An Endocrine Cause of Acute Post-partum Hypertension

Abstract

This is a case of acute peri-partum hypertension secondary to Conn's syndrome. The timing of presentation offers a rare insight into the hormonal physiology of pregnancy and its impact on blood pressure regulation. This case highlights the challenges of diagnosing primary hyperaldosteronism in the peripartum period and the high index of suspicion required by the obstetric physician.

Primary hyperaldosteronism presenting as persistent postpartum hypertension: Illustrative case and systematic review

“…Our searched yielded 316 titles and abstracts, of which 14 publications were retrieved for full text review. Eighteen cases of postpartum PA were identified; 16 were documented in case reports 10,[13][14][15][16][17][18][19][20][21][22][23][24] and two were identified in a retrospective cohort study 25 (data provided by T Podymow) ( Figure 1). Six cases (33%) experienced complications in pregnancy including gestational hypertension (n ¼ 2), preeclampsia (n ¼ 2), small for gestational age (n ¼ 1), or stillbirth (n ¼ 1).…”

“…Blood pressure was elevated in the severe range after delivery in all cases. Fifteen cases were noted to have hypokalemia postpartum; 10,13,15,16,[18][19][20][21][22][23][24][25] however, most studies did not report potassium concentration during pregnancy. Aldosterone to renin ratios ranged from 20 to >1400.…”

“…Six cases (33%) experienced complications in pregnancy including gestational hypertension ( n = 2), preeclampsia ( n = 2), small for gestational age ( n = 1), or stillbirth (n = 1). However, eight cases (44%) were normotensive during pregnancy and only experienced hypertension in the postpartum period 10,13,18,19,21 (Table 1). Blood pressure was elevated in the severe range after delivery in all cases.…”

“…13 The withdrawal of circulating progesterone levels towards the end of pregnancy allows the increased aldosterone to act unopposed, thereby precipitating the peri-partum and postpartum presentation of hypertension. 13 Activating somatic mutations involved in the Wnt cell-differentiation pathway may also play a potential role in PA with worsening in pregnancy. 30 The women in our review who were diagnosed with an aldosterone-producing adenoma were identified postpartum.…”

“…13,14 This can be explained by the direct natriuretic effect of high progesterone levels during pregnancy acting on the renal proximal tubule and competitive inhibition of aldosterone at the mineralocorticoid receptors in the distal tubules, interrupting the effects of aldosterone. 13 The withdrawal of circulating progesterone levels towards the end of pregnancy allows the increased aldosterone to act unopposed, thereby precipitating the peri-partum and postpartum presentation of hypertension. 13 Activating somatic mutations involved in the Wnt cell-differentiation pathway may also play a potential role in PA with worsening in pregnancy.…”