impact of oxidative stress on the activity of adenosine deaminase and its isoenzymes in nephropathy patients from Wasit-Iraq

Abstract

Diabetes mellitus is a group of metabolic disorders that share with symptoms of hyperglycemia led to elevated free radical activity. Hyperglycemia is linked to a higher level of (ADA), which is one of the factors that cause oxidative stress by creating reactive oxygen species (ROS), that leads to insulin resistance. This study aimed to determine the relationship between serum total adenosine deaminase(TADA) and its isoenzyme (ADA1and ADA2) with the progression of nephropathy in patients with type 2 diabetes using a case-control study from Wasit-Iraq. In addition, we aimed to find if there is a link between oxidative stress with TADA and its isoenzyme. The One-way ANOVA was used to compare the mean values of fasting plasma sugar (FPS), total oxidant status (TOS), total antioxidant status (TAS), malondialdehyde (MDA), microalbumin in urine, HbA1c, and TADA, ADA1, ADA2 between the three studied groups (Control(C), diabetic patients(DM), and diabetic nephropathy patient(DN). The results of our study revealed that there was a highly significant increase in TADA and its isoenzyme activities of DM and DN groups, as compared to the C group.

Assessment the Role of Kidney Function and Total Proteins in Patients with Diabetic Nephropathy in Kirkuk City/ Iraq

“…The findings in Table 1 reveal a notable elevation (P ≤ 0.05) in the levels of urea in patients with diabetes, as it reached (43.82 ± 9.87) mg / 100 ml, compared to the control group amounted to (29.45± 4.27) mg / 100 ml, and these results agreed with the results of [21] with regard to the level of urea in the blood, which found an increase in the average concentration of blood urea in diabetics compared to the healthy group, According to the age groups in Table 2, the results indicate because there are no discernible variations between the different age groups among patients with diabetes, as the concentration of urea in the first age group (35-45) amounted to (39.56 ± 8.44) mg / 100 ml, compared to in the second age group (46-55) amounted to ( 46.35 ± 9.87) mg / 100 ml, in the third age group (56-65) amounted to (43.30 ± 10.35) mg / 100 ml, and in the fourth age group (66-75) amounted to (46.05± 9.92 (mg/100 ml). Because the concentration of urea in serum demonstrates the ratio between the urea generated by the liver and urea elimination in the urine by the renal system, an excess of urea in plasma may be caused by raised urea manufacturing, reduced urea elimination, or an amalgamation of the two; the highest concentrations occur in the setting of decreased the urea removal in the urine because of chronic kidney disease and the associated significant decrease in glomerular filtration rate.…”