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Antidiuretic Principle in Tuberculous Lung Tissue of a Patient with Pulmonary Tuberculosis and Hyponatremia

[+] Article, Author, and Disclosure Information

Supported by grant DRG-981, the Damon Runyon Memorial Fund, New York, N. Y.; and grant AM-12639, U. S. Public Health Service, Washington, D.C.

Dr. Vorherr is presently at the Department of Obstetrics and Gynecology, The University of New Mexico School of Medicine.

Dr. Massry is an Established Investigator of the American Heart Association, New York, N. Y.

Dr. Fallet was supported in this study as a Postdoctoral Fellow by training grant HE 5705, U. S. Public Health Service.

▸Requests for reprints should be addressed to Charles R. Kleeman, M.D., Cedars-Sinai Medical Center, 8720 Beverly Blvd., Los Angeles, Calif. 90048

Los Angeles and San Francisco, California

Ann Intern Med. 1970;72(3):383-387. doi:10.7326/0003-4819-72-3-383
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A 51-year-old white man had advanced pulmonary tuberculosis without renal or adrenal involvement, hyponatremia, and high urinary osmolality. The tuberculous lung tissue and the urine from the patient contained antidiuretic activity (assayed in rats undergoing water-ethanol diuresis) equivalent to 22 ±8 µunits/mg tissue powder and 57 ±8 µunits/ml of arginine vasopressin, respectively, and the patient's plasma did not contain detectable antidiuretic activity. It is indicated that the antidiuretic principle is either very similar or identical to arginine vasopressin. Uninvolved lung tissue from the patient, suspension of Mycobacterium tuberculosis, or culture media containing metabolites of M. tuberculosis did not have antidiuretic properties. Tuberculous lung tissue may either produce antidiuretic hormone or adsorb an inappropriately released hormone from the posterior pituitary. This is the first demonstration of a relation between antidiuretic hormone and hyponatremia in a patient with pulmonary tuberculosis.





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