Abstract: SA-PO370
A Rare Cause of Resistant Hypertension
Session Information
- Genetic and Diagnostic Trainee Case Reports
November 09, 2019 | Location: Exhibit Hall, Walter E. Washington Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Trainee Case Report
- 1403 Hypertension and CVD: Mechanisms
Authors
- Singh, Amardeep, Centra Medical Group, Farmville, Virginia, United States
- Bali, Atul, UVA Dialysis, Farmville, Virginia, United States
Introduction
Resistant hypertension is defined as suboptimally controlled blood pressure despite concurrent use of three antihypertensive agents of different classes, including a diuretic. A thorough evaluation for secondary causes of hypertension is crucial to allow timely institution of treatment to limit end-organ damage and associated morbidity and mortality.
Case Description
A 66-year-old African American gentleman was referred for evaluation of uncontrolled hypertension and declining renal function. His antihypertensive regimen consisted of maximal doses of Valsartan, Verapamil ER and Clonidine. Diuretics were being held due to persistent hypokalemia despite potassium supplementation. Family history was notable for his father succumbing to renal failure of unclear etiology at age 50, his sister passing from her ESRD, and his mother having well controlled hypertension. Physical exam was otherwise unremarkable, with the patient appearing euvolemic. Lab review suggested progressive decline in GFR, equating to CKD stage 3 with minimal proteinuria, with mild but persistent hypokalemia and metabolic alkalosis. An arterial blood gas confirmed chronic metabolic alkalosis. Both plasma renin activity and aldosterone were undetectable. Based on the above findings, a diagnosis of Liddle syndrome was made. Amiloride was started and gradually uptitrated. He had a reassuring response to treatment which translated into stability of his GFR (Figure 1).
Discussion
Liddle Syndrome is a rare autosomal dominant disorder associated with a gain-of-function mutation involving the epithelial sodium channels, which mimics the manifestations of hyperaldosteronism, without a demonstrable elevation in serum aldosterone. Our case illustrates the benefits of prompt diagnosis and treatment to arrest the progression of hypertension mediated end-organ damage.