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.