Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2007) 14 P487


General Hospital of Athens ‘G. Gennimatas’, Department of Endocrinology & Diabetes Center, Athens, Greece.

Background: The renin-angiotensin system is important for blood pressure control. Screening and diagnostic tests used so far to diagnose patients with aldosterone related hypertension does not take into consideration the stimulating ACTH effect on aldosterone secretion.

Objective: To assess the role of aldosterone in essential hypertension using a modified suppression test, performed under suppressed ACTH levels.

Subjects and methods: 117 hypertensive patients with essential hypertension and 34 age and sex matched normotensive controls were studied. A modified fludrocortisone suppression test (FST) under suppressed ACTH levels was performed to all participants (fludrocortisone 0.4 mg daily in 4 divided doses for 4 days and overnight dexamethasone suppression with 1 mg on day 4). Basic biochemical parameters, ACTH, plasma aldosterone and plasma active renin were measured at 08.00 am on day 1 and 5. Median value of aldosterone to renin ratio (ARR) +2 standard deviations in the control group after the test was used to define normal cut-off.

Results: Basal aldosterone, renin, ARR, K+, and urine 24-hour K+ did not differ between the two groups. Post-test aldosterone and ARR were significantly higher in hypertensives compared to controls (47.79±3.97 (mean±S.E.M) vs 132.2±11.18 pmol/L, P<0.0001 and 23.4±3.25 vs 55.54±7.53 pmol/L/pg/ml, P<0.0001). Baseline K+ levels were inversely correlated to post-test aldosterone and ARR only in the hypertensive group (r=−0.21, P<0.05 and r=−0.24, P<0.01 respectively). A significant proportion of hypertensives (29.05%) failed to suppress aldosterone levels to normal range after the test.

Conclusions: A modified FST revealed that a high percentage (29.05%) of patients who were thought to have essential hypertension, have autonomy of aldosterone secretion. This observation could possibly explain the cause of the low renin levels of the 25% of patients with essential hypertension reported in literature.

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