{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,28]],"date-time":"2026-06-28T09:45:15Z","timestamp":1782639915998,"version":"3.54.5"},"reference-count":23,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2026,6,28]],"date-time":"2026-06-28T00:00:00Z","timestamp":1782604800000},"content-version":"vor","delay-in-days":178,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,1,1]],"date-time":"2026-01-01T00:00:00Z","timestamp":1767225600000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Case Reports in Nephrology"],"published-print":{"date-parts":[[2026,1]]},"abstract":"<jats:sec>\n                    <jats:title>Introduction<\/jats:title>\n                    <jats:p>Liddle\u2019s syndrome is a rare inherited disorder associated with early\u2010onset and resistant hypertension due to hyperactivity of epithelial sodium channels (ENaCs). The condition is caused by mutations in the genes SCNN1A, SCNN1B, and SCNN1G. Liddle\u2019s syndrome leads to hypertension, hypokalemia, and metabolic alkalosis.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Case Presentation<\/jats:title>\n                    <jats:p>A previously healthy 21\u2010year\u2010old male patient complained of severe central chest pain radiating to both arms and had a hypertensive emergency with a BP reading of 267\/170\u2009mmHg. The patient had marked elevation in troponin I (13.9\u2009ng\/mL), hypokalemia (2.8\u2009mmol\/L), and metabolic alkalosis. The electrocardiogram showed left ventricular hypertrophy with a strain pattern and QTc prolongation due to hypokalemia. Coronary angiography ruled out the possibility of primary acute coronary syndrome by revealing normal coronary arteries. Echocardiogram showed concentric left ventricular hypertrophy with normal ejection fraction and no wall motion abnormalities. In search of the secondary cause of hypertension, renal Doppler ultrasonography and aldosterone\u2010to\u2010renin ratio were normal, thus ruling out primary hyperaldosteronism. About the typical clinical and biochemical presentation, a clinical diagnosis of Liddle syndrome was highly likely. Genetic tests were not performed owing to financial constraints. However, treatment with amiloride brought about remarkable improvement in the control of hypertension and normalization of potassium levels.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Liddle\u2019s syndrome should be suspected in cases where there are young individuals who have severe hypertension, hypokalaemia, and an aldosterone\u2010to\u2010renin ratio that is normal or low. The diagnosis must be made promptly because delay may lead to complications. In instances where molecular testing is impractical, treatment with ENaC inhibition using amiloride is diagnostic and potentially life\u2010saving.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1155\/crin\/7218869","type":"journal-article","created":{"date-parts":[[2026,6,28]],"date-time":"2026-06-28T09:13:17Z","timestamp":1782637997000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Liddle Syndrome Presenting as Hypertensive Crisis and Myocardial Injury in a Young Male: A Case Report"],"prefix":"10.1155","volume":"2026","author":[{"ORCID":"https:\/\/orcid.org\/0009-0005-8844-6094","authenticated-orcid":false,"given":"Abbas","family":"Khan","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0009-7179-3662","authenticated-orcid":false,"given":"Alina","family":"Batool","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0006-2867-5159","authenticated-orcid":false,"given":"Askar","family":"Nisar","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0007-3042-8402","authenticated-orcid":false,"given":"Jaweria","family":"Farman","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0001-5747-6507","authenticated-orcid":false,"given":"Okasha","family":"Tahir","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0000-1800-1800","authenticated-orcid":false,"given":"Muhammad Hassaan","family":"Javaid","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0009-9434-1650","authenticated-orcid":false,"given":"Raghabendra Kumar","family":"Mahato","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0005-9771-1339","authenticated-orcid":false,"given":"Tayyeb","family":"Ali","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2026,6,28]]},"reference":[{"key":"e_1_2_13_1_2","first-page":"199","article-title":"A Familial Renal Disorder Simulating Primary Aldosteronism But With Negligible Aldosterone Secretion","volume":"76","author":"Liddle G. 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