INTRODUCTION
Increased uric acid by endothelial dysfunction, mitochondrial dysfunction and glomerular arteriopathy, tubular obstruction of urate crystal formation can be cause of structural damage of the kidney1. Elevated serum uric acid levels (SUA) appear to be associated with accelerated renal dysfunction in chronic kidney disease (CKD) patients2,3. There are also serious arguments that there may be an additional risk factor for graft loss in KTRs4. There are studies showing the loss of function in renal allograft as well as chronic kidney disease of hyperuricemia5,6.
Xanthine oxidase inhibitor allopurinol increases urinary excretion of uric acid and is well tolerated. Allopurinol has been reported to slow GFR loss in renal KTRs7,8. However, another study was found to be ineffective in KTRs8. In this retrospective observational cohort study; effects of elevated serum uric acid and reduction of serum uric acid by allopurinolon renal function were evaluated.