Endocrine Hypertension: A Practical Approach

Pappachan, Joseph M; Buch, Harit

doi:10.1007/5584_2016_26

Cited by 26 publications

(25 citation statements)

References 93 publications

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“…Primary aldosteronism (PA) is the most common cause of endocrine hypertension. 1 Recent studies have revealed that the prevalence of PA is between 3.2% and 12.7% in primary care or between 1% and 29.8% in referral centers of hypertensive patients. 2 PA is characterized by inappropriate aldosterone secretion, hypertension, hypokalemia, and suppressed plasma renin.…”

Section: Introductionmentioning

confidence: 99%

Comparison of biomarkers of endothelial dysfunction and microvascular endothelial function in patients with primary aldosteronism and essential hypertension

Sang

Wei

et al. 2021

J Renin Angiotensin Aldosterone Syst

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Introduction: Studies have shown that primary aldosteronism (PA) has a higher risk of cardiovascular events than essential hypertension (EH). Endothelial dysfunction is an independent predictor of cardiovascular events. Whether PA and EH differ in the endothelial dysfunction is uncertain. Our study was designed to investigate the levels of biomarkers of endothelial dysfunction (Asymmetric dimethylarginine, ADMA; E-selectin, and Plasminogen activator inhibitor-1, PAI-1) and assess the microvascular endothelial function in patients with PA and EH, respectively. Methods: The biomarkers of endothelial dysfunction were measured by enzyme-linked immunosorbent assay (ELISA). Microvascular endothelial function was evaluated by Pulse amplitude tonometry (PAT). Results: Thirty-one subjects with EH and 36 subjects with PA including 22 with aldosterone-producing adenoma (APA) and 14 with idiopathic hyperaldosteronism (IHA) were enrolled in our study. The ADMA levels among the three groups were different (APA 47.83 (27.50, 87.74) ng/ml vs EH 25.08 (22.44, 39.79) ng/ml vs IHA 26.00 (22.23, 33.75) ng/ml; p = 0.04), however, when the APA group was compared with EH and IHA group, there was no statistical significance (47.83 (27.50, 87.74) ng/ml vs 25.08 (22.44, 39.79) ng/ml for EH, p = 0.11; 47.83 (27.50, 87.74) ng/ml vs IHA 26.00 (33.75) ng/ml, p = 0.07). The results of ADMA levels are presented as Median (p25, p75). Whereas, levels of PAI-1 and E-selectin, microvascular endothelial function were not significantly different between PA and EH subjects. Conclusions: Our study shows no significant differences between PA and EH in terms of biomarkers of endothelial dysfunction and microvascular endothelial function. The microvascular endothelial function of PA and EH patients is comparable.

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Section: Introductionmentioning

confidence: 99%

Comparison of biomarkers of endothelial dysfunction and microvascular endothelial function in patients with primary aldosteronism and essential hypertension

Sang

Wei

et al. 2021

J Renin Angiotensin Aldosterone Syst

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“…Since increased luminal ENaC in the distal nephron is the common final mechanism for MR-mediated sodium reabsorption, Liddle syndrome resembles states of mineralocorticoid excess. The classical clinical presentation is severe hypertension in a young patient, with hypokalemia and metabolic alkalosis, in the setting of suppressed renin; however, unlike PA, aldosterone levels are low or undetectable and the syndrome does not improve with MR antagonist therapy [ 73 , 74 , 75 , 76 ]. The diagnosis of Liddle syndrome can be confirmed by genetic sequencing of the SCNN1B and SCNN1G genes, which encode for the β and γ subunits of ENaC [ 75 ], or the SCNN1A gene [ 77 ], and the treatment of choice are ENaC inhibitors such as amiloride or triamterene [ 74 ].…”

Section: Liddle Syndromementioning

confidence: 99%

The Low-Renin Hypertension Phenotype: Genetics and the Role of the Mineralocorticoid Receptor

Baudrand

Vaidya

2018

IJMS

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A substantial proportion of patients with hypertension have a low or suppressed renin. This phenotype of low-renin hypertension (LRH) may be the manifestation of inherited genetic syndromes, acquired somatic mutations, or environmental exposures. Activation of the mineralocorticoid receptor is a common final mechanism for the development of LRH. Classically, the individual causes of LRH have been considered to be rare diseases; however, recent advances suggest that there are milder and “non-classical” variants of many LRH-inducing conditions. In this regard, our understanding of the underlying genetics and mechanisms accounting for LRH, and therefore, potentially the pathogenesis of a large subset of essential hypertension, is evolving. This review will discuss the potential causes of LRH, with a focus on implicated genetic mechanisms, the expanding recognition of non-classical variants of conditions that induce LRH, and the role of the mineralocorticoid receptor in determining this phenotype.

