Primary Hyperaldosteronism: When to Suspect It and How to Confirm Its Diagnosis

The definition of primary hyperaldosteronism (PA) has shifted, as progress has been made in understanding the disease. PA can be produced by unilateral or bilateral cortical adrenal hyperproduction of aldosterone, due to hyperplasia, aldosterone-secreting cell clusters, aldosterone-producing macro or micro adenoma/s, and combinations of the above, or by an aldosterone-producing carcinoma. PA is a highly prevalent disease, affecting close to 10% of the hypertensive population. However, PA is clearly underdiagnosed. The purpose of this review is to address current knowledge of PA’s clinical manifestations, as well as current methods of diagnosis. PA is associated with a higher cardiovascular morbidity and mortality than essential hypertension with similar blood pressure control. Young hypertensive patients, those with a first-degree relative with PA or ictus, and/or those with apnea/hypopnea syndrome, moderate/severe/resistant hypertension, adrenal incidentaloma, and/or hypokalemia should be screened for PA. PA can induce atrial fibrillation (AF), and those patients should also be screened for PA. We propose the use of the Captopril challenge test (CCT), oral salt loading, or intravenous salt loading for PA diagnosis, given their availability in the majority of hospital centers. CCT could be first-line, since it is safe and easy to perform.

Abstract 16932: Primary Hyperaldosteronism And Resistant Hypertension In Pregnancy

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.

Primary Hyperaldosteronism: A Rare Cause of Malignant Hypertension with Thrombotic Microangiopathy in a Kidney Transplant Recipient

Thrombotic microangiopathy (TMA) is a rare disease that presents with haemolysis and organ damage. The kidney is one of the main affected organs, and TMA is associated with serious complications and increased mortality. In transplanted patients, TMA is even less common and has a variety of possible causes, including thrombotic thrombocytopenic purpura (TTP) and haemolytic-uremic syndrome (HUS), infections, drugs, autoimmune disease, tumours, and malignant hypertension. Transplant-related causes, such as antibody-mediated rejection, calcineurin inhibitors, and viral infections, need to be considered as well. The authors report a rare case of TMA in a kidney transplant recipient, whose investigation revealed malignant hypertension secondary to primary hyperaldosteronism.

MANAGEMENT OF PRIMARY HYPERADOSTERONISM : DON'T WAIT UNTIL IT'S TOO LATE

Introduction: Arterial hypertension by primary hyperaldosteronism is the most frequent cause of endocrine hypertension. It is responsible for 10% of endocrine arterial hypertension. In our context, there is a delay in the diagnosis of primary hyperaldosteronism because it is under traked and also because of the high cost of check-ups. The aim of our study is to highlight the challenges in the management of these patients. This observational study i Material And Method: ncludes patients admitted at the department of endocrinology of Sheikh Khalifa Ibn Zayd universitary hospital for primary aldosteronism between January 2019 and January 2021. Primary hyperaldosteronism was dened according to the Consensus on Primary Hyperaldosteronism of The French Society of Endocrinology (SFE), in collaboration with the French Society of Hypertension (SFHTA) and the French Association of Endocrine Surgery (AFCE). For all patients, we collected demographic characteristics, familial history of hypertension and cardiovascular diseases, patient's history of hypertension and its complications. We performed biological assessments and imaging investigations. We included 10 patients .The mean age of patients Results: was 42.5 years (+/-12.06). 7/10 of patients was males. We found a family history of hypertension in 7/10 of the cases . The mean age of onset of arterial hypertension was 36.4 years (+/-7,87) . Grade 3-hypertension was found in 4/10 of the cases. Hypokalemia was found in 6/10 of the cases. The etiological investigation found bilateral adrenal hyperplasia in 4/10 of the cases. Among them 5/10 have performed catheterization of the adrenal veins, which revealed lateralization of aldosterone secretion. Conn's adenoma was found in 4/10 of the cases and unilateral adrenal hyperplasia in 2/10 of the cases. Our study illustrate the value of screening for Conclusion: primary hyperaldosteronism in young subjects with severe hypertension associated with hypokalemia and also given the curable and reversible nature of hypertension.