Evaluation of the Relationship Between Microalbuminuria and Urine Ischemia-Modified Albumin Levels in Patients with Diabetic Nephropathy.

INTRODUCTION: Ischemia-modified albumin (IMA) is a marker which can be associated with oxidative stress in various ischemic and non-ischemic processes. Oxidative stress plays roles in diabetes mellitus, its complications and pathogenesis. Serum IMA levels are examined in various clinical events. However, urine IMA levels have not yet been evaluated in diabetic patients. In this study, we aim to examine the relationship between metabolic features and urine microalbuminuria levels of diabetic patients and their urine IMA levels. MATERIALS AND METHODS: There were totally 50 type 2 diabetic patients in the study at the Mevlana University Hospital. Patients with cerebrovascular disease, acute myocardial infarction, hemodialysis patients with end stage chronic renal failure, pulmonary embolism, and malignant disease were excluded from the study. Metabolic features, urine IMA levels and cardiological parameters of patients were evaluated. RESULTS: Mean age of patients was 59 ± 9 years, 20 of them (40%) were male and 30 of them (60%) were female. There were six patients with albuminuria value of <0.03 mg/g (normal), there were 39 patients with microalbuminuria value of 0.03-0.3 mg/g and there were five patients with macroalbuminuria of >0.3 mg/g. According to the analysis of patients with microalbuminuria (n = 39), there was no correlation between IMA levels and numerical demographic data, albuminuria, glucose, HbA1c, lipid profile, creatinine, uric acid, hematological parameters. DISCUSSION: Conclusively, there was no relationship between urine IMA levels and microalbuminuria related to the diabetic nephropathy. These findings can be associated with urinary excretion mechanisms of IMA.

Efficacy of different therapeutic regimens on hepatic osteodystrophy in chronic viral liver disease.

BACKGROUND AND AIMS: Metabolic bone disease is common in patients with chronic liver disease. Comparative studies on the efficacies of antiosteoporotic agents in hepatic osteodystrophy have not been conducted yet. The aim of this study was to evaluate the safety and efficacy of different therapeutic regimens on hepatic osteodystrophy. METHODS: Eighty-one patients (mean age 48.9 ± 10 years; 50 cases with chronic viral hepatitis and 31 patients with cirrhosis) were enrolled in the study. Treatment groups consisted of 61 patients who had reduced T scores in at least one region, selected randomly and treated for 1 year with vitamin D 400 IU, calcitonin 200 IU, alendronate 10 mg, alendronate 70 mg, or risedronate 5 mg. An untreated group consisting of 20 patients who had no reduction in T scores was followed up during the study period. RESULTS: No significant adverse effects, including esophageal variceal hemorrhage, were detected. According to the T score at the end of the first year compared with baseline, significant improvements in bone mineral density were observed at all regions with alendronate 70 mg; improvements at the lumbar spine (LS) and distal radius regions with alendronate 10 mg; at the LS and distal radius regions with risedronate; at the LS region with calcitonin; and at the femoral neck region with vitamin D. CONCLUSION: All therapeutic regimens seemed to be safe, and oral biphosphonates were the most effective in preventing both cortical and trabecular bone loss in patients with chronic viral liver disease. Larger studies with longer follow-up are warranted in hepatic osteodystrophy of chronic viral liver diseases.