| 초록 |
Acute Kidney Injury (AKI), biochemically characterized as abnormality in kidney function test which causes accumulation of creatinine and blood urea and functionally by a rapid decline in the glomerular filtration rate (GFR). Oxidative stress plays an important role in the development vascular complications in type 2 diabetes. Oxidant derived tissue injury occurs when production of oxidants or reactive oxygen species (ROS) exceeds local antioxidant capacity. Inflammatory cytokines such as tumor necrosis factor-alpha (TNF-a) and interleukin (IL-6) and various growth factors in renal cells modulate the local response are responsible for AKI. 10 ml of fasting venous blood was collected from the anticubital vein in a plain, fluoride and EDTA vacutainers. The blood sample was centrifuged and stored at 40 C for biochemical and immunological investigations. The study group consisted of n=50 healthy individuals (Group I), n=25 Type II Diabetic without AKI (Group II), n=25 Type II diabetic with AKI (Group III) of either sex aged between 50-65 years. Type II Diabetic presented with clinical signs and symptoms of Acute Kidney Injury without Nephropathy. Serum levels of inflammatory markers (IL-6 & TNF-a), antioxidants (Glutathione reductase), plasma malondialdehyde (MDA), hs-CRP were estimated. Concentration of inflammatory molecules such as TNF-a 9.32±1.08, 14.04±1.42 and 36.56±10.50; IL-6 9.24±1.20, 14.14±1.50 and 36.76±11.56; hs-CRP 0.90±1.10, 1.96±0.50 and 2.18±0.90 was significantly elevated in Group III. GSH were significantly lower in both the groups of Diabetic with and without AKI when compared to controls. 7.10±0.58, 6.90±0.70 and 5.80±0.80. Mean value of total MDA 2.32±0.98, 8.68±2.50 and 9.80±2.72 was significantly more in Group III as compared to Group I and Group II. Results of the present study indicates that inflammatory markers and oxidative stress are increased with decreased antioxidant defense levels in patients with AKI due to DM induced oxidative stress. |