Conn's Syndrome With Severe Hypertension

Chalmers, T. M.; Fitzgerald, M. G.; James, A. H.; Scarborough, Harold

doi:10.1016/s0140-6736(56)91092-3

Cited by 77 publications

(13 citation statements)

References 14 publications

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“…Severe nephrosclerosis has been found in renal biopsy specimens from two patients (11,12). Our patients 2 and 3 demonstrate functional evidence thereof.…”

Section: Renal Hemodynamicssupporting

confidence: 51%

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Renal Function in Primary Aldosteronism 1

Dustan¹,

Corcoran²,

Page³

1956

J. Clin. Invest.

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Primary aldosteronism is characterized by weakness-a sequel to potassium loss; hypertensionattributed to sodium retention; thirst and polyuria; and excretion of dilute, alkaline urine (1). These defects imply significant changes in renal function.The purpose of this report is to describe preand postoperative observations of renal function in three patients suffering from aldosterone-secreting adrenal cortical tumors.The data indicate that excess urinary potassium excretion is attributable to aldosteronism as such, and may bear on the basic cellular mechanism of action of aldosterone. The polyuria and excretion of dilute urine are recognized sequelae of potassium deficiency and probably not directly due to hormonal action. It also seems likely that renal tubular fluid as delivered from some proximal site to more distal tubules may be hypotonic rather than isotonic. The data suggest that aldosterone has profound effects on the maintenance of renal blood flow and glomerular filtration rates. From the clinical aspect, the diagnosis of aldosteronism should be strongly suspected in patients with hypertension of unknown origin who, in the presence of adequate renal excretory function, excrete alkaline urine and show loss of urinary concentrating power. METHODS AND PROCEDURESThe three patients studied suffered from primary aldosteronism which was cured by resection of small adrenal cortical adenomata. Detailed diagnostic data together with evidences of impaired glucose tolerance are reported elsewhere (2). All three had had hypertension for years, all showed hypokalemia with hypochloremic alkalosis, impairment of urinary concentrating power and persistently alkaline urine. Preoperatively, the aldosterone content of the urine was increased in each.

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“…Severe nephrosclerosis has been found in renal biopsy specimens from two patients (11,12). