Endocrine Abstracts (2018) 55 WE13 | DOI: 10.1530/endoabs.55.WE13

Primary hyperaldosteronism presenting following a miscarriage

Layla Thurston, Sheharyar Qureshi & Marcus Martineau


West Middlesex University Hospital, London, UK.


Case history: A 35-year-old female was found to be significantly hypertensive (181/91 mmHg) following a first trimester miscarriage (at 8 weeks gestation) during her first pregnancy.

Investigations: Blood tests demonstrated moderate hypokalaemia (2.6 mmol/l) with a normal serum sodium (140 mmol/l) and eGFR (>90 ml/min). ECG showed hypokalaemic changes with prolongation of the PR interval and T wave flattening. To avoid potential misinterpretation, additional blood tests were performed prior to commencing antihypertensive therapy. Her potassium was replaced intravenously and an aldosterone: renin ratio was performed.

Results: Aldosterone 940 pmol/l, Renin <0.2 nmol/l per h with a ratio of >4700. Testing was repeated a week later, Aldosterone 1180 pmol/l, Renin <0.2 nmol/l per h with a ratio >5900. A saline infusion test (with 2 litres of 0.9% NaCl) was undertaken and further bloods drawn. Aldosterone 1380 pmol/l, Renin <0.2 nmol/l per h with a ratio of >6900 supporting a diagnosis of primary hyperaldosteronism. Adrenal MR imaging identified a 2 cm right adrenal lesion with loss of signal on the out of phase image in keeping with benign, lipid-rich adenoma.

Management: Given her suitability for a laparoscopic adrenalectomy, adrenal venous sampling (AVS) was undertaken in order to localise the source of aldosterone hypersecretion (results pending).

Conclusion: This patient was asymptomatic and her hypertension and hypokalaemia only identified following early pregnancy loss (with progesterone acting as a potential aldosterone antagonist). Whilst her MRI is suggestive of an adrenal adenoma, it is important that her initial blood results and imaging are interpreted in concert with AVS in order to guide targeted removal of the appropriate gland. 35% of cases of primary hyperaldosteronism are caused by a unilateral adenoma whilst 60% are the result of bilateral adrenal hyperplasia (bilateral idiopathic hyperaldosteronism). Whilst a laparoscopic adrenalectomy is the treatment of choice for unilateral aldosterone-secreting adenomas (with around 70% of patients being cured for hypertension following surgery); medical management (with Aldosterone antagonists such as Spironolactone/Eplerenone) should be considered in the management of bilateral disease.

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