Association of Kidney Function With Residual Hypertension After Treatment of Aldosterone-Producing Adenoma

Wu, Vin‐Cent; Chueh, Shih-Chieh; Chang, Hung-Wei; Lin, Lian‐Yu; Liu, Kao–Lang; Lin, Yen‐Hung; Ho, Yen Teng; Lin, Wei-Chou; Wang, Shuo-Meng; Huang, Kuo‐How; Hung, Kuan‐Yu; Kao, Tze-Wah; Lin, Shuei‐Liong; Yen, Ruoh‐Fang; Chen, Ming-Fong; Hsieh, Bor‐Shen; Wu, Kwan‐Dun

doi:10.1053/j.ajkd.2009.06.014

Cited by 91 publications

(77 citation statements)

References 42 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…with PA after adrenalectomy in the TAIPAI (Taiwan Primary Aldosteronism Investigation) study, and residual hypertension was thought to be a result of renal parenchymal injury. 16 We hypothesized that renal RI might be a predictor of blood pressure (BP) outcome in patients with APA after adrenalectomy. Thus, in this prospective study, we measured the RI before and after adrenalectomy in patients with APA and investigated whether preoperative renal RI was independently associated with the postoperative BP level.…”

mentioning

confidence: 99%

Renal Resistive Index Predicts Postoperative Blood Pressure Outcome in Primary Aldosteronism

et al. 2016

View full text Add to dashboard Cite

show abstract

mentioning

confidence: 99%

Renal Resistive Index Predicts Postoperative Blood Pressure Outcome in Primary Aldosteronism

et al. 2016

View full text Add to dashboard Cite

show abstract

“…Patients were followed monthly for the first three months after the operation, and then every three months. Assessment of cure rate of hypertension has been described previously 30 . Briefly, hypertension was considered cured if 75% of their recorded systolic BP was <140 mmHg and their diastolic BP was <90 mmHg with no use of anti-hypertensive medications for at least 1 year after adrenalectomy 30,31 .…”

Section: Methodsmentioning

confidence: 99%

Prevalence and Clinical Correlates of Somatic Mutation in Aldosterone Producing Adenoma-Taiwanese population

Huang

et al. 2015

Journal of Hypertension

Self Cite

View full text Add to dashboard Cite

Primary aldosteronism (PA) is a common form of secondary hypertension and has significant cardiovascular consequences. Mutated channelopathy due to the activation of calcium channels has been recently described in aldosterone-producing adenoma (APA). The study involved 148 consecutive PA patients, (66 males; aged 56.3 ± 12.3years) who received adrenalectomy, and were collected from the Taiwan PA investigator (TAIPAI) group. A high rate of somatic mutation in APA was found (n = 91, 61.5%); including mutations in KCNJ5 (n = 88, 59.5%), ATP1A1 (n = 2, 1.4%), and ATP2B3 (n = 1, 0.7%); however, no mutations in CACNA1D were identified. Mutation-carriers were younger (<0.001), had lower Cyst C (p = 0.042), pulse wave velocity (p = 0.027), C-reactive protein (p = 0.042) and a lower rate of proteinuria (p = 0.031) than non-carriers. After multivariate adjustment, mutation carriers had lower serum CRP levels than non-carriers (p = 0.031. Patients with mutation also had a greater chance of recovery from hypertension after operation (p = 0.005). A high incidence of somatic mutations in APA was identified in the Taiwanese population. Mutationcarriers had lower CRP levels and a higher rate of cure of hypertension after adrenalectomy. This raises the possibility of using mutation screening as a tool in predicting long-term outcome after adrenalectomy.Primary aldosteronism (PA), characterized by the autonomous production of aldosterone, is a common potentially curable cause of secondary hypertension 1 . It affects 5-13% of patients with hypertension in specialized centers 2,3 . PA patients have a high incidence of cardiovascular events in comparison with essential hypertension (EH) patients 4,5 . Somatic mutations in the selectivity filter of the KCNJ5 channel in APA result in a loss of selectivity for potassium and the entry of sodium, resulting in membrane depolarization, calcium mobilization, increased CYP11B2 expression, and aldosteronism 6 . Further exome sequencing of aldosterone producing adenoma (APA) has identified ATPase mutations in ATP1A1 and ATP2B3, which could lead to the opening of voltage-dependent calcium (Ca 2+ ) channels 7,8 . The CACNA1D mutation induced a shift in voltage-dependent gating to a more negative voltage, again implicating gain-of-function Ca 2+ channel mutations in APAs 9,10 . Therefore, aldosterone secretion is regulated

show abstract

“…There is accumulating evidence indicating that aldosterone-dependent kidney damage is a major determinant of blood pressure outcome following treatment in patients with PA (70). Prospective studies have reported a higher glomerular filtration rate and albuminuria in patients with APA or BAH compared with essential hypertension and significant reduction in urinary albumin excretion and glomerular filtration rate following adrenalectomy or treatment with spironolactone (71,72).…”

Section: Pathological Consequences Of Mineralocorticoid Excess Beyondmentioning

confidence: 99%

Genetics in endocrinology: Genetics of mineralocorticoid excess: an update for clinicians

Zennaro

Rickard

Boulkroun

2013

European Journal of Endocrinology

View full text Add to dashboard Cite

Aldosterone plays a major role in the regulation of sodium and potassium homeostasis and blood pressure. More recently, aldosterone has emerged as a key hormone mediating end organ damage. In extreme cases, dysregulated aldosterone production leads to primary aldosteronism (PA), the most common form of secondary hypertension. However, even within the physiological range, high levels of aldosterone are associated with an increased risk of developing hypertension over time. PA represents the most common and curable form of hypertension, with a prevalence that increases with the severity of hypertension. Although genetic causes underlying glucocorticoid-remediable aldosteronism, one of the three Mendelian forms of PA, were established some time ago, somatic and inherited mutations in the potassium channel GIRK4 have only recently been implicated in the formation of aldosteroneproducing adenoma (APA) and in familial hyperaldosteronism type 3. Moreover, recent findings have shown somatic mutations in two additional genes, involved in maintaining intracellular ionic homeostasis and cell membrane potential, in a subset of APAs.This review summarizes our current knowledge on the genetic determinants that contribute to variations in plasma aldosterone and renin levels in the general population and the genetics of familial and sporadic PA. Various animal models that have significantly improved our understanding of the pathophysiology of excess aldosterone production are also discussed. Finally, we outline the cardiovascular, renal, and metabolic consequences of mineralocorticoid excess beyond blood pressure regulation.European Journal of Endocrinology 169 R15-R25

show abstract

Association of Kidney Function With Residual Hypertension After Treatment of Aldosterone-Producing Adenoma

Cited by 91 publications

References 42 publications

Renal Resistive Index Predicts Postoperative Blood Pressure Outcome in Primary Aldosteronism

Renal Resistive Index Predicts Postoperative Blood Pressure Outcome in Primary Aldosteronism

Prevalence and Clinical Correlates of Somatic Mutation in Aldosterone Producing Adenoma-Taiwanese population

Genetics in endocrinology: Genetics of mineralocorticoid excess: an update for clinicians

Contact Info

Product

Resources

About