Abstract
Introduction At the time of his historic discovery of hyperuricemia in gout, A. B. Garrod stated that Gout would thus appear, at least partly, to depend on a loss of power (temporary or permanent) in the uric acid-excreting function of the kidneys.1Thus began a century of interest and controversy over the role of the kidney in the pathogenesis of gout. The fact that renal mechanisms, as well as metabolic considerations, are important in some cases of gout has been demonstrated by several investigators and accepted by most workers in the field.2In addition, the kidney is one of the major sites for the deposition of uric acid crystals.3-6Nonspecific findings such as proteinuria, a decrease in the ability of the kidney to concentrate the urine, and a decrease of phenolsulfonphthalein (PSP) excretion by the kidney are the early manifestations of this derangement. In recent years uricosuric
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