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The Primary Aldosteronism Foundation [36] is a patient-driven initiative committed to creating the paradigm shift that will lead to optimum diagnosis and treatment of primary aldosteronism by raising awareness, fostering research, and providing support to patients and healthcare professionals worldwide.
Primary aldosteronism (hyporeninemic hyperaldosteronism) is most often caused by bilateral idiopathic (micronodular) adrenal hyperplasia (almost 70% of cases) [4] and adrenal adenoma (Conn's syndrome) (about 30% of cases). [4] These cause hyperplasia of aldosterone-producing cells of the adrenal cortex resulting in primary hyperaldosteronism.
The cutoff normal individuals from those with primary hyperaldosteronism is significantly affected by the conditions of testing, such as posture and time of day. On average, an ARR cutoff of 23.6 ng/dL per ng/(mL·h), expressed in alternative units as 651 pmol/L per μg/(L·h), has been estimated to have a sensitivity of 97% and specificity of 94%. [2]
On one hand, mutations on the gene NR3C2 (coding the mineralocorticoid receptor) cause the synthesis of a non-functional receptor which is unable to bind aldosterone or function correctly. In the kidney, aldosterone plays an important role of regulating sodium and potassium homeostasis by its actions on distal nephron cells. [3]
The Randomized Aldactone Evaluation Study (RALES) trial is a landmark clinical study that assessed the impact of spironolactone, an aldosterone antagonist, on morbidity and mortality in patients with severe heart failure due to systolic dysfunction. [1] The findings from this trial significantly influenced the treatment guidelines for heart ...
Adrenocortical adenomas are classified as ACTH-independent disorders, and are commonly associated with conditions linked to hyperadrenalism such as Cushing's syndrome (hypercortisolism) or Conn's syndrome (hyperaldosteronism), which is also known as primary aldosteronism. [1]
Pseudohyperaldosteronism (also pseudoaldosteronism) is a medical condition which mimics the effects of elevated aldosterone (hyperaldosteronism) by presenting with high blood pressure, low blood potassium levels (hypokalemia), metabolic alkalosis, and low levels of plasma renin activity (PRA).
The difference between primary hyperaldosteronism and secondary hyperaldosteronism lies in the causation of excess aldosterone, where primary hyperaldosteronism refers to the overproduction of aldosterone from the adrenal glands, and secondary hyperaldosteronism refers to the overactivation of the RAAS system.