Determination of urinary 18-hydroxycortisol in the diagnosis of primary aldosteronism

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Abstract
Urinary excretion of 18-hydroxycortisol (18-OHF), 18-hydroxycorticosterone (18-OHB) and aldosterone 18-glucuronide (Aldo-18-glu) was measured in 10 patients with primary aldosteronism; 5 with aldosterone-producing adenoma (APA) and 5 with idiopathic hyperaldosteronism (IHA), 10 patients with essential hypertension (EHT) and 11 nor-motensive subjects. In EHT patients, urinary 18-OHF (172 ± 15 μ/24h) and 18-OHB (3.1 ± 0.6 μ/24h) values were not significantly different from 18-OHF (142 ± 35 jig/24h) and 18-OHB (3.6 ± 0.5 μg/24h) in the controls. Urinary 18-OHF values were significantly higher in APA (640 ± 213 μg/24h) when compared with controls and EHT, whereas 18-OHB (11.3 ± 1.5 μ/24h) values were only slightly elevated. Both 18-OHF and 18-OHB were significantly increased in APA compared with 18-OHF (232 ± 56 μg/24h) and 18-OHB (4.6 ± 0.3 μ/24h) in IHA. The two urinary steroids, especially 18-OHF proved to be a useful marker for the diagnosis of APA, confirming the previous findings. Aldo-18-glu was not significantly different between APA and IHA. In normal subjects when sodium intake was restricted to 48meq/day for four days the urinary 18-OHF was increased two fold to 383 ± 59 μ/24h (p < 0.01 vs control period) associated with comparable rise in plasma renin activity. This suggests that the biosynthesis of 18-OHF is partly under control of renin-angiotensin axis in normal subjects.