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Sodium and Water Regulation in a Patient With Cerebral Salt Wasting
Michael Diringer, MD;
Paul W. Ladenson, MD;
Cecil Borel, MD;
Graeme K. Hart, FFARACS;
Jeffrey R. Kirsch, MD;
Daniel F. Hanley, MD
Arch Neurol. 1989;46(8):928-930.
Abstract
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Hyponatremia, in patients with central nervous system disease, can be attributable to impaired free water excretion (syndrome of inappropriate secretion of antidiuretic hormone) or to excessive sodium excretion (cerebral salt wasting). We present a patient with a parietal glioma and hyponatremia characterized by salt wasting and dehydration. Rehydration and sodium repletion corrected the sodium and volume deficits; withdrawal of supplemental sodium resulted in recurrence of dehydration and hyponatremia. We determined sodium and water balance and measured plasma atriopeptin, antidiuretic hormone, and aldosterone. Plasma atriopeptin ranged from 8 to 44 pg/mL (normal, <45 pg/mL); antidiuretic hormone was not elevated at 4 to 5 pg/mL, and aldosterone was slightly elevated at 1040.25 pmol/L. The concentrations of these hormones could not directly explain the natriuresis; interactions with neural or other humoral factors may be involved. In evaluating such patients, careful attention to sodium and water balance is important to guide appropriate therapy.
Author Affiliations
From the Departments of Neurology, Neuroscience Critical Care Unit (Drs Borel, Diringer, and Hanley), Anesthesiology and Critical Care Medicine (Drs Borel, Hanley, Hart, and Kirsch), and Medicine, Division of Endocrinology and Metabolism (Dr Ladenson), The Johns Hopkins Medical Institutions, Baltimore.
Footnotes
Accepted for publication Oct 19, 1988.
Reprint requests to Department of Neurology, The Johns Hopkins Medical Institutions, Meyer 8-139, 600 N Wolfe St, Baltimore, MD 21205 (Dr Diringer).
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