BACKGROUND/AIM: A high uric acid (UA) level is demonstrated as a major risk factor of nephropathy and cardiovascular events in people with type 2 diabetes (T2D). This study aimed to evaluate the lovastatin effect on serum UA levels in people with type 2 diabetic nephropathy (T2DN). METHODS: Thirty patients completed the study course, out of 38 adult male patients with T2DN who were initially enrolled. Lovastatin, 20 mg/d, was administered for 90 days. Afterwards, lovastatin was withdrawn for the next 30 days. Blood samples were obtained at baseline, after 45 and 90 days of intervention, and 30 days after the withdrawal of lovastatin. The serum level of UA was assessed by the uricase/PAP method. The lipid profile and high-sensitivity C-reactive protein (hs-CRP) were determined using commercial reagents and the ELISA method. RESULTS: After 90 days of lovastatin intervention, cholesterol (Chol) and low-density lipoprotein cholesterol (LDL-C) levels significantly decreased and the high-density lipoprotein cholesterol (HDL-C) level increased significantly, despite the unchanged level of triglyceride (TG). After withdrawal, Chol, TG, and LDL-C levels were significantly increased, without any change in the HDL-C level. The baseline serum UA level was 5.94 ± 2.02 mg/dL and not changed after the intervention (5.95 ± 2.21 mg/dL; p = 0.969) and withdrawal period (5.80 ± 1.51 mg/dL; p = 0.647). The changes of serum UA levels were not correlated with the changes of serum hs-CRP levels, both after intervention and withdrawal (p = 0.963 & p = 0.835). CONCLUSIONS: Lovastatin does not have any effect on the serum UA level in people with T2DN. There is no correlation between the anti-lipidemic and anti-inflammatory effects of lovastatin and its effect on serum UA.
BACKGROUND/AIM: A high uric acid (UA) level is demonstrated as a major risk factor of nephropathy and cardiovascular events in people with type 2 diabetes (T2D). This study aimed to evaluate the lovastatin effect on serum UA levels in people with type 2 diabetic nephropathy (T2DN). METHODS: Thirty patients completed the study course, out of 38 adult male patients with T2DN who were initially enrolled. Lovastatin, 20 mg/d, was administered for 90 days. Afterwards, lovastatin was withdrawn for the next 30 days. Blood samples were obtained at baseline, after 45 and 90 days of intervention, and 30 days after the withdrawal of lovastatin. The serum level of UA was assessed by the uricase/PAP method. The lipid profile and high-sensitivity C-reactive protein (hs-CRP) were determined using commercial reagents and the ELISA method. RESULTS: After 90 days of lovastatin intervention, cholesterol (Chol) and low-density lipoprotein cholesterol (LDL-C) levels significantly decreased and the high-density lipoprotein cholesterol (HDL-C) level increased significantly, despite the unchanged level of triglyceride (TG). After withdrawal, Chol, TG, and LDL-C levels were significantly increased, without any change in the HDL-C level. The baseline serum UA level was 5.94 ± 2.02 mg/dL and not changed after the intervention (5.95 ± 2.21 mg/dL; p = 0.969) and withdrawal period (5.80 ± 1.51 mg/dL; p = 0.647). The changes of serum UA levels were not correlated with the changes of serum hs-CRP levels, both after intervention and withdrawal (p = 0.963 & p = 0.835). CONCLUSIONS:Lovastatin does not have any effect on the serum UA level in people with T2DN. There is no correlation between the anti-lipidemic and anti-inflammatory effects of lovastatin and its effect on serum UA.