Interleukin-18 expression in PBMC of type 2 diabetes mellitus patients with early kidney damage

Abstract

Objective To investigate the correlation between the expression of mononuclear cells Interleukin-18(IL-18)and early renal damage in diabetic patients. Methods 480 cases with type 2 diabetes mellitus(T2DM)in our hospital from Jan. 2010 to Dec. 2012 were selected. According to urine albumin excretion rate, They were randomly divided into diabetic group, micro proteinuria group, and proteinuria group. 160 cases of normal people were selected as the control group. Glycosylated hemoglobin, serum cholesterol, serum triglycerides, serum creatinine, blood urea nitrogen. 2 h postprandial blood glucose and urine protein were detected. After mononuclear cells being isolated and cultured for 12 h and 24 h, IL-18 was detected. -137G/C and -607C/A gene polymorphism were detected. Results Normal group were significantly lower than diabetes group, micro proteinuria group, and proteinuria group(P<0.01)in BMI, 2 h postprandial blood sugar, cholesterol, glycosylated protein, urea nitrogen and serum creatinine index. Micro proteinuria group and proteinuria group were higher than diabetic group in 2 h blood sugar, cholesterol, glycosylated protein, urea nitrogen and serum creatinine index(P<0.05). Diabetes group, micro proteinuria group, and proteinuria group were significantly higher than normal group in urine protein, 12 h IL 18 and 24 h IL-18(P< 0.01). Micro albuminuria and proteinuria group was significantly higher than diabetic group in urine protein, 12 h IL 18 and 24 h IL-18(P< 0.01). There were positive correlation between urine protein and 12 h, 24 h IL-18(r=0.454, P< 0.01; r=0.479, P<0.01). There was statistical difference between albuminuria group and diabetes group in -137G/C genotype frequency(χ2=5.45, P< 0.05)and there was statistical differencebetween the allele frequency distribution(χ2=5.76, P<0.05). Conclusions IL-18 can be used as an indicator for detecting early renal damage. Gene -137G/C polymorphism may increase the risk of diabetic nephropathy by upregulating the expression of IL-18. Key words: Type 2 diabetes mellitus; Mononuclear cells; IL- 8; Renal damage