Abstract
Hematologic disorders which result in increased cell turnover rates are frequently associated with hyperuricemia and secondary gout due to increased uric acid synthesis. Although sickle cell anemia is characterized by a 6–8 fold increase in red cell turnover, gout is thought to be an uncommon complication of this disease. Since impaired renal concentrating ability is a common and early manifestation of sickle cell disease, and other defects of renal tubular transport such as diminished tubular maxima for PAH and renal tubular acidosis have been described, the present study was designed to investigate tubular transport of urate in sickle cell anemia, and to evaluate the hypothesis that hyperuricosuria due to defective renal tubular transport of urate might protect sickle cell anemia patients against gout.
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