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Companion Animals Models of Human Disease
Published in Rebecca A. Krimins, Learning from Disease in Pets, 2020
Primary hyperaldosteronism, also referred to as Conn’s syndrome, is an adrenocortical disorder characterized by excessive, autonomous secretion of mineralocorticoids, mainly aldosterone, leading to systemic arterial hypertension and/or hypokalemia. After its first description in man in 1955, Conn suggested that as many as 20% of people with arterial hypertension would have primary hyper-aldosteronism. Nevertheless, primary hyperaldosteronism was considered a very rare condition for several decades. With improved screening tests, however, detection has increased, and recent studies have shown that primary hyperaldosteronism is found in about 6% of all human patients with arterial hypertension and up to 11% of those selected for therapy-resistant hypertension. Primary hyperaldosteronism has also been reported in dogs and, much more frequently, in cats. It is probably the most common adrenocortical disorder in cats, and it may be an important cause of arterial hypertension in this species, as it is in man(26–28).
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
The Adrenal Glands
Published in E. George Elias, CRC Handbook of Surgical Oncology, 2020
The diagnosis of primary hyperaldosteronism is difficult but can be established by one of the following tests: The saline infusion test; the infusion of 2 1 of normal saline over 4 hr i.v. will result in suppression of the renin-angiotensin system which will lower the serum aldosterone level in normal individuals, but fail to do so in patients with primary hyperaldosteronism. However, this test cannot be administered to patients with severe hypertension or congestive heart disease.Captopril test; the administration of 25 mg of Captopril orally will result in significant decrease in serum aldosterone within 2 hr in normal individuals as well as in those with essential hypertension, but there is no such response in patients with primary aldosteronism.
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.
The randomised Oslo study of renal denervation vs. Antihypertensive drug adjustments: efficacy and safety through 7 years of follow-up
Published in Blood Pressure, 2021
Ola Undrum Bergland, Camilla Lund Søraas, Anne Cecilie K. Larstorp, Lene V. Halvorsen, Ulla Hjørnholm, Pavel Hoffman, Aud Høieggen, Fadl Elmula M. Fadl Elmula
Seven patients in the Drug Adjustment group experienced adverse events and received appropriate treatment. These events were unrelated to study participation. The first patient experienced a fall accident with only minor head trauma approximately 2 years after randomisation, causing sequelae of chronic tiredness. The same patient died from complications of emphysema 7 years after randomisation. The second patient was diagnosed with claudication. The third and fourth patients were diagnosed with benign prostate hyperplasia, while one of them was additionally found to have sleep apnoea. The fifth patient was diagnosed with primary hyperaldosteronism (without Conn adenoma) approximately 1 year after randomisation, and was treated with an aldosterone antagonist. The last two patients were diagnosed with atrial fibrillation.
Effect of sample delivery conditions on Renin-Angiotensin-Aldosterone System (RAAS) assay
Published in Scandinavian Journal of Clinical and Laboratory Investigation, 2020
Yu Fu, Shibin Ge, Xueting Qiu, Rongrong Cui, Chen Zhang, Xindan Xu, Jianhua Li, Jianlin Feng, Jianling Bai, Min Sun, Wei Liu
Based on the important physiology of RAAS, blockade of this system is the most effective strategy for the prevention of renal disease progression, heart failure, and cardiovascular death. Indeed, Renin inhibitors (e.g. Aliskiren) [6], ACE inhibitors [7], angiotensin receptor blockers (ARBs, e.g. losartan) [8], and aldosterone antagonists (e.g. spironolactone) [9] act to decrease the effect induced by RAAS. Moreover, by detection of the levels of RAAS-related assays in patients, the therapeutic effect can be evaluated by clinicians who can tailor the program to the patient’s needs. In addition, detection of RAAS-related assays might facilitate the diagnosis of diseases. For example, identifying the aldosterone-renin activity ratio or aldosterone-renin ratio may be a helpful tool in screening for primary hyperaldosteronism (PHA) [10–13]. Overall, an exact assessment of the activity of RAAS is essential for diagnostic and therapeutic purposes.