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Abstract
Primary aldosteronism is the most common cause of secondary hypertension; however, the dynamic regulation of aldosterone by potassium is less well studied and current diagnostic recommendations are imprecise. We describe a young man who presented with resistant hypertension and severe hypokalemia. The workup initially revealed undetectable aldosterone despite acute potassium repletion. Chronic potassium supplementation eventually uncovered hyperaldosteronism. In situ genetic studies revealed a gain-of-function KCNJ5 mutation within an aldosterone-producing adenoma that was clinically responsive to changes in extracellular potassium. We highlight a unique presentation of Conn’s syndrome and discuss the implications for the molecular mechanisms of potassium regulation of aldosterone.
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Details
1 Stanford Hypertension Center, Department of Medicine, Stanford University School of Medicine, Stanford, CA, USA; Division of Nephrology, Department of Medicine, Stanford University School of Medicine, Stanford, CA, USA; Stanford HealthCare, Stanford Hospital, Stanford, CA, USA
2 Department of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, MI, USA; Division of Metabolism, Endocrinology, and Diabetes, Department of Internal Medicine, University of Michigan, Ann Arbor, MI, USA
3 Department of Pathology, Stanford University School of Medicine, Stanford, CA, USA
4 Stanford Hypertension Center, Department of Medicine, Stanford University School of Medicine, Stanford, CA, USA; Division of Nephrology, Department of Medicine, Stanford University School of Medicine, Stanford, CA, USA