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Research Article Free access | 10.1172/JCI106047

Plasma and urinary amino acids in primary gout, with special reference to glutamine

Ts'Ai-Fan Yü, Max Adler, Elias Bobrow, and Alexander B. Gutman

1Department of Medicine, Mount Sinai School of Medicine of the City University of New York, New York 10029

Find articles by Yü, T. in: PubMed | Google Scholar

1Department of Medicine, Mount Sinai School of Medicine of the City University of New York, New York 10029

Find articles by Adler, M. in: PubMed | Google Scholar

1Department of Medicine, Mount Sinai School of Medicine of the City University of New York, New York 10029

Find articles by Bobrow, E. in: PubMed | Google Scholar

1Department of Medicine, Mount Sinai School of Medicine of the City University of New York, New York 10029

Find articles by Gutman, A. in: PubMed | Google Scholar

Published May 1, 1969 - More info

Published in Volume 48, Issue 5 on May 1, 1969
J Clin Invest. 1969;48(5):885–894. https://doi.org/10.1172/JCI106047.
© 1969 The American Society for Clinical Investigation
Published May 1, 1969 - Version history
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Abstract

Measurement of the plasma free amino acids by column chromatography (AutoAnalyzer) in 32 patients with primary gout showed statistically significant increases or decreases in several components when compared with the spectrum in 18 control subjects, but the absolute amounts involved were small and the mean total plasma amino acid concentrations in both groups were the same. In the urine all major amino acid components, notably glutamine, serine, threonine, and leucine, were lower in our gouty than in our nongouty subjects, as were also the corresponding renal clearance ratios. These deficits could be reproduced by restricting dietary protein, so appear to be due largely to the some-what reduced mean dietary protein intake of our gouty subjects. However, the low renal clearance of glutamine, the most striking and consistent of the deficits in urinary amino acids noted, could not be accounted for by dietary or other relevant factors, and is interpreted as indicating increased tubular reabsorption of glutamine in primary gout. This interpretation was supported by the results of glutamine loading. The possible compensatory relationship of the abnormality in renal handling of glutamine to the deficiency in renal production of ammonia previously reported is discussed.

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