DISCUSSION
The prevalence of hyperuricemia in KTRs is between 15-52%6,9. It can even be detected in 30-84% of those using cyclosporine as calcıneurin inhibitor (CNI)10. In the normal population, the prevalence is around 10-15%11. Older age, male gender, low GFR, drugs such as diuretic, beta blocker, CNI (especially cyclosporine), high body mass index, duration of dialysis treatment during pretransplant are the factors that increase the tendency to hyperuricemia7,11-13.
Some data suggest that hyperuricemia is related to severity of CKD2,3 or shows progression to end stage renal disaase (ESRD)14. In addition, there are studies on the treatment of hyperuricemia improves renal function8. Renal graft survival is still controversial, with some benefits, and may be the result of chronic allograft nephropathy and graft failure15-17. Meanwhile, the SYMPHONY study suggests that hyperuricemia is not an independent risk factor for graft failure18. In addition, Kim et al. concluded that there is no risk factor for graft outcome according to the data obtained using the Marginal Structural Model19. According to the Korean-based meta-analysis of Miyeun et al, hyperuricemia is an indicator of renal damage due to decreased excretion, but its association with normal renal function may be indicative of a negative endpoint, such as ESRD4. According to the recent meta-analysis of Liu et al, high SUA treatment, albeit with different drugs, slows the development of CKD20.
In our study, high SUA levels can be considered as a possible risk factor for graft loss in the first two years. Although treatment with allopurinol does not prevent graft loss, it decreases the progression of kidney function and even improves it initially. Also interesting allopurinol therapy prevented loss of GFR both first 2 and first 5. year follow up periods.
In order to investigate the effect of elevated SUA levels on CKD progression in KTRs, multicenter studies that exclude the effect of rejection and graft dysfunction by biopsy will further explain the adverse effects of hyperuricemia. Because uric acid itself is a source of oxidative stress and inflammation, although it is the result of renal failure. In our study, allopurinol therapy of high SUA had a positive effect on renal function. According to the results of studies in KTRs hyperuricemia is bad for kidney function4,13,17,21, there is no relationship7,9 or treatment of hyperuricemia preserves kidney function. or treatment of uric acid elevation preserves kidney function20,22.
In conclusion we found that in kidney transplant recipients in 2 years and 5 years; hyperuricemia accompaning loss of GFR and alIopurinol therapy in hyperuricemic patients preserved the renal function. So that hyperuricemia should be treated and low dose allopurinol can be option for treatment of hyperuricemia thefore prevention of loss of kidney function in kidney transplant recipients.