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Primary aldosteronism presenting as post-partum pre-eclampsia (#411)

Shivangi Gupta 1 , Braden Engelbogen 1 , Aidan Kashyap 2 , Paul Moench 1 , Carolyn Allan 1
  1. Department of Endocrinology, Monash Health, Clayton, Victoria, Australia
  2. Department of Obstetrics & Gynaecology, Monash Health, Clayton, Victoria, Australia

Primary aldosteronism (PA) is an under-diagnosed cause of hypertension. Recognition may be delayed during pregnancy where physiological changes and pre-eclampsia can obscure the diagnosis.

A 31-year-old woman presented with postpartum pre-eclampsia. Hypertension had been diagnosed aged 17 years. On no anti-hypertensive during her first pregnancy, average systolic blood pressure (SBP) was 112 mmHg. Following a spontaneous vaginal birth, she was re-admitted day 5 postpartum with hypertension (SBP 160 mmHg) and hypokalaemia (3.3mmol/L) and was discharged on enalapril which was discontinued after blood pressure normalised within one year. She then had recurrent presentations with hypertension (peak SBP 200 mmHg) and hypokalaemia (3.4 mmol/L) treated with telmisartan (ceased pre-conception). During her second pregnancy average SBP was 123 mmHg on no antihypertensive therapy. Following a spontaneous vaginal birth at term she developed hypertension (peak SBP 180 mmHg) two hours postpartum, resistant to anti-hypertensive therapy (labetalol 400 mg QID, nifedipine XR 60 mg BD, enalapril 10 mg BD), prompting investigation for secondary hypertension. Evaluation at day 11 postpartum (on the above medications) demonstrated hypokalaemia (3.1 mmol/L), urine protein-to-creatinine ratio (164.3mg/mmol) and aldosterone-renin ratio (592.6 pmol/munit; aldosterone 1600 pmol/L, renin 2.7 munit/L). CT - normal adrenal glands. A presumptive diagnosis of PA was made, and commencement of spironolactone resulted in blood pressure improvement. On discharge at day 15 postpartum SBP was 115-138mmHg on labetalol 400 mg QID, nifedipine XR 30 mg daily, enalapril 10mg BD and spironolactone 25mg daily. Confirmatory PA testing is pending. 

Postpartum hypertension is a possible discriminating feature of PA. Across both these pregnancies blood pressure normalised antenatally but relapsed with recurrent hypokalaemia in the immediate postpartum period. Antenatally, rising placental production of progesterone competes with aldosterone at the distal convoluted tubule and mitigates mineralocorticoid effects of PA. Postpartum, abrupt withdrawal of progesterone unmasks autonomous aldosterone activity, mediating postpartum hypertension [1,2].

 

  1. Ronconi V, Turchi F, Zennaro MC, Boscaro M, Giacchetti G. Progesterone increase counteracts aldosterone action in a pregnant woman with primary aldosteronism. Clin Endocrinol (Oxf). 2011;74(2):278–9.
  2. Forestiero V, Sconfienza E, Mulatero P, Monticone S. Primary aldosteronism in pregnancy. Rev Endocr Metab Disord. 2023 Feb;24(1):39-48.