Background: Hyperuricemia often causes kidney dysfunction which increases serum urate, forming a vicious cycle in the kidney. In this study, urate-lowering therapy was demonstrated in type 2 diabetic patients with hyperuricemia to evaluate the effect on diabetic nephropathy.
Methods: Type 2 diabetic patients with hyperuricemia (n = 34) were treated by urate-lowering drugs. Serum urate levels, estimated glomerular filtration rate (eGFR), blood pressure, HbA1c, and urinary albumin-to-creatinine ratio (UACR) were measured for 52 weeks. The parameters at the endpoint when serum urate decreased to below 6.0 mg/dL and at 52 weeks were compared to the initial levels at week 0.
Results: Serum urate level decreased to the endpoint in all patients and was maintained at under 6.0 mg/dL throughout the observation period. eGFR significantly increased at the endpoint and also at 52 weeks. Overall UACR did not change after 52 weeks; however, the treatment decreased UACR significantly in patients with no microalbuminuria. There was a negative relationship between the change of serum urate levels and the change of eGFR, and a negative relationship between the baseline UACR and the change of UACR when patients with macroalbuminuria were excluded. There were no changes in HbA1c levels and blood pressure before and after the treatment.
Conclusions: There were significant improvements in kidney function by lowering serum urate levels to under 6.0 mg/dL and the effect was maintained for at least 52 weeks. This treatment may be one strategy to slow the progression of nephropathy in type 2 diabetic patients with hyperuricemia.
Keywords: Diabetic nephropathy; Estimated glomerular filtration rate; Hyperuricemia; Type 2 diabetes; Urinary albumin-to-creatinine ratio.