Endocrine Abstracts

Case history: 48 year old man presented in the endocrinology clinic for further evaluation of hypertension (HTN). He had a hospital admission 2 months ago with worsening dyspnoea and markedly elevated BP (236/149 mmHg). He denied any visual disturbances or chest pain. There were no symptoms to suggest any endocrinopathy. His PMH included previous inguinal hernia repair. He was not on regular medications and he had no allergies. He lived with his family, worked as a manager and he was a smoker. There was a family history of HTN in his father but no other cardiovascular conditions. On examination, he appeared overweight but he had no stigmata of any endocrine conditions. Respiratory and cardiovascular examination were unremarkable

Investigations: During his hospital admission, he was investigated for end organ damage and underlying secondary causes. These included baseline blood tests, chest x-ray, ECHO, urine dipstick, fundoscopy, ARR and 24-h-urine catecholamines, HBA1c and lipid profile.

Results and Treatment: Investigations revealed evidence of end-organ damage (LVH pattern with left strain on ECG, LVH on ECHO, Grade 3 retinopathy on fundoscopy, Creatinine:117) and hyperreninemic hyperaldosteronism (Renin: 20.4-H, Aldosterone: 760-H, ARR: 37. 24 urine metadrenalins: 1.4 (<1.2), normetadrenalins: 4.5 (< 2.9) 3-methoxytyramine 1.7 (<1.3). In addition, he was diagnosed with impaired glucose regulation and hyperlipidaemia. He was commenced on Ramipril, amlodipine, bisoprolol and Furosemide. In view of the above, he had a CT with contrast to visualize the adrenals and renal arteries. This showed a 13mm myolipoma on the right adrenal, normal kidneys with no masses and bilateral slightly beaded renal arteries suggestive of fibromuscular dysplasia (FMD). He repeated urine collection for catecholamines three times and were all negative. At follow up, he remained on 4 different antihypertensive agents, with moderate control of his HTN. He has been referred to the Vascular team for further evaluation.

Conclusions and points of discussion: FMD is a non-inflammatory, non-atherosclerotic disorder that leads to arterial stenosis, occlusion, aneurysm and dissection and is more common in women. Its exact prevalence is unknown and although the disease is thought to be rare, recent studies have suggested that it may be underdiagnosed. In our case, demographics, personal and family history would suggest a likely diagnosis of essential hypertension. However, in light of evidence of accelerated hypertension, further assessment of secondary causes was warranted. Hyperreninemic hyperaldosteronism with hypertension is indicative of renovascular disease. In the abscence of more common causes, FMD should remain in the differential diagnosis and appropriate imaging considered.