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Primary hyperaldosteronism
Published in Nadia Barghouthi, Jessica Perini, Endocrine Diseases in Pregnancy and the Postpartum Period, 2021
Vivek Alaigh, Amanda Fernandes
Primary hyperaldosteronism is one of the more common causes of secondary hypertension in the nonpregnant adult population, with a prevalence of 5–10%.3 Its prevalence in the pregnant population is unknown due to limited data.
Hormones of the Adrenal Gland
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
Secondary hyperaldosteronism arises when there is excess renin and, hence, angiotensin II stimulation of the zona glomerulosa. The causes of secondary hyperaldosteronism may be divided into two groups: (i) normotensive and (ii) hypertensive groups. The normotensive group includes cirrhosis (reduced metabolism of aldosterone) and cardiac failure (due to renin release caused by low renal perfusion), and oedema is a feature of the primary disease. The hypertensive group includes renal artery stenosis and accelerated hypertension, and oedema is not a feature of this group.
Pituitary and adrenal disease
Published in Catherine Nelson-Piercy, Handbook of Obstetric Medicine, 2020
Primary hyperaldosteronism may be due to the following: Adrenal aldosterone-secreting adenomaAdrenal carcinomaBilateral adrenal hyperplasia
Pre-bout hypertension in the combat sports athlete: clearance recommendations
Published in The Physician and Sportsmedicine, 2023
Kevin deWeber, Ken S Ota, Cicely Dye
High BP is the most common abnormal finding during pre-participation cardiovascular screening in athletes [5]. Hypertension is very common, with prevalence of 41% in men age 20–44 and 29% in women age 20–44 using JNC-8 criteria [1]. The prevalence rises dramatically with age. African Americans have the highest overall prevalence among the various races/ethnicities, followed by Asians, Caucasians, and Hispanics. The vast majority of hypertension is ‘essential’ and is caused by several factors including but not limited to advancing age, genetics, excessive salt use, inadequate exercise/fitness, and obesity. Secondary hypertension, which occurs in about 10% of adults, is caused by more specific and often remediable causes such as renal parenchymal disease, renovascular disease, aortic coarctation, drugs (prescription or illicit), obstructive sleep apnea, primary hyperaldosteronism, Cushing’s syndrome, hyperthyroidism, primary hyperparathyroidism, congenital adrenal hyperplasia, pheochromocytoma, and acromegaly [1].
A patent review of aldosterone synthase inhibitors (2014-present)
Published in Expert Opinion on Therapeutic Patents, 2022
As a key component of the renin-angiotensin-aldosterone system (RAAS), mineralocorticoid aldosterone has been well recognized for its principal role in regulating fluid and electrolyte balance [1]. It promotes renal sodium (Na+) and water reabsorption, and induces potassium (K+) and hydrogen (H+) excretion in epithelial cells of the distal nephron [2]. Not surprisingly, dysregulation of aldosterone, either excess or deficiency, has been linked to the clinical conditions of various cardiovascular and metabolic diseases. ‘Hyperaldosteronism’ (excess aldosterone) contributes to arterial hypertension (AH), congestive heart failure, and chronic kidney disease (CKD) [3,4]. Meanwhile, aldosterone deficiency or ‘hypoaldosteronism’ results in hyponatremia, hyperkalemia, and acidosis [5,6].
An evaluation of KBP-5074 in advanced chronic kidney disease with uncontrolled hypertension
Published in Expert Opinion on Investigational Drugs, 2021
Bertram Pitt, Frederic Jaisser, George Bakris
Primary hyperaldosteronism has been reported in approximately 10 to 20% of patients with RH [16]. However, more recent data suggest the prevalence may be as high as 58% due to unrecognized forms of this condition that may elude detection when using current diagnostic thresholds [17]. This high and largely unrecognized incidence of primary hyperaldosteronism in RH and its causative effects on cardiorenal disease progression make the advent of a clinically suitable MRA that much more relevant. In addition to high MR-binding affinity, an agent with a long half-life would be of great utility in clinical practice as this allows for 24-hour BP control. Currently there is no clinically useful MRA that could serve as a suitable fourth-line agent to treat RH in stage 3B/4 CKD that also provides vascular and end organ protection, without unwanted hormonal side effects, and is well tolerated with a low incidence of hyperkalemia, thereby avoiding or minimizing the need for oral potassium binders.