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Reduced uric acid excretion can occur after renal transplantation, leading to hyperuricemia and, in some cases, gouty arthritis [1-3]. This problem is more common with cyclosporine [1,2,4,5]:
The lower GFR induced by cyclosporine probably contributes to uric acid retention [1], but tubular damage may also be important by impairing urate secretion [2]. Concurrent diuretic use and renal insufficiency due to rejection are other risk factors for hyperuricemia [2]. (See "Diuretic-induced hyperuricemia and gout".)
Although renal insufficiency predisposes to hyperuricemia and gout, patients with advanced renal failure may be at lesser risk of symptomatic disease. This hypothesis derives from observations in patients with end-stage renal disease treated with maintenance dialysis. Despite persistent hyperuricemia, patients with previous gouty arthritis note a marked reduction in symptomatic episodes, and de novo gout is a rare event [6]. Why this occurs and whether it is applicable to transplant recipients are not clear; it is possible that the antiinflammatory effect of uremia is an important protective factor [6,7].
The hyperuricemia induced by cyclosporine is not restricted to renal transplant recipients but is also frequent in heart or heart-lung transplant patients [8]. In these patients, hyperuricemia is associated with an increased risk of symptomatic gout. Gouty arthritis has been reported in 7 to 24 percent of cyclosporine-treated transplant recipients but only occasionally in transplant patients receiving azathioprine [1,2]; in severe cases, the gout may be polyarticular and tophi may be seen [8]. Gout frequently occurs as a de novo event, although patients with a prior history of gout are at higher risk [8]. De novo gout generally begins 17 to 24 months after transplantation [1].
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