Gout is a common problem among renal transplant patients with a prevalence of 2 to 13%. Hyperuricemia is even more common (1–7). This association is important in two respects. First, gout is a disabling disease, and may cloud the outcome of a patient for whom rehabilitation has been particularly hard fought. Second, the treatment of gout in renal allograft recip-ients poses more potential pitfalls than in the general popula-tion. This article will explore the metabolic basis of gout in allograft recipients. The currently available methods for treat-ing gout will be examined with particular emphasis on drug interactions and specific needs of the transplant patient. Pathophysiology of Hyperuricemia and Gout Gout is a painful disorder caused by an inflammatory reac-tion to monosodium urate crystals in joint fluid and periartic-
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David M. Clive (2000) studied this question.
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