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Hyperkalemic periodic paralysis in Gordon's syndrome: A possible defect in atrial natriretic peptide function
Author(s) -
Pasman J. W.,
Gabreëls F. J. M.,
Semmekrot B.,
Renier W. O.,
Monnens L. A. H.
Publication year - 1989
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/ana.410260314
Subject(s) - periodic paralysis , hyperkalemia , pathophysiology , medicine , hypokalemic periodic paralysis , endocrinology , paralysis , renal function , blood pressure , atrial natriuretic peptide , acidosis , aldosterone , cardiology , hypokalemia , surgery
We present the case of a 14‐year‐old boy who had secondary hyperkalemic periodic paralysis caused by Gordon's syndrome. This syndrome consists of hypertension, tubular acidosis, and hyperkalemia with normal glomerular filtration rate. The pathophysiological mechanism is still unknown. Pathophysiological studies suggest that in this disorder the kidney lacks sensitivity to atrial natriretic peptide. After treatment with hydrochlorothiazide, serum potassium and plasma aldosterone values, plasma rennin activity, and blood pressure became normal and the attacks of periodic paralysis disappeared.

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