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 of 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-) and interleukin (IL-6) and various growth factors in renal cells modulate the local response are responsible for AKI.
Material and Methods: 10 ml of fasting venous blood was collected from the antecubital 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-), antioxidants (Glutathione reductase), plasma malondialdehyde (MDA), hs-CRP were estimated.
Results: Concentration of inflammatory molecules such as TNF- 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.
Conclusion: 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.