Endocrine Abstracts

Background: Endocrine hypertension accounts for around 3% of the secondary forms of hypertension and screening of young hypertensive patients for secondary causes is mandatory.

Aim: To present difficulties in endocrine assessment of arterial hypertension in people younger than 40 years.

Patients and methods: Twenty-two patients (15 M/7 F), aged 27.1±7.7 years (range:16-40 years), with systemic hypertension (systolic blood pressure=187.5±24.6 mmHg) were evaluated for endocrine hypertension. Cardiac and renal causes of secondary hypertension were previously excluded. Plasma catecholamines were measured by ELISA, aldosterone by radioimmunoassay or ELISA, plasma cortisol, direct renin by immunochemiluminescence.

Results: Essential hypertension with normal hormonal assessment was diagnosed in 21 patients (95.4%) and one patient presented subclinical Cushing due to a right adrenal tumour. Hormonal assessment in our series revealed: basal 0800. cortisol levels=18.6±4.6 (μg/dl, 0800 cortisol levels after 1 mg overnight dexamethasone suppression test=1±0.1 μg/dl; median plasma metanephrines=14.5 pg/ml (25th percentile:10 pg/ml; 75th percentile: 26 pg/ml), median plasma normetanephrines=34 pg/ml (25th percentile:20.75 pg/ml; 75th percentile: 70.5 pg/ml), upright morning aldosterone=161.8±65.7 pg/ml with aldosterone:renin ratio=3.5±1.6 ng/mIU. One male patient, aged 18, presented with paroxysmal hypertension (240/130 mmHg) and mild hypokaliemia (3.1 mmol/l). The patient’s morning upright plasma aldosterone concentration was normal (247.1 pg/ml; reference range 38.1-313.3), but his plasma active renin concentration was extremely high (>500 mIU/l) with very low aldosterone:renin ratio. CT scan revealed a 17 mm lesion in the right renal kidney, suggesting a possible reninoma. Because therapy with sartans was stopped only 4 days prior to renin measurement, a prolonged 6 weeks withdrawal was made prior to a second renin assessment, which showed normal values (54.8 mIU/l). Renal MRI revealed cystic nature of the renal lesion.

Conclusion: Drugs interfering with renin-aldosterone axis should be stopped a longer period for avoiding false increase of direct renin.