Hyperuricemia is a mediator of endothelial dysfunction and inflammation in renal allograft recipients

Hyperuricemia is common in renal transplant recipients treated with calcineurin inhibitors. Uric acid induces glomerular hypertension, microvascular disease, and renal interstitial fibrosis and is an independent risk factor for cardiovascular complications. The mechanisms by which uric acid injures renal allografts and the cardiovascular system remain unclear.

To assess the influence of uric acid on biomarkers of endothelial dysfunction and inflammation in renal allograft recipients.

The study included 78 allograft recipients with normal allograft function. Exclusion criteria were abnormal renal function, proteinuria, diabetes mellitus, obesity, and inflammation. Participants were divided into 2 groups: 48 patients with hyperuricemia (mean [SD] uric acid concentration, 7.72 [1.33] mg/dL) and 30 patients with normouricemia (5.48 [0.92] mg/dL; control group). Concentrations of plasma resistin, CD146, and soluble vascular cell adhesion molecule-1 (sVCAM-1), which are markers of endothelial dysfunction and inflammation, were assessed in both groups. No significant differences were noted for patient demographic data including age, sex, cause of renal failure, number of HLA mismatches, delayed graft function, and number of acute rejection episodes.

Concentrations of the examined biomarkers were increased in the group with hyperuricemia compared with the control group: plasma resistin, 7.15 (2.42) ng/mL vs 6.29 (2.76) ng/mL; CD146, 389.7 (150.0) microg/mL vs 330 (117) microg/mL; and sVCAM-1, 1126 (371) ng/mL vs 955 (269) ng/mL (P < .03). In addition, resistin correlated significantly with sVCAM-1 (P < .01).

Hyperuricemia mediates endothelial dysfunction and inflammation and via this pathway, possibly contributes to chronic allograft injury and cardiovascular events in renal allograft recipients.