including smooth eye tracking movements and auditory gating, possibly through decreased expression of the α-7 nicotinic acetylcholine receptor (Durson and Kutcher, 1999; Leonard et al., 2000). Furthermore, cigarette smoking has been found to reduce monoamine oxidase activity, which is thought to increase vulnerability to the development of schizophrenia (Fowler et al., 1996; Simpson et al., 1999).


Depression has consistently been linked with smoking (Breslau and Johnson, 2000; Glassman, 1993). Studies have demonstrated that a history

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