The Effect of Hyperuricemia on Endothelial Biomarkers and Renal Function in Kidney Allograft Recipients

Background. Uric acid may play a pathogenic role in hypertension, cardiovascular morbidity, and kidney disease. The aim of this study was to assess the effect of serum uric acid on biomarkers of endothelial activation and renal function in kidney allograft recipients during 30 months of follow-up. Methods. The study included 100 allograft recipients with stable renal function (estimated glomerular filtration rate (eGFR) >60 mL/min). The study was performed 34 +/- 12 months after transplantation. The patients were followed prospectively for 30 months. Seventy patients displayed hyperuricemia (uric acid 7.5 +/- 1.0 mg/dL) and 30 normouricemia (5.5 +/- 0.9 mg/dL). Concentrations of plasma resistin, soluble vascular cell adhesion molecule 1 (sVCAM-1), soluble CD146, and high-sensitivity C-reactive protein (hs-CRP) were assessed in patients at the beginning and after 30 months of follow-up. Clinical outcomes and biomarker values were analyzed in these groups and compared to a control group of 26 healthy volunteers. Results. Concentrations of resistin and CD 146 were increased among the hyperuricemia versus the normouricemic group (P < .05). Serum uric acid level correlated with sVCAM-1, hs-CRP, resistin, and sCD146 concentration in both groups of kidney recipients (P < .01). Serum creatinine concentrations correlated with sVCAM-1, resistin, and sCD146 concentrations (P < .01). There were significant direct correlations between uric acid and the number of antihypertensive agents (P < .001) and inverse correlations between eGFR (P < .001) and high-density lipoprotein cholesterol (P < .04). Pulse pressure increased in hyperuricemic patients during follow-up (P < .05). The decrease in eGFR during the 30-month follow-up was similar in both groups. No subject progressed to kidney allograft failure. Patient and graft survivals were 98% among hyperuricemic and 96.7% among normouricemic individuals. Conclusions. Hyperuricemia may injure endothelial function via resistin-dependent mechanisms. It represents a risk factor for arterial stiffness. The elevated serum uric acid may not have a causal role in the progression of renal transplant injury over 30 months of follow-up.