Aldosterone-producing adrenal adenoma and idiopathic intracranial hypertension--a pathogenetic link for aldosterone?

Abstract

A 49-year-old Caucasian male with poorly controlled hypertension was admitted to St George’s Hospital in 1998 with a 6-week history of headaches and visual obscuration. He had an episode of left ventricular failure 8 months previously. A subsequent coronary and renal angiogram were normal. Hypertension was diagnosed 5 years previously and he was on treatment with amlodipine 10 mg od, methyldopa 250 mg tds, doxazosin 2 mg qds, labetalol 200 mg bd and furosemide 40 mg bd. His blood pressure (BP) was 160/90 mmHg on admission. Visual acuity was reduced in both eyes with bilateral papilloedema worse on the left than on the right. Magnetic resonance imaging (MRI) of his brain was normal. Diagnostic lumbar puncture (LP) revealed a high cerebrospinal fluid (CSF) opening pressure at 270 mmH2O (reference range 60–220 mmH2O). CSF of 4.5 ml was drained with a fall in CSF pressure to 165 mmH2O along with subjective improvement in headaches. On the basis of a normal MRI brain, bilateral papilloedema and high CSF pressure, he was diagnosed with idiopathic intracranial hypertension (IIH). His vision, however, did not improve and he underwent an optic nerve sheath fenestration to relieve the pressure on the left optic nerve. The patient was referred to the Blood Pressure Unit at St George’s Hospital in January 2003 with resistant hypertension with a BP of 210/100 mmHg. Initial investigations showed serum Na+ 139 mmol/l, serum K+ 3.5 mmol/l and bicarbonate 29 mmol/l. His plasma aldosterone concentration was 1476 pmol/l (normal range of 100–600 pmol/l) and his plasma renin activity (PRA) was suppressed at 0.1 ng/ml/h (normal upright range of 0.5–4.5 ng/ml/h) giving a plasma aldosterone concentration to PRA [aldosterone to renin (ARR)] ratio of 14760. Urinary catecholamines were normal. A computerized tomography (CT) scan of his …