Endocrine Abstracts (2018) 55 P26 | DOI: 10.1530/endoabs.55.P26

Normotensive hypokalemic primary aldosteronism: How is this Possible?

Andrew Tang, Janice Pasieka & Gregory Kline


University of Calgary, Calgary, Canada.


Case history: A 40-year-old woman presented with long-standing hypokalemia fluctuating between 2.3 and 2.5 mmol/l. She had episodes of right-sided weakness and was seen by Neurologists without a clear diagnosis. She had no other past medical history. Physical examination was unremarkable. Her blood pressure (BP) was 116/63.

Investigations: Plasma aldosterone was 1363 pmol/l. Plasma renin activity was 0.18 ng/ml/h. Aldosterone-renin ratio (ARR) was 7570 (normal < 550). There was inappropriate kaliuresis (173.2 mmol in 24 h). Her natriuresis was 315 mmol in 24 h. 24-hour ambulatory BP was 129/79. Her magnesium was normal at 0.88. MRI abdomen showed a 2-cm mass in the left adrenal gland. Adrenal vein sampling demonstrated lateralization to the left with an aldosterone-cortisol ratio of 36.49 in the left adrenal, 0.78 in the right adrenal, and 6.21 in the common femoral vein.

Results and treatment: She underwent a left laparoscopic adrenalectomy. Pathology revealed a 1.9×1.5×1.5 cm adrenocortical adenoma. Post-operatively, her BP was 110/70. Her ARR normalized and her potassium normalized.

Conclusions and points for discussion: 38 cases of normotensive primary aldosteronism (PA) have been reported since 1972. The majority of cases are in females (28/38) from Europe (15/38) and Japan (15/38). 31 cases of were detected due to hypokalemia. There are numerous proposed mechanisms of normotensive PA. It is thought that these individuals were detected at an early stage of the disease. However, data from PA registries suggest that the development of hypokalemia is a late development in PA. As most patients are female, estrogen and progesterone may counteract the effects of hyperaldosteronism. However, it is still common to see hypertensive PA in pre-menopausal women and in pregnancy. Partial resistance to aldosterone is an unlikely explanation as the patient had severe hypokalemia and a suppressed renin despite a normal BP. Normotensive PA has occurred patients with Gitelman’s syndrome; however, this patient’s magnesium was normal and her hypokalemia resolved preoperatively. Perhaps this patient’s normal BP and salt-wasting was due to the natriuretic peptide system. Sodium and water retention from excess aldosterone leads to release of atrial natriuretic peptide (ANP). ANP induces systemic vasodilation. Furthermore, ANP increases glomerular filtration rate through vasodilation, promoting natriuresis and diuresis. Although there is no prospective data demonstrating long-term benefits in the diagnosis and treatment of normotensive PA, this case illustrates that PA is not confined to patients with hypertension.

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