Urinary tetrahydroaldosterone in low renin hypertension

Suppression of plasma aldosterone (PA) after saline infusion (SI) and determination of urinary aldosterone (UA) during high salt diet are utilized widely to identify patients (pts) with primary aldosteronism. Since about 4 x more aldosterone is metabolized to 3α,5β-tetrahydroaldosterone (THA) than to the aldosterone-18-oxo-glucuronide metabolite measures as UA, urinary THA (UTHA) sould more accurately identify subtle abnormalities in aldosterone production. A new RIA for UTHA was validated. UTHA in 74 normal subjects during outpatient diet was 29.4 ± 30 (mean ± 2 SD). Seventy-eight pts with low renin hypertension (LRH) were identified. Ten pts had classical primary aldosteronism with elevated UTHA and UA and abnormal SI (PA >8.0 ng/dl). Six pts had elevated UTHA with normal SI; one had elevated UA. Thirty of the pts with LRH (23 black, 7 white) and normal SI received 200 mEq Na⁺ diet for 6 days with Florinef (0.5 mg BID) during the last 3. Daily PA (0600, overnight supine, and 0800, 2-hr ambulation), 24-hr UA, and 24-hr UTHA were compared with values obtained during identical studies in 13 agematched normal subjects (4 black). Eleven pts (9 black) failed to suppress UTHA (10 pts), PA (5 pts), and/or UA (2 pts) normally. Mean plasma K⁺ was 3.4 mEq/l but only 1 of 11 pts had plasma K⁺ <3.2 mEq/l. Thus, UTHA determinations in pts with LRH and normal SI, particularly after Florinef suppression, identify a significant number of pts with evidence of aldosterone overproduction or abnormal aldosterone metabolism.