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.