scholarly journals Evolution of the Primary Aldosteronism Syndrome: Updating the Approach

2020 ◽  
Vol 105 (12) ◽  
pp. 3771-3783 ◽  
Author(s):  
Anand Vaidya ◽  
Robert M Carey

Abstract Context New approaches are needed to address the evolution of the primary aldosteronism syndrome and to increase its recognition. Herein, we review evidence indicating that primary aldosteronism is a prevalent syndrome that is mostly unrecognized, and present a pragmatic and pathophysiology-based approach to improve diagnosis and treatment. Methods Evidence was gathered from published guidelines and studies identified from PubMed by searching for primary aldosteronism, aldosterone, renin, and hypertension. This evidence was supplemented by the authors’ personal knowledge, research experience, and clinical encounters in primary aldosteronism. Interpretation of Evidence Renin-independent aldosterone production is a prevalent phenotype that is diagnosed as primary aldosteronism when severe in magnitude, but is largely unrecognized when milder in severity. Renin-independent aldosterone production can be detected in normotensive and hypertensive individuals, and the magnitude of this biochemical phenotype parallels the magnitude of blood pressure elevation, the risk for incident hypertension and cardiovascular disease, and the likelihood and magnitude of blood pressure reduction with mineralocorticoid receptor antagonist therapy. Expansion of the indications to screen for primary aldosteronism, combined with the use of a pathophysiology-based approach that emphasizes inappropriate aldosterone production in the context of renin suppression, will substantially increase the diagnostic and therapeutic yields for primary aldosteronism. Conclusions The landscape of primary aldosteronism has evolved to recognize that it is a prevalent syndrome of renin-independent aldosterone production that contributes to the pathogenesis of hypertension and cardiovascular disease. Expanding screening indications and simplifying the diagnostic approach will enable implementation of targeted treatment for primary aldosteronism.

PEDIATRICS ◽  
1992 ◽  
Vol 89 (2) ◽  
pp. 262-268
Author(s):  
Trudy L. Burns ◽  
Patricia P. Moll ◽  
Ronald M. Lauer

Total and cause-specific mortality was investigated in 387 first- and second-degree deceased adult relatives of three groups of children selected from those who participated in three biennial school surveys in Muscatine, Iowa: the lean group (students in the first quintile of relative weight on all three surveys); the random group (a random sample of all eligible students); and the heavy group (students in the fifth quintile of relative weight on all three surveys). A greater proportion of death certificates for heavy group relatives listed a cardiovascular cause of death (60%) compared with lean (48%) and random (43%) group relatives. The relative risk of dying of cardiovascular disease for heavy group vs random group relatives was 1.41 (95% confidence interval 1.01, 1.98). In a subset of heavy group families identified by children with elevated systolic blood pressure, the proportion of death certificates listing a cardiovascular cause was even higher (76%) and the estimate of relative risk vs random group relatives was 2.20 (95% confidence interval 1.43, 3.37). These results indicate that persistent obesity in children, particularly when accompanied by persistent blood pressure elevation, identifies families whose members are at increased risk of dying of cardiovascular disease.


2019 ◽  
Vol 240 (2) ◽  
pp. 111-122 ◽  
Author(s):  
Yuefei Huang ◽  
Pei Yee Ting ◽  
Tham M Yao ◽  
Tsuyoshi Homma ◽  
Danielle Brooks ◽  
...  

Human risk allele carriers of lysine-specific demethylase 1 (LSD1) and LSD1-deficient mice have salt-sensitive hypertension for unclear reasons. We hypothesized that LSD1 deficiency causes dysregulation of aldosterone’s response to salt intake resulting in increased cardiovascular risk factors (blood pressure and microalbumin). Furthermore, we determined the effect of biological sex on these potential abnormalities. To test our hypotheses, LSD1 male and female heterozygote-knockout (LSD1+/−) and WT mice were assigned to two age groups: 18 weeks and 36 weeks. Plasma aldosterone levels and aldosterone production from zona glomerulosa cells studied ex vivo were greater in both male and female LSD1+/− mice consuming a liberal salt diet as compared to WT mice consuming the same diet. However, salt-sensitive blood pressure elevation and increased microalbuminuria were only observed in male LSD1+/− mice. These data suggest that LSD1 interacts with aldosterone’s secretory response to salt intake. Lack of LSD1 causes inappropriate aldosterone production on a liberal salt diet; males appear to be more sensitive to this aldosterone increase as males, but not females, develop salt sensitivity of blood pressure and increased microalbuminuria. The mechanism responsible for the cardiovascular protective effect in females is uncertain but may be related to estrogen modulating the effect of mineralocorticoid receptor activation.


2017 ◽  
Vol 2 (7) ◽  
pp. 775 ◽  
Author(s):  
Joshua D. Bundy ◽  
Changwei Li ◽  
Patrick Stuchlik ◽  
Xiaoqing Bu ◽  
Tanika N. Kelly ◽  
...  

2021 ◽  

The blood pressure response to physical activities is an essential contributor to ambulatory blood pressure and a risk factor for future cardiovascular disease. Peak exercise blood pressure and the blood pressure elevation from rest to peak exercise are higher in apparently healthy men without a prior history of hypertension than in their female peers. Lifestyle modifications can decrease blood pressure during aerobic and resistance exercise. However, there may be sex differences in the effects of lifestyle modifications on blood pressure responses to exercise. Additionally, the optimal blood pressure interventions probably differ between men and women due to sex differences in lifestyles. In men, hypertension not only increases the risk of cardiovascular disease but also worsens quality of life by contributing to erectile dysfunction. Further studies are warranted to attenuate the exaggerated blood pressure response to exercise in men.


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