Hyperuricemia is a common complication in organ transplant recipients, with a higher incidence in kidney and heart recipients. Risk factors for post-transplant hyperuricemia include reduced glomerular filtration rate, diuretic use, cyclosporine therapy, increasing age at transplant, obesity, and metabolic syndrome, as well as the presence of pretransplant hyperuricemia. The impact of hyperuricemia in patient and graft survival is unclear because uric acid only recently has been considered a risk factor for cardiovascular disease and graft survival. The effect of uric acid on graft function remains controversial, with studies suggesting that uric acid is an independent risk factor for chronic allograft dysfunction, contrasting with other studies suggesting that hyperuricemia is only a marker of reduced glomerular filtration rate. Strategies to reduce uric acid levels include reduction or avoidance of cyclosporine treatment, adequacy of antihypertension treatment, avoidance of diuretics, nutritional management, and use of uric acid-lowering agents. In this article, we review the incidence and risk factors for the development of post-transplant hyperuricemia, the effect of different immunosuppressive regimens in uric acid handling, and recent results from studies comparing uric acid levels and renal function in organ transplant recipients that try to identify which comes first: hyperuricemia or chronic allograft dysfunction?