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Background Cigarette smoking is an important modifiable risk factor in kidney disease progression. Although long-term smoking has been associated with chronic kidney disease (CKD), its effect on kidney function in early stages has not been clarified. Objective To detect the early effects of smoking either active or passive on kidney functions. Methodology The current study was comparative cross sectional study conducted on 280 participants, 140 were non‑smokers and 140 were smokers (70 passive smokers and 70 active smokers). The two groups were comparable in terms of all parameters. We investigated the possible effects of smoking on kidney functions using both serum kidney function tests especially; serum urea, serum creatinine, serum cotinine levels and detection of albumin in urine. Smoking history, full Laboratory investigations, Ventilatory function test including (FEV1/FVC, FEV1, FEF 25–75%, VC and FVC) were done. Results Serum urea, serum creatinine, serum cotinine levels and urinary albumin were statistically significant higher in smokers group in comparison to nonsmokers, also the serum cotinine levels and urinary albumin were statistically significant in active smokers in comparison to passive smokers. There were positive correlations between the level of urinary albumin and pack/year (r = 0.9, p<0.05), smoking index (r = 0.9, p<0.05), smoking duration (r = 0.4, p<0.05), and serum cotinine (r = 0.6, p<0.050) with good statistical significance. The most significant predictive risk factors of microalbuminuria among smokers group in descending orders were active smoking, passive smoking, age and serum cotinine level. Conclusion Both active and passive smoking, especially among heavy smokers, is a significant risk factor for microalbuminuria. This finding increase the importance of early cessation of smoking in order to minimize early renal affection among healthy smokers that may not be discovered by routine renal function tests.

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Background Activated platelets and platelet indices have a vital role in bronchial hyper-responsiveness, bronchoconstriction, bronchial inflammation, airway remodeling, angiogenesis, allergic reactions, and repair and renewal of tissues; platelets contain mediators that lead to inflammatory response. AimThe aim was to assess the use of platelet indices [mean platelet volume (MPV), platelet distribution width (PDW), plateletcrit (PCT), and platelet large cell ratio (PLCR)] as cheap and readily available biomarkers for bronchial asthma exacerbation.Patients and methods A case-control study involved 45 bronchial asthma female patients during both stable and exacerbation phases, and 45 age-matched healthy female patients as a control group. Measurements of platelet counts, MPV, PDW, PCT, PLCR, C-reactive protein (CRP), spirometric indices, and arterial blood gases were performed for all participants.Results The MPV and PDW were significantly lower, whereas the PCT and PLCR were considerably higher in exacerbation phase compared with stable phase and in stable phase in comparison with controls (P<0.001). The MPV and PDW were negatively correlated with white blood cells, PaCO 2 , symptoms duration, and hs-CRP (high sensitive), with positive correlation with forced expiratory volume in the first second and PaO 2 (P<0.001). PCT and PLCR were positively correlated with white blood cells, PaO 2 , and symptoms duration, and negatively correlated with forced expiratory volume in the first second, symptoms duration, and hs-CRP (P<0.001). ConclusionThe platelet indices were altered in exacerbation phase compared with stable phase and control group. Therefore, clinicians should not ignore interpreting platelet indices during asthma exacerbation, especially as these tests are simple, readily available, and of lower cost. It appears that measurement of the platelet indices is a valuable indicator of asthma severity/activity and appears as a useful screening test for asthma exacerbation.