Through the progress of modern molecular biology, primary aldosteronism (PA) has been re-defined from a rare endocrine disorder, into a common cause of hypertension in clinical practice. PA can be categorized as unilateral (e.g. aldosterone-producing adenoma, APA) or bilateral (e.g. idiopathic hyperaldosteronism, IHA) disease, clinically not only distinct in pathogenesis, but also different in treatment modality.
Although hyperaldosteronism was considered the original cause of disease, PA presents many faces of clinical presentation, such as hypokalemia, refractory hypertension, and various associated comorbidities. In consistent, various driver gene (such as KCNJ5, CACNA1D, ATP1A1, ATP2B3 and CTNNB1) mutations have been documented in alone or in various combination in a single individual.
Base on the complexity of PA, many unsolved issues need to be answered, for which we will invite all the researchers to discuss in the following issues
1. What is the correlation between histopathologic feature and genetic mutation in APA and/or IHA?
2. Is there a second or sequential event to drive the ontology of PA?
3. Is the aldosterone and cortisol co-secreting adrenal tumor distinct from the classical APA?
4. Through the understanding of pathogenesis of PA, can we develop new treatment modalities targeting on the driver gene mutation?
Through the progress of modern molecular biology, primary aldosteronism (PA) has been re-defined from a rare endocrine disorder, into a common cause of hypertension in clinical practice. PA can be categorized as unilateral (e.g. aldosterone-producing adenoma, APA) or bilateral (e.g. idiopathic hyperaldosteronism, IHA) disease, clinically not only distinct in pathogenesis, but also different in treatment modality.
Although hyperaldosteronism was considered the original cause of disease, PA presents many faces of clinical presentation, such as hypokalemia, refractory hypertension, and various associated comorbidities. In consistent, various driver gene (such as KCNJ5, CACNA1D, ATP1A1, ATP2B3 and CTNNB1) mutations have been documented in alone or in various combination in a single individual.
Base on the complexity of PA, many unsolved issues need to be answered, for which we will invite all the researchers to discuss in the following issues
1. What is the correlation between histopathologic feature and genetic mutation in APA and/or IHA?
2. Is there a second or sequential event to drive the ontology of PA?
3. Is the aldosterone and cortisol co-secreting adrenal tumor distinct from the classical APA?
4. Through the understanding of pathogenesis of PA, can we develop new treatment modalities targeting on the driver gene mutation?
