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https://www.selleckchem.com/products/Roscovitine.html Dysregulated vitamin D metabolism is one of the most important issues in chronic kidney disease- mineral and bone disorder (CKD-MBD). Patients with end-stage kidney disease (ESKD) receive large amounts of calcitriol, i.e., 1,25 -dihydroxy vitamin D [1-25(OH)2D], for suppression of parathyroid hormone (PTH). The aim of this study was to evaluate the 1-25(OH)2D status in maintenance hemodialysis patients and its correlation with 25(OH) D level and calcitriol consumption and to determine whether the usual practice of administrating large amounts of calcitriol for suppression of PTH may lead to toxic serum levels. One hundred and fifty-six maintenance hemodialysis patients were enrolled. Demographic data, comorbid conditions and history of medication use (cumulative and current doses) were retrieved from Hemodialysis Data Processor Software previously designed for our center. Predialysis serum samples were measured for serum levels of 25(OH)D and 1-25(OH)2D accompanying by markers of mineral bone metabolism acontinued, though we are not yet aware of the 1,25(OH)2D status at the cellular levels. Data on the effects of melatonin administration on metabolic parameters in patients with diabetic nephropathy (DN) is limited and controversial. This study was performed to analyze the effects of melatonin administration on metabolic status in patients with DN. This randomized, double blind, placebo-controlled clinical trial was performed on 60 patients with DN. Patients were randomly assigned into two groups to take either 10 mg/d of melatonin (n = 30) or placebo (n = 30) for 12 weeks. Fasting blood samples were taken at baseline and 12 weeks after intervention to quantify metabolic parameters. Melatonin administration significantly reduced plasma fasting glucose (β = -10.64 mg/dL; 95% CI -20.37 to -0.90; P < .05), insulin (β = -2.37 μIU/mL, 95% CI -3.33 to -1.41; P < .001), insulin resistance (β = -0.67, 95% CI -0.98 to -0.3

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