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Vitamin D is claimed to have an adjuvant effect on glycemic control by dual action on pancreatic β-cells and insulin resistance. The aim of this study was to assess the possible effect of short-term alfacalcidol supply on glycemic control in type 2 diabetic hemodialysis (HD) patients. Twenty type 2 diabetic HD patients (using diet and oral drugs but not insulin) were randomly selected from our dialysis unit as well as 20 non-diabetic HD patients as control. A third group of 12 healthy subjects were studied as well. All three groups were similar in age, sex, and body mass index. Oral alfacalcidol therapy was administrated daily as recommended by Kidney Disease Outcomes Quality Initiative (K/DOQI) guidelines for 12 weeks guided by monthly serum phosphorus and Cax PO4 product. Corrected total calcium, phosphorus, intact parathyroid hormone, 25-hydroxy vitamin D (25[OH]D), and glucoparameters (fasting blood glucose, glycated hemoglobin [HbA1c%], insulin resistance by homeostatic model assessment, and β-cell function by HOMA-β%) were measured under basal conditions and after 3 months of therapy. 25(OH)D was non-significantly lower in diabetic than non-diabetic HD patients, but significantly lower than healthy subjects at the start of the study. However, vitamin D level increased significantly after 3 months of trial, although the levels did not reach normal values. This vitamin D rise was associated with highly significant improvement in concentrations of fasting blood sugar (FBS), fasting insulin, HbA1c%, and HOMA-β-cell function in diabetic and non-diabetic controls. However, there was a significant rise in insulin resistance after treatment. The percentage of change was evident more in diabetics regarding FBS and 25(OH)D concentration. Adjustment of 25(OH)D level in type 2 diabetic prevalent HD patients may improve, at least with short-term therapy, glycemic control mainly through improving β-cell function.

Background: Hyperuricemia is commonly associated with hypertension. Also, it is well known to coincide with the metabolic syndrome but is still not recognized as a risk factor. So, we aimed to evaluate hyperuricemia among a sample of hypertensive Egyptians with normal renal function. Methods: this study was performed on 303 hypertensive patients aged 30-69 years. Patients were divided into 2 groups according to the level of uric acid: group 1 composed of 168 hypertensive hyperuricemic patient sand group2 composed of 135 hypertensive normouricemic patients. All patients were subjected to complete medical history and detailed clinical examination including body mass index (BMI), complete blood count (CBC), serum creatinine, BUN, FBS, cholesterol, triglycerides, uric acid, sodium, potassium, urinary uric acid, urinary creatinine, urinary uric acid to creatinine ratio and fractional excretion of uric acid(FEUA). Results: The overall prevalence of hyperuricemia was 55.4%. Uric acid correlated significantly with age (p<0.05). BMI was significantly higher in group1 than in group 2(p<0.05), and there was a significant positive correlation between serum uric acid and BMI (p<0.01).Serum triglycerides and cholesterol were significantly higher in group 1than in group 2 (p<0.05for both) denoting risky metabolic effects. Serum uric acid correlated significantly with systolic blood pressure (p<0.05), but not with diastolic blood pressure. No significant difference found between group 1 and group 2 as regards SBP, DBP or blood pressure control(all p values>0.05). Serum uric acid found to correlate significantly (p<0.001) with urinary uric acid, urinary creatinine and negatively with FEUA denoting early tubular defect of the kidney. Also, Urinary uric acid, urinary creatinine and urinary uric acid/creatinine ratio were higher in group 1than in group 2 (p values were<0.001, <0.001 and <0.05 respectively). FEUA was found to be significantly lower in group 1 than in group 2 (p<0.01). We found, also, that serum sodium level was significantly higher in the hyperuricemic group than in the normouricemic group (p<0.001) denoting the role of Na + in the development of hypertension and defective renal excretion of uric acid. Conclusion: We conclude that the incidence hyperuricemia in our sample of Egyptian hypertensive patients was (55.4%). Impaired renal clearance of uric acid occurs before deterioration of GFR. Serum uric acid should be measured in all cases of hypertension together with BMI, total cholesterol, triglycerides and should be treated to avoid consequent metabolic complications. Hypertensive patients with hyperuricemia should be warned strictly of high sodium diet.