The Effects Of Pioglitazone On Urinary MCP-1 And ICAM-1 Excretions In Type 2 Diabetic Patients

Aim To observe the effects of pioglitazone therapy on urinary monocyte chemoattractant protein-1 (MCP-1) and intercellular adhesion molecule-1 (ICAM-1) excretions in Type 2 diabetic patients and probe into its possible reno-protective mechanisms. Methods 98 uncontrolled Type 2 diabetic patients with fasting blood glucose (FBG) 7.0~13.0mmol/L and glycosylated hemoglobin A1C (GHbA1c)≥7.0% were assigned randomly into group DP (pioglitazone add-on) and group DS (sulfonylureas add-on). FBG, GHbA1c, urinary albumin (Alb) and monocyte chemoattractant protein-1 (MCP-1) and intercellular adhesion molecule-1 (ICAM-1) and creatinine(Cr)levels were determined at baseline and the 12th week. In order to eliminate the volume of urine, Alb/Cr (mg/gCr), MCP-1/Cr (pg/ngCr) and ICAM-1/Cr (pg/ngCr) were used to represent the urinary excretions of Alb, MCP-1 and ICAM-1.Results 1) At baseline, there were significant deifference in FBG, GHbA1c, Alb/Cr, MCP-1/Cr and ICAM-1/Cr (P<0.01) in group DP and group DS. The difference between the two treatment groups had no statistical difference (P> 0.05). 2) After 12 weeks treatment, FBG and GHbA1c levels decreased obviously in both groups (P<0.01), however, there was no significant diffirence between the two therapy groups (P> 0.05) .3) Urinary Alb/Cr was obviously decreased in group DP (P<0.01) and slightly decreased in group DS (P>0.05). 4) Meanwhile, the urinary MCP-1/Cr was significantly declined in group DP and group DS (P<0.01) after treatment. The ICAM-1/Cr was obviously decreased in group DP (P<0.01) and slightly decreased in group DS (P> 0.05). Compared to group DS, the Alb/Cr, MCP-1/Cr and ICAM-1/Cr were lowered significantly in group DP at the 12th week (P<0.05). 5) The MCP-1/Cr and ICAM-1/Cr levels were positive associated with Alb/Cr, respectively (r=0.695 and r=0.705), P<0.01.Conclusion Pioglitazone can protect against kidney injury through lessening the increased inflammatory reaction, which partly due to inhibition of urinary MCP-1 and ICAM-1 excretions in local kidney of type 2 diabetic patients.