Orginal Publication Date
MCV/Q, Medical College of Virginia Quarterly
In order to provide a point of reference for a rational approach to the therapy of acute uricemic nephropathy, the metabolic pathways leading to the production of uric acid will be briefly reviewed. Uric acid is the end-product of adenine and guanine metabolism. Relevant to this discussion is the xanthine oxidase enzyme which catalyzes the conversion of hypoxanthine to xanthine and xanthine to uric acid. In children with acute leukemia the increasing production and subsequent destruction of white blood cells result in the rapid elevation of uric acid concentration in the plasma, especially during treatment with antineoplastic drugs. This in turn may lead to the development of acute hyperuricemic nephropathy. The uric acid deposition in the renal medulla causes obstructive uropathies. This occurrence is not uncommon in children treated for reticuloendothelial malignancies, sarcoma and acute lymphocytic leukemia.
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