Liddle syndrome: clinical and cellular abnormalities.
Clinical findings resemble those of primary hyperaldosteronism, except that aldosterone secretion is negligible. The fault appears to lie with continuously avid sodium channels in the distal nephron, resulting in excessive salt absorption, potassium wasting, and severe hypertension. Insights gained in this disorder may help clarify more common forms of low-renin hypertension.
Department of Medicine, University of Alabama School of Medicine, Birmingham.
D G
DG
Warnock
J K
JK
Bubien
D000293:Adolescent; D000471:Alkalosis / Q000235:genetics / Q000378:metabolism / Q000503:physiopathology*; D005260:Female; D006801:Humans; D006973:Hypertension / Q000235:genetics / Q000378:metabolism / Q000503:physiopathology*; D007008:Hypokalemia / Q000235:genetics / Q000378:metabolism / Q000503:physiopathology*; D008297:Male; D010375:Pedigree; D015222:Sodium Channels / Q000502:physiology; D013577:Syndrome
D015222:Sodium Channels