Case report
Symptomatic normovolemic essential hypernatremia: A clinical and physiologic study

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Abstract

A 23 year old man presenting with episodic muscle paralysis and persistent normovolemic hypernatremia and hyperosmolality was investigated. Metabolic studies at the time of presentation and during a 10 hour fast, and the responses to acute and chronic water loading, alcohol, vasopressin and nicotine infusion, sodium restriction and intravenous sodium loading were all normal, with the exception of the acute water load. These results suggested abnormal hypothalamic function leading to an altered regulation of the central osmoreceptors controlling thirst and sodium metabolism; however, no central nervous system lesion was demonstrable. Despite normal levels of plasma [potassium], total exchangeable body potassium was reduced. It is proposed that the muscle paralysis was secondary to both the hypernatremia and the reduced total body potassium status. Progressive symptomatic improvement with lowering of plasma sodium and osmolality occurred following 24 months on a low sodium-high potassium-high fluid regimen although total body potassium status has remained low.

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    This work was supported in part by the National Institutes of Health, HE 11580-01 (GMB), the National Medical Research Council of Australia and the National Heart Foundation of Australia.

    Present address: Department of Medicine, Stanford University Medical School, Palo Alto, California 94305.

    1

    From the Department of Endocrinology, Royal Melbourne Hospital and the Howard Florey Institute of Experimental Physiology and Medicine, University of Melbourne, Victoria, Australia.

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