[Symposium] Adrenal (1)
20 Mar 2026
13:50
15:20
201BC
Update in Primary Aldosteronism
| Time | Session |
|---|---|
|
13:50
14:20
|
Hirotaka ShibataJapan
Speaker
2026 Update in Primary AldosteronismDiagnosis and Management of Adrenal Insufficiency
201BC
|
|
14:20
14:50
|
Edith ChowHong Kong, China
Speaker
Personalizing Hypertension Treatment through Renin-Angiotensin-Aldosterone Physiology: Are We There Yet?Hypertension is the leading cardiovascular risk factor accounting for the global burden of cardiovascular disease and death. Renin-angiotensin-aldosterone-system takes a crucial role as the regulator in maintaining the body’s electrolyte homeostasis. RAAS overactivity is a key pathophysiological mechanism in hypertension. Dysregulation of the RAAS is closely tied to development of hypertension.
Primary aldosteronism is a disorder characterised by renin-independent aldosterone excess, manifesting as hypertension with greater risk of end-organ damage compared to individuals with essential hypertension. Recent guidelines for hypertension and primary aldosteronism have uniformly advocated for an expanded screening strategy for primary aldosteronism to improve awareness and detection of this treatable secondary cause of hypertension.
Traditionally, screening for primary aldosteronism has relied on the conception that it is a dichotomous condition. However, increasing evidence have suggested that renin and aldosterone abnormalities may exist on a continuum of clinical severity. In individuals with elevated blood pressure and family history of hypertension, higher levels of aldosterone are associated with greater risks of incident hypertension. Among normotensive individuals, the association between high aldosterone and incident hypertension were only evident among those with a suppressed renin, suggesting a phenotype of subclinical aldosterone excess. On the other hand, among individuals with resistant hypertension, targeting RAAS overactivity with mineralocorticoid antagonists have demonstrated superior blood pressure reduction compared to beta-blockers or alpha-blockers, especially in those with lower renin levels. With the development of novel treatments for hypertension that target RAAS, including aldosterone synthase inhibitors and non-steroidal mineralocorticoid inhibitors, there is growing interest in the role of RAAS hormones or metabolites as biomarkers to guide diagnosis, prognostication and management of hypertension.
Building upon this foundation, this talk will explore the potential role of aldosterone, renin and their metabolites as biomarkers in diagnosing and treating individuals with hypertension.
201BC
|
|
14:50
15:20
|
Vincent WuTaiwan
Speaker
From Taiwan to the World: The TAIPAI Journey Transforming Primary AldosteronismPrimary aldosteronism (PA) is an increasingly recognized cause of secondary hypertension, affecting an estimated 5%-15% of hypertensive patients. This condition, once thought to be rare, is now understood to be a relatively common contributor to high blood pressure, particularly in cases resistant to standard antihypertensive therapies. PA arises primarily from either bilateral adrenal hyperplasia or an aldosterone-producing adenoma. The pathophysiology of PA is characterized by excessive and autonomous secretion of aldosterone, an adrenal hormone that plays a critical role in regulating blood pressure and fluid balance.
Diagnosing PA involves a multi-step process, beginning with screening tests to identify at-risk individuals, followed by confirmatory tests, and finally, subtype differentiation to determine the specific cause of the condition. Screening is especially recommended for patients who present with certain risk factors, such as resistant hypertension, unexplained hypokalemia, or an onset of hypertension at a young age (under 40 years). Family history of PA, early signs of target organ damage, the presence of an adrenal incidentaloma, obstructive sleep apnea, unexplained atrial fibrillation, and psychosomatic symptoms are also significant indicators warranting screening. Additionally, patients with hypertension but no other comorbidities should be evaluated for PA, as it could be the underlying cause.
PA does not occur in isolation; it is often found to coexist with Mild Autonomous Cortisol Secretion (MACS). This co-occurrence presents a more complex clinical picture, as MACS can further aggravate the cardio-renal-vascular complications already associated with PA. Moreover, it can contribute to abnormalities in glucose metabolism, increasing the risk of diabetes and other metabolic disorders. One of the key challenges in the diagnosis and management of PA, particularly when MACS is present, lies in accurately interpreting the aldosterone-to-cortisol ratios during adrenal venous sampling, a critical step in subtype differentiation.
201BC
|