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“…Most studies about primary AHT have being focused in genetic alterations associated with the onset and progression of AHT affecting cardiac, endocrine, and renal systems ( 1 , 2 , 30 – 32 ). Gene-specific ( 31 , 33 , 34 ), genome-wide association ( 35 – 39 ), and epigenetic studies ( 40 , 41 ) support the knowledge about the genetic components related to AHT.…”

Section: Arterial Hypertension (Aht)mentioning

confidence: 99%

“…Some of the main players in sodium/water balance are the NHE3 ( SLC9A3 , sodium-hydrogen exchanger 3) ( 86 ) present in the renal proximal tubule, the Na–K–Cl cotransporter NKCC2 (SLC12A1 ) in the thick ascending loop of Henle (LoH) ( 84 , 87 , 88 ) and the NCC (SLC12A3) along with the ENaC ( SCNN1 ) on the distal nephron (distal convoluted tubules and collecting duct). Altered function of these leads to hypertensive syndromes, such as Liddle (increased ENaC activity) ( 89 ) and Gordon (WNK4-NCC) ( 90 , 91 ), or hypotensive syndromes, such as Gitelman (NCC) ( 92 ) and Bartter (NKCC2) ( 30 ) (see Figure 1 ).…”

Section: Water-electrolytic Balance: Taking Advantage Of Exosomesmentioning

confidence: 99%

Urinary Exosomes and Their Cargo: Potential Biomarkers for Mineralocorticoid Arterial Hypertension?

Barros

Carvajal

2017

Front. Endocrinol.

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Arterial hypertension (AHT) currently affects approximately 40% of adults worldwide, and its pathological mechanisms are mainly related to renal, vascular, and endocrine systems. Steroid hormones as aldosterone and cortisol are highly relevant to human endocrine physiology, and also to endocrine hypertension. Pathophysiological conditions, such as primary aldosteronism, affect approximately 10% of patients diagnosed with AHT and are secondary to a high production of aldosterone, increasing the risk also for cardiovascular damage and heart diseases. Excess of aldosterone or cortisol increases the activity of the mineralocorticoid receptor (MR) in epithelial and non-epithelial cells. Current research in this field highlights the potential regulatory mechanisms of the MR pathway, including pre-receptor regulation of the MR (action of 11BHSD2), MR activating proteins, and the downstream genes/proteins sensitive to MR (e.g., epithelial sodium channel, NCC, NKCC2). Mineralocorticoid AHT is present in 15–20% of hypertensive subjects, but the mechanisms associated to this condition have been poorly described, due mainly to the absence of reliable biomarkers. In this way, steroids, peptides, and lately urinary exosomes are thought to be potential reporters of biological processes. This review highlight exosomes and their cargo as potential biomarkers of metabolic changes associated to mineralocorticoid AHT. Recent reports have shown the presence of RNA, microRNAs, and proteins in urinary exosomes, which could be used as biomarkers in physiological and pathophysiological conditions. However, more studies are needed in order to benefit from exosomes and the exosomal cargo as a diagnostic tool in mineralocorticoid AHT.

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Endocrine Hypertension: A Practical Approach

Cited by 26 publications

References 93 publications

Comparison of biomarkers of endothelial dysfunction and microvascular endothelial function in patients with primary aldosteronism and essential hypertension

Comparison of biomarkers of endothelial dysfunction and microvascular endothelial function in patients with primary aldosteronism and essential hypertension

The Low-Renin Hypertension Phenotype: Genetics and the Role of the Mineralocorticoid Receptor

Urinary Exosomes and Their Cargo: Potential Biomarkers for Mineralocorticoid Arterial Hypertension?

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