There is accumulating evidence that
advanced glycation end products (AGEs) play a role in the development and progression of
chronic kidney disease (CKD). We have previously found that
atorvastatin treatment significantly reduces serum levels of AGEs in type 2 diabetic patients and subjects with non-
alcoholic steatohepatitis in a
cholesterol lowering-independent manner. In this study, we examined whether
atorvastatin could reduce
proteinuria partly via reduction of serum levels of AGEs in non-diabetic CKD patients. Ten non-diabetic normotensive stage I or II CKD patients with
dyslipidemia were enrolled. Patients were treated with
atorvastatin (10 mg/day) for 1 year. All subjects underwent determination of blood chemistries,
proteinuria and serum levels of AGEs at baseline and after 1 year.
Atorvastatin treatment for 1 year significantly decreased circulating levels of total
cholesterol, LDL-
cholesterol,
triglycerides, and AGEs, while it increased
HDL-cholesterol levels. Further, although
atorvastatin treatment did not affect estimated glomerular filtration rate, it significantly reduced
proteinuria. In univariate analyses,
proteinuria levels were correlated with total
cholesterol, LDL-
cholesterol,
triglycerides,
HDL-cholesterol (inversely) and AGEs. Multiple stepwise regression analysis revealed that AGE level was a sole independent correlate of
proteinuria. In this initial examination of the patients in this study, our present study suggests that
atorvastatin could decrease
proteinuria in non-diabetic CKD patients with
dyslipidemia partly via reduction of serum levels of AGEs.
Atorvastatin may have AGE-lowering effects in CKD patients as well that could contribute to renoprotective properties of this agent.