Abstract: SA-PO370
A Curious Case of Salt-Sensitive Hypertension
Session Information
- Hypertension, CVD, and the Kidneys: Clinical Research
October 26, 2024 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Hypertension and CVD
- 1602 Hypertension and CVD: Clinical
Authors
- Rajagopal, Madhumitha, Icahn School of Medicine at Mount Sinai, New York, New York, United States
- Rein, Joshua L., Icahn School of Medicine at Mount Sinai, New York, New York, United States
Introduction
Excess NaCl consumption is the top modifiable risk factor for HTN. Despite clear evidence, adherence to dietary NaCl restriction is low. HTN affects half of US adults and among them, half have salt-sensitive (SS)-HTN. We present a case of SS-HTN and its unique management.
Case Description
Patient is a 70 yo Black man with PMHx of resistant HTN (despite clonidine 0.3mcg TID, hydralazine 100mg TID, lisinopril 40mg TID, and labetalol 800mg BID). Over the years, he developed severe constipation from Ca2+ channel blockers, gynecomastia from spironolactone, and HCTZ induced hyponatremia. He weighed 95kg, had no edema, and BP was labile, 124-200/68-104 mmHg. Labs were notable for K+ 3.5-4.0 mEq/L, TCO2 23-28 mEq/L, creatinine (SCr) 1.3-1.6 mg/dL, and PAC/PRA < 1.0-2.3 ng/dL / 0.3-1.4 ng/mL/hr. Renal US was unremarkable and CT showed bilateral adrenal thickening.
A positive correlation was observed between BP and NaCl intake based on 24h dietary recall (24H). Given suppressed RAAS (volume expanded state), low dose torsemide (10mg QD) and amiloride (5mg QD) were started, lisinopril was continued, and hydralazine, labetalol, and clonidine doses were halved. Two weeks later, he was hypotensive (90/60) with pre-renal AKI (SCr 2.8) that improved with IV fluids. Diuretics, lisinopril, and hydralazine were stopped, and clonidine dosing was decreased. However, BP rebounded over a few weeks to 158-190/88-108. Torsemide+amiloride were resumed and BP improved within 1 week to 106-144/68-85, allowing for a lower labetalol dose. Over the next 6 months, BP was controlled (106-144/68-85) and hypervolemia improved (PAC/PRA 6.5/0.8) with torsemide 10 QD, amiloride 5 QD, labetalol 200 BID, and clonidine 0.1 BID. Natera Renasight genetic testing revealed a heterozygous VUS in NR3C1, encoding the glucocorticoid (GC) receptor. Pathogenic homozygous mutations cause GC resistance, with elevated ACTH and cortisol levels leading to SS-HTN from mineralocorticoid receptor activation.
Discussion
After years of ineffective anti-HTN therapy missing the mechanism of SS-HTN, serial PAC/PRA measurements with 24H, prompted an unconventional diuretic combination to achieve HTN control and reduce pill burden. This case highlights: 1) the utility of serial PAC/PRA with 24H to diagnose SS-HTN; 2) the efficacy of non-thiazide distal diuretics to treat SS-HTN; and 3) an evolving role for genetic testing to further our understanding of SS-HTN.