Abstract

Case Presentation: A 42-year-old woman with history of primary hyperaldosteronism (PA), IDDM and chronic kidney disease stage 3b (baseline Cr 2.5 mg/dl) presented at 10 weeks gestation with uncontrolled hypertension during pregnancy. Given prior difficulties conceiving and lack of discussions surrounding pregnancy risks, preconception counseling had not been done. She was taking carvedilol, spironolactone, and furosemide at pregnancy diagnosis. Given unclear safety profile in pregnancy, her spironolactone was discontinued. Her regimen was uptitrated to nifedipine 90 mmHg, carvedilol 50mg BID, hydralazine 50mg TID and furosemide 80mg BID. At 18 weeks gestation, she was readmitted with severe range hypertension and fluid overload unresponsive to escalating diuretic dosing. Due to poor urine output and creatinine to 5.5 mg/dl, she was initiated on dialysis. Her fetus was diagnosed with severe intrauterine growth restriction (IUGR) and umbilical doppler noted reversal of umbilical artery end-diastolic flow indicating severely elevated arterial resistance (Figure). During admission, she developed resistant hypertension requiring nicardipine and esmolol drips and severe headache, concerning for superimposed preeclampsia (SIPE). At 25 weeks gestation, she was taken for urgent c-section. Given extreme prematurity and growth restriction, her newborn baby passed away shortly after delivery. Discussion: This case highlights complications which arise from PA and antepartum persistent hypertension including progression of kidney disease, heart failure, IUGR, SIPE, and preterm delivery. It further highlights unique challenges using targeted therapies of mineralocorticoid receptor antagonists in PA in pregnancy. This information is crucial as PA is an increasingly recognized cause of resistant hypertension in young adults. Both PA and preeclampsia involve pathophysiologic mechanisms in the RAAS pathway and deserve further attention and research.

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