Association of Uric Acid With Inflammation, Progressive Renal Allograft Dysfunction and Post-Transplant Cardiovascular Risk

Hyperuricemia is common after kidney transplantation. Although its risk factors are well established, its relation to inflammation, progressive renal dysfunction, and cardiovascular events is unknown. In this study, 405 stable renal transplant recipients with ≥3 uric acid (UA) and C-reactive protein measurements from January 2005 to April 2008 were identified to determine the relations between UA and C-reactive protein and between UA and the rate of decrease in the estimated glomerular filtration rate (eGFR; using the Modification of Diet in Renal Disease equation) and cardiovascular events. Hyperuricemia was defined as UA >7.1 mg/dl (420 μmol/L) in men and >6.1 mg/dl (360 μmol/L) in women. The prevalence of hyperuricemia was 44% (180 of 405). Hyperuricemia was negatively associated with eGFR (p <0.0001) and positively associated with diuretic use (p = 0.013), time since transplantation (p = 0.014), and triglycerides (p = 0.04). Although UA was correlated with C-reactive protein (p = 0.003), adjustment for eGFR rendered this relation nonsignificant (p = 0.225). The slope of eGFR was +0.144 ± 0.85 ml/min/1.73 m2/month (95% confidence interval 0.032 to 0.257) in those with normal UA levels and −0.091 ± 0.93 ml/min/1.73 m2/month (95% confidence interval −0.235 to +0.054) in patients with hyperuricemia (p = 0.003). There were 17 cardiovascular events in the patients with hyperuricemia and 4 in those with normal UA levels (p = 0.001). In conclusion, hyperuricemia is associated with a decrease in renal allograft function and may be an independent cardiovascular risk factor in transplant recipients. Further studies are needed to establish its role in post-transplantation cardiovascular disease.