Background : Preclinical data suggest that cilostazol  might reduce urinary albumin excretion in patients with microalbuminuric diabetic kidney disease (DKD)by reduce renal production  of thromboxane B2 (TXB2).

Objective : To evaluate the effects of cilostazol on urinary albumin and serum of plasminogen-activator inhibitor type 1 (PAI-1) activity in type 2 diabetic patients with microalbuminuric and macroalbuminuric DKD.

Method : Patients were randomly assigned to: (1) 12  weeks of cilostazol 100 mg/day and (2) 12 weeks of placebo. All patients were received  angiotensin converting enzyme inhibitor (ACEI) or angiotensin receptor blocker (ARB) and aspirin less than 120 mg/day. Urinary albumin creatinine ratio (UACR) and urine plasminogen-activator (U-PA) that inversely correlated to serum PAI-1 activity were measured before and after interventions.                                

Results : There was no statistical significant of UACR and serum creatinine within group and between groups. U-PA increased significantly from 1.46±0.08 to 1.53±0.1 (p=0.006) in the cilostazol group but no significantly in the placebo group. However, there  was no statistical significant difference of U-PA between groups (p=0.926). In addition, there was significant increase in high density lipoprotein (HDL) in the cilostazol group from 52.45±13.38 to 58.09±16.48 mg/dl (p=0.002). Adverse events were similar in both groups.

Conclusions :  This study demonstrated that cilostazol could increase U-PA or decrease serum PAI-1activity and increase HDL but it did not reduce albuminuria in type 2 DKD.