Quadric analysis in the preoperative distinction between patients with and without adrenocortical tumors in hypertension with aldosterone excess and low plasma renin

Aitchison, J.; Brown, J. J.; Ferriss, J. B.; Fraser, Robert; Kay, A. W.; Lever, A. F.; Neville, A. Munro; Symington, T.; Robertson, James I.

doi:10.1016/0002-8703(71)90336-x

Cited by 62 publications

(23 citation statements)

References 16 publications

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“…The leading symptom of primary aldoste ronism is hypokalemia which is reported to be more severe in patients with APA than in those with 1AH [1,9], In this study serum potassium levels were lower (although not significantly) in APA than in IAH.…”

Section: Discussioncontrasting

confidence: 41%

Primary Aldosteronism: Diagnosis and Noninvasive Lateralization Procedures

Vetter¹,

Fischer²,

Galanski³

et al. 1985

Cardiology

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In 72 patients with primary aldosteronism who were classified on the basis of adrenal pathology after adrenalectomy, analysis of routine clinical and laboratory data, of supine and upright plasma aldosterone, and of plasma renin activity were of limited value in differentiating patients with aldosterone-producing adenoma(s) (APA, n = 59) from those with idiopathic adrenal hyperplasia (IAH, n = 13). Normokalemic aldosteronism occurred in 6 patients (3 APA, 3 IAH). A correct classification of the adrenal lesion(s) was obtained in 80% of the patients by computed tomography and only in 69% by adrenal scintiscan. In addition, adrenal scintiscan was hampered by a relatively high rate of incorrect results independent of whether dexamethasone was used or not. Small adenomas ( < 1 cm) and more often adrenal hyperplasia may escape visualization by computed tomography.

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Section: Discussioncontrasting

confidence: 41%

Primary Aldosteronism: Diagnosis and Noninvasive Lateralization Procedures

Vetter¹,

Fischer²,

Galanski³

et al. 1985

Cardiology

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“…Because of this, attempts have been made to develop multi-parameter biochemical models to distinguish the two subtypes (14,148). Parameters typically included in such models have included plasma sodium, potassium, total carbon dioxide, aldosterone, and renin.…”

Section: Biochemical Approachesmentioning

confidence: 99%

Primary Aldosteronism: Changing Definitions and New Concepts of Physiology and Pathophysiology Both Inside and Outside the Kidney

Stowasser

Gordon

2016

Physiological Reviews

125

134

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In the 60 years that have passed since the discovery of the mineralocorticoid hormone aldosterone, much has been learned about its synthesis (both adrenal and extraadrenal), regulation (by renin-angiotensin II, potassium, adrenocorticotrophin, and other factors), and effects (on both epithelial and nonepithelial tissues). Once thought to be rare, primary aldosteronism (PA, in which aldosterone secretion by the adrenal is excessive and autonomous of its principal regulator, angiotensin II) is now known to be the most common specifically treatable and potentially curable form of hypertension, with most patients lacking the clinical feature of hypokalemia, the presence of which was previously considered to be necessary to warrant further efforts towards confirming a diagnosis of PA. This, and the appreciation that aldosterone excess leads to adverse cardiovascular, renal, central nervous, and psychological effects, that are at least partly independent of its effects on blood pressure, have had a profound influence on raising clinical and research interest in PA. Such research on patients with PA has, in turn, furthered knowledge regarding aldosterone synthesis, regulation, and effects. This review summarizes current progress in our understanding of the physiology of aldosterone, and towards defining the causes (including genetic bases), epidemiology, outcomes, and clinical approaches to diagnostic workup (including screening, diagnostic confirmation, and subtype differentiation) and treatment of PA.

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“…The presence of an adenoma was established by surgery or adrenal venography in all but one. This patient had very high plasma aldosterone, sodium, and bicarbonate concentrations, markedly suppressed plasma renin activity, and a very low plasma potassium concentration as is characteristic of patients with an adrenal adenoma rather than hyperplasia (17 2400 0600 1200 1800 2400 0600 200 1800 TIME OF DAY FIGURE 2 The circadian rhythm of plasma aldosterone (PA) and plasma cortisol (PC) have been superimposed for seven patients with primary aldosteronism and adenoma and two patients with hyperplasia. The 2400 hour absolute concentration of each hormone is included.…”

Section: Introductionmentioning

confidence: 96%

Circadian Rhythm of Plasma Aldosterone Concentration in Patients with Primary Aldosteronism

Kem¹,

Weinberger²,

Gómez-Sánchez³

et al. 1973

J. Clin. Invest.

120

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A B S TRA CT Plasma aldosteronie, cortisol, and renin activity were measured in nine recumbent patients with hyperaldosteronism, including seven with adenomas, one with idiopathic hyperplasia, and one with glucocorticoid suppressible hyperplasia. All had peak values of plasma aldosterone concentration from 3 a.m. to noon and lowest values at 6 p.m. or midnight. This rhythm was similar to the circadian pattern of plasma cortisol in the same patients. When these data were normalized to eliminate the wide variation in ranges of plasma aldosterone and cortisol between individuals, there was an excellent correlation (r = + 0.87, P < 0.005) between the two hormones. In contrast, plasma aldosterone concentrations did not correlate with plasmla renin activity before or after normalization of data.Short term suppression of ACTH by adniinistration of dexamethasone eliminated the circadian variation of plasma aldosterone in both patients with hyperplasia and in four of five patients witlh adenomas, while it markedly altered the rhythm in the fifth. Similar doses of dexamethasone were administered to four normal subjects and did not flatten the circadian rhyrthm of plasma aldosterone.These data suggest that patients witlh primary aldosteronism have a circadian rhythm of plasma aldosterone mediated by changes in ACTH.This work was presented in part at the Westerni Section

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Quadric analysis in the preoperative distinction between patients with and without adrenocortical tumors in hypertension with aldosterone excess and low plasma renin

Cited by 62 publications

References 16 publications

Primary Aldosteronism: Diagnosis and Noninvasive Lateralization Procedures

Primary Aldosteronism: Diagnosis and Noninvasive Lateralization Procedures

Primary Aldosteronism: Changing Definitions and New Concepts of Physiology and Pathophysiology Both Inside and Outside the Kidney

Circadian Rhythm of Plasma Aldosterone Concentration in Patients with Primary Aldosteronism

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