The literature on the pathogenesis of hyperuricemia have been limited to the discussion of metabolic syndromes associated with risk factors for atherosclerosis and hyperuricemia and the genetics of the juvenile form of hyperuricemic nephropathies. A few new mutations in the hypoxanthine-guanine phosphoribosyltransferase gene, which result in Lesch-Nyhan syndrome, have been described. In addition, some new insight has been gained in the renal handling of uric acid by the human kidney.
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