The Renal Effect of Intravenous Adenine in Humans

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Abstract
The purine base, adenine, improves the posttransfusion viability of liquid stored blood. However, adenine in high doses may cause kidney damage because of the precipitation in renal tubules of its insoluble metabolite, 2,8‐dioxyadenine. Adenine is not licensed for use in the United States because it may be nephrotoxic. In a controlled, randomized, double‐blind study, eight human subjects received 10 mg/kg of adenine infused intravenously over one hour, four subjects received 5 mg/kg, and four subjects received no adenine. Renal function tests were performed on each subject before adenine infusion and one day and one week following the infusion. Tests included an assessment of glomerular function (serum creatinine, creatinine clearance, protein excretion), proximal tubular function (amino acid and glucose excretion), and distal tubular function (maximal acidifying and concentrating ability). Plasma and urine levels of adenine and 2,8‐dioxyadenine were measured. Renal function tests showed no evidence of kidney damage secondary to adenine.