Endocrine Abstracts

Background: Over 90% of hypertension cases are classed as primary, with no single identifiable cause. Of cases with a secondary cause, most are attributable to renal/renovascular disease. While the impact of renal arterial stenosis is well-established, it is less apparent whether a stenosed accessory renal artery contributes to systemic hypertension. An accessory renal artery is a common anatomical variant found in 20-30% of the population. Emerging literature has highlighted cases of resistant hypertension in the context of a stenosed accessory renal artery, which showed improvement post intervention.

Case report: A 38-year-old gentleman with a known small ventricular septal defect presented to hospital with a hypertensive crisis and flash pulmonary oedema, where he was commenced on IV duresis and a GTN infusion. An echocardiogram revealed a dilated LV with an EF of 19%, attributed to long-standing hypertension. The patient was offloaded and subsequently discharged on ramipril, hydralazine, alongside other cardiac modulators, with a blood pressure in the range of 140/85mmHg. As part of a secondary hypertension workup, Plasma Metanephrines were essentially normal, and an MIBG scan ruled out a Phaeochromocytoma. The initial aldosterone renin ratio was 3, and a 24hr urinary free cortisol was slightly raised however with no clinical features of Cushings syndrome. A renal MRA revealed normal right and left renal arteries, with a highly stenosed right inferior accessory renal artery. There was no evidence of adrenal pathology. In view of the patients’ flash pulmonary oedema presentation and sub-optimal BP control, he was referred to the vascular team for consideration of arterial stenting.

Discussion: This case highlights the role of a stenosed accessory renal artery as a secondary cause of systemic hypertension. It also highlights the importance of a multi-disciplinary approach in not only ruling out other secondary causes, but also in devising optimal pharmacological and interventional strategies.