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Background <p>Primary 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.</p> Case presentation <p>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.</p> Conclusion <p>PA 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.</p> Clinical trial number <p>Not applicable.</p>

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Paradoxical gestational normotension in primary aldosteronism: a case report of diagnostic challenges and postpartum rebound hypertension

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年12月26日

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  • Yuzhu Fan,
  • Bing Wang,
  • Leilei Xing,
  • Guiting Liang,
  • Junhong Duan,
  • Chunliang Wang,
  • Yu Lai

摘要

Background

Primary 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.

Conclusion

PA 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.