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The Patient with Renal Dysfunction
Published in Andreas P. Kalogeropoulos, Hal A. Skopicki, Javed Butler, Heart Failure, 2023
Alexandros Briasoulis, Ily Kristine T. Yumul-Non, Paulino Alvarez
Evidence of benefit from administration of ACEi/ARB in patients with HF and ESRD is scarce. In the randomized Fosinopril in Dialysis (FOSIDIAL) trial, there was a non-significant trend toward fewer cardiovascular events with fosinopril compared with placebo among dialysis patients with LV hypertrophy.90 Although clinical data from randomized, controlled trials are lacking, the favorable effects of ACE inhibitors on neurohormonal activation and ventricular remodeling may translate into a reduction in cardiovascular events in dialysis patients with LV dysfunction and HF.93,94 However, careful monitoring of serum potassium concentration is required, as these patients carry a significant risk of hyperkalemia. The use of mineralocorticoid receptor antagonists is controversial in dialysis patients because of the risk of hyperkalemia.95 Finally, digoxin is not routinely used in dialysis patients because of the higher risk of digoxin toxicity.96 Newer additions to the therapeutic armamentarium of HF, such as ivabradine and angiotensin receptor-neprilysin inhibitors, have not been tested in patients with ESRD.
Adrenal insufficiency
Published in Nadia Barghouthi, Jessica Perini, Endocrine Diseases in Pregnancy and the Postpartum Period, 2021
Progesterone levels increase in parallel with increases in plasma estradiol levels over the course of pregnancy. Progesterone acts as a mineralocorticoid receptor antagonist, displacing aldosterone from its renal receptors.12 By near term, the human fetal adrenal gland is capable of aldosterone secretion due to development of the zona glomerulosa.10,17
Endocrine and Neuroendocrine Tumors
Published in Pat Price, Karol Sikora, Treatment of Cancer, 2020
Natasha Shrikrishnapalasuriyar, P.N. Plowman, Márta Korbonits, Ashley B. Grossman
Hypercortisolism is the most common presenting hormone excess which causes symptoms of diabetes mellitus, muscles weakness, atrophy, and osteoporosis. Adult ACC can be associated with virilization alone or a mixed syndrome of virilization and Cushing’s syndrome. Excessive release of androgens causes hirsutism and virilization, which is a common presentation in children. Hypokalemia and hypertension may occur due to the saturation of the renal enzyme 11-HSD2 which leads to activation of the mineralocorticoid receptor by high levels of glucocorticoids.73
Autophagosome protects proximal tubular cells from aldosterone-induced senescence through improving oxidative stress
Published in Renal Failure, 2021
Jing-Yuan Cao, Li-lu Ling, Wei-Jie Ni, Hong-Lei Guo, Min Yang
In order to further explore the role of autophagy in PTC senescence, a rat model induced by Aldo was established. As shown in Supplementary Figure 1, Aldo significantly increased the levels of serum creatinine (SCr) and blood urea nitrogen (BUN), while the treatment of Rap attenuated the kidney injury. In contrast, CQ treatment worsened the Aldo-induced damage (Supplementary Figure 1). Figure 4(A) showed that Aldo significantly up-regulated the ratio of LC3-II/LC3-I in renal tissues and enhanced degradation of p62 (Figure 4(A,B)). Immunohistochemical staining of LC3 showed the formation of autophagosomes in kidneys. Consistent with the above results, LC3 was diffusely distributed throughout the cells, while LC3 was punctated in control group. Furthermore, intense dot-like LC3 staining puncta appeared in Aldo treated group indicating the formation of autophagosomes (Figure 4(C)). To further detect the autophagy flux in proximal tubule cells, electron microscopy was used to evaluate the formation of autophagic vacuoles (Figure 4(D,E)). We explored the levels of mineralocorticoid receptor at the same time. It showed that Rap or CQ did not change the expression of mineralocorticoid receptor (Supplementary Figure 2). In brief, these results provided convincing proof for the occurrence of autophagy in Aldo-induced renal damage. As expected, treatment with Rap increased autophagic activity, whereas CQ treatment blocked autophagy in Aldo-infused rats (Figure 4).
Effects of eplerenone on cerebral aldosterone levels and brain lesions in spontaneously hypertensive rats
Published in Clinical and Experimental Hypertension, 2020
Xue Wang, Yuhai Zhu, Shuanglin Wang, Zhuoqun Wang, Haonan Sun, Yujie He, Wei Yao
Adverse cardiovascular effects may occur in response to aldosterone escape during chronic angiotensin-converting enzyme inhibitor (ACEI) or angiotensin receptor blocker (ARB) therapy (11), which are often used to treat hypertension. As a result, mineralocorticoid receptor antagonists have been increasingly used in patients with treatment-resistant hypertension. Several studies have shown that aldosterone receptor antagonism can protect organs and vasculature without significantly lowering blood pressure (BP), which is consistent with a major role for endogenous mineralocorticoids as mediators of cardiovascular injury (12). Blocking aldosterone receptors is an important goal in the clinical treatment of patients with heart or kidney dysfunction. As a selective aldosterone receptor blocker, eplerenone has advantages such as low sex hormone-related side effetcs and has exhibited therapeutic value in preventing cardiovascular disease and associated end organ damage (13). However, whether or not it has a role in protecting brain tissue remains unclear. Thus, hypothesizing that eplerenone could alleviate the brain damage caused by hypertension is tempting. The aim of the present study was to verify the relationship between cerebral aldosterone levels and brain tissue damage of spontaneously hypertensive rats (SHRs), and to determine the effects of eplerenone on BP and in protecting brain tissue.
Blockade of mineralocorticoid receptor ameliorates oral contraceptive-induced insulin resistance by suppressing elevated uric acid and glycogen synthase kinase-3 instead of circulating mineralocorticoid
Published in Archives of Physiology and Biochemistry, 2020
O. A. Adeyanju, O. S. Michael, A. O. Soladoye, L. A. Olatunji
The mineralocorticoid receptor (MR) was originally thought to be activated only by the aldosterone and to act primarily by promoting sodium retention and potassium excretion in the kidney resulting in increased blood pressure (Nagata 2008). However, it is now known to be expressed in nonepithelial cells, including cardiomyocytes. The MR is capable of binding multiple classes of steroids with high affinity, including the mineralocorticoids, aldosterone and deoxycorticosterone; the glucocorticoids such as cortisol (in humans) or corticosterone (in rodents); and progesterone (Sutanto and De Kloet 1991). Aldosterone is considered the primary physiological MR ligand but in some tissues, cortisol may be the primary ligand for MR (Fagart et al.1998). It has been shown that aldosterone and corticosterone activates the MR with equal efficiency and glucocorticoids circulate at concentrations much higher than that of aldosterone under normal circumstances (Fuller and Young 2005, Funder 2009).