ArticleBMC endocrine disorders2025
Paradoxical gestational normotension in primary aldosteronism: a case report of diagnostic challenges and postpartum rebound hypertension.
Article in BMC endocrine disorders, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundPrimary aldosteronism (PA), characterized by dysregulated aldosterone secretion, is a leading cause of endocrine hypertension. While its association with cardiovascular morbidity is well-established, pregnancy-related PA remains understudied, with limited data on hemodynamic fluctuations and diagnostic pitfalls. Transient blood pressure normalization during gestation, attributed to progesterone-mediated mineralocorticoid receptor antagonism, often masks underlying pathology, delaying diagnosis and increasing postpartum complications. CASE PRESENTATION: A 29-year-old woman presented with recurrent dizziness and labile hypertension (ambulatory BP: 135–163/85–108 mmHg). The initial evaluation did not include assessment for secondary hypertension, with symptoms attributed to essential hypertension. Following pregnancy confirmation, amlodipine was discontinued due to teratogenicity concerns. Paradoxically, first-trimester stage 1 hypertension (119–142/72–83 mmHg) normalized by the third trimester (108–126/72–79 mmHg) without gestational hypertensive disorders. At 6 weeks postpartum, progressive rebound hypertension (145–167/92–105 mmHg) prompted tertiary referral. Biochemical profiling revealed suppressed plasma renin (2.81 mU/L) and elevated aldosterone-to-renin ratio [ARR: 5.427(ng/dL)/(mU/L)]. Confirmatory testing (seated saline infusion and captopril suppression tests) demonstrated dysregulated aldosterone secretion. Adrenal CT identified an 8-mm right adrenal nodule, with adrenal vein sampling confirming lateralized secretion (lateralization index: 7.46). Laparoscopic right adrenalectomy achieved hypertension remission and complete biochemical remission.
conclusionPA should be suspected in hypertensive women of reproductive age, irrespective of potassium status. Pregnancy-induced blood pressure normalization does not preclude PA diagnosis, mandating systematic postpartum reassessment. Early subtype differentiation and targeted intervention mitigate long-term cardiovascular risks. CLINICAL TRIAL NUMBER: Not applicable.
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