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Research Article Free access | 10.1172/JCI106948

A natriuretic factor in the serum of patients with chronic uremia

Jacques J. Bourgoignie, Kuo Hwa Hwang, Carlos Espinel, Saulo Klahr, and Neal S. Bricker

1Renal Division, Department of Internal Medicine, Washington University Medical School, St. Louis, Missouri 63110

Find articles by Bourgoignie, J. in: PubMed | Google Scholar

1Renal Division, Department of Internal Medicine, Washington University Medical School, St. Louis, Missouri 63110

Find articles by Hwang, K. in: PubMed | Google Scholar

1Renal Division, Department of Internal Medicine, Washington University Medical School, St. Louis, Missouri 63110

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1Renal Division, Department of Internal Medicine, Washington University Medical School, St. Louis, Missouri 63110

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1Renal Division, Department of Internal Medicine, Washington University Medical School, St. Louis, Missouri 63110

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Published June 1, 1972 - More info

Published in Volume 51, Issue 6 on June 1, 1972
J Clin Invest. 1972;51(6):1514–1527. https://doi.org/10.1172/JCI106948.
© 1972 The American Society for Clinical Investigation
Published June 1, 1972 - Version history
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Abstract

Sera from chronically uremic and normal individuals were subjected to gel filtration with Sephadex G-25 and the same fraction of both was infused into rats with a decreased nephron population to determine the effects on sodium excretion. Sodium excretion rate and fractional sodium excretion increased slightly with the normal fractions; but the increase in both functional parameters produced by the uremic fractions was substantially and significantly greater. The natriuresis could not be explained by associated changes in glomerular filtration rate (GFR), para-aminohippurate (PAH) clearance, filtration fraction, hematocrit, or blood pressure. The possibility thus exists that the inhibitor affected some component part of the transepithelial sodium transport system. The elution characteristics of the fraction plus certain of its physicochemical properties suggest that the inhibitor of sodium reabsorption by the rat nephron may be identical with the inhibitor of PAH uptake by kidney slices and the inhibitor of transepithelial sodium transport by the frog skin and toad bladder previously found in the serum of chronically uremic patients.

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