{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,4]],"date-time":"2026-10-04T06:24:16Z","timestamp":1791095056310,"version":"4.1.0"},"reference-count":19,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2004,10,8]],"date-time":"2004-10-08T00:00:00Z","timestamp":1097193600000},"content-version":"vor","delay-in-days":5516,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Annals of Neurology"],"published-print":{"date-parts":[[1989,9]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>We present the case of a 14\u2010year\u2010old 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.<\/jats:p>","DOI":"10.1002\/ana.410260314","type":"journal-article","created":{"date-parts":[[2005,1,1]],"date-time":"2005-01-01T14:14:36Z","timestamp":1104588876000},"page":"392-395","source":"Crossref","is-referenced-by-count":9,"title":["Hyperkalemic periodic paralysis in Gordon's syndrome: A possible defect in atrial natriretic peptide function"],"prefix":"10.1002","volume":"26","author":[{"given":"J. W.","family":"Pasman","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"F. J. 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