Abstract
THE recent demonstration that patients with primary hyperuricaemia are also hyperaminoacidaemic1 has suggested the possibility that the presumptive renal tubular defect in the handling of uric acid by these patients2 may be only one manifestation of a more generalized transport defect that involves other substances. The amino-acid glycine, a purine precursor, has been investigated with the view of determining whether the elevated serum level of glycine can be explained on a renal basis.
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KAPLAN, D., WALLACE, S. & HALBERSTAM, D. Renal Handling of Glycine in Primary Hyperuricaemia. Nature 209, 213–214 (1966). https://doi.org/10.1038/209213a0
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DOI: https://doi.org/10.1038/209213a0
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