ABSTRACT
Background: The acute effects of cigarette smoking in smokers include dyslipidemia and impaired insulin action that leads to abnormal glucose metabolism. Both dyslipidemia and insulin resistance are well-established major risk factor for cardiovascular disease. Aims & Objective: To ascertain the prevalence of several degrees of glucose abnormalities in smokers and to assess the impact of active tobacco smoking on lipids profile in adult male population. Material and Methods: A cross-sectional study was conducted with one hundred and fifty two active adult male smokers defined by persons smoking cigarettes over 2 pack years and fifty age and Body Mass Index (BMI) matched healthy control. Smokers were classified into mild to moderate (Group I) and severe (Group II) based on the number of pack years as 2 – 10 and more than 10 respectively. Glucose tolerance was assessed according to American Diabetes Association (ADA) guidelines and standard methods were adopted to check the lipid levels. Data analyses were performed with the SPSS 15.0 statistical software. Results: An abnormal glucose metabolism was diagnosed in 66% (95% confidence interval [CI], 61.4%-71.6%) of the smokers. The mean HOMA-IR (Homeostasis model assessment-insulin resistance) in smokers was 6.8 + 3.1. Decreasing glucose tolerance was associated with insulin resistance i.e. from normal glucose tolerance condition through IGT, IFG to diabetic, the HOMA IR progressively increased (4.9 + 2.1, 6.7 + 4.2, 7.4 + 3.1 and 8.9 + 3.7 respectively). Atherogenic index as indicated by total cholesterol/HDL cholesterol and LDL cholesterol/HDL cholesterol ratio was significantly elevated in both the smoker groups as compared to non-smokers. According to the Adult Treatment Program III criteria, the metabolic syndrome was diagnosed in 44.07% (95% CI, 35.9%-47.3%) of the smokers. In fact only 10 participants (6%, 95% CI, 5.4% - 7.1%) showed good control of cardiovascular risk factors. Conclusion: Abnormalities in lipid profile and glucose tolerance are directly correlated with smoking pack years in this study. Intense education program about adverse health events of smoking should be under taken through all means.
ABSTRACT
Diabetic nephropathy is the leading cause of kidney disease in patients starting renal replacement therapy and affects ~30% of type 1 and type 2 diabetic patients. This review focuses on the progression and pathophysiological aspects of the condition. The natural history of diabetic nephropathy is characterized by specific renal morphological and functional alterations. Features of early diabetic renal changes are microalbuminuria (30-300mg/day), glomerular hyperfiltration, glomerular and renal hypertrophy, increased basement membrane thickness, and mesangial expansion with the accumulation of extracellular matrix proteins such as collagen, fibronectin, and laminin. Advanced diabetic nephropathy is characterized by macroalbuminuria ( >300mg/day), a progressive decline in glomerular filtration rate, decreasing creatinine clearance, glomerulosclerosis, and interstitial fibrosis. Although poor glycemic control is an important risk factor, glycemia does not fully explain why only a subset of diabetic patients progress to end stage renal disease. Several decades of extensive research has elucidated various pathways to be implicated in the development of diabetic kidney disease such as systemic and glomerular hypertension, advanced glycation endproducts and the aldose reductase system. Furthermore, hemodynamic factors, the reninangiotensin system, the endothelin system, the intracellular signaling molecule protein kinase C, transforming growth factor-ß, growth hormone, insulin like growth factors, vascular endothelial growth factor, and platelet-derived growth factor are believed to be involved in the pathogenesis. Thus, there are clearly many points at which therapeutic approaches could be tried to provide renoprotection in diabetes. It is likely that due to its complexity, targeting multiple points in altered metabolism in the diabetic kidney will be more successful in attenuating the development of diabetic nephropathy, rather than a single approach.