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Case Due to Renal Tubular Acidosis

RICHARD A. HERRMANN, M.D.; ALLEN W. MEAD, M.D.; NORTON SPRITZ, M.D.; ALBERT L. RUBIN, M.D.

Arch Intern Med. 1961;108(6):925-928.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

In renal tubular acidosis, potassium depletion, severe enough to produce flaccid paralysis with life-threatening respiratory embarrassment, is a relatively uncommon manifestation of the syndrome and one which may easily be mistaken for organic neurological disease. Owen and Verner, in a recent review, added 9 such cases to the previously reported 13, and they suggested that this syndrome may be more common than previously thought.¹ The associated diagnostic findings, the remediable nature of the defect, and the magnitude of the potassium deficit which may be present are illustrated by this case.

Report of Case

The patient was a 42-year-old Polish-born white male admitted to the Neurological Service (Cornell) of Bellevue Hospital on Sept. 18, 1958, at 4 A.M., after transfer from another hospital with the tentative diagnosis of alcoholic polyneuritis.

He admitted to an alcoholic consumption of 8 to 9 ounces of whiskey per day; there was no history of . . . [Full Text PDF of this Article]

Author Affiliations
NEW YORK

From the Cardiorenal Laboratory of the Second (Cornell) Medical Division, Bellevue Hospital, and the Department of Medicine, Cornell University Medical College.

Footnotes
Submitted for publication Oct. 25, 1960.

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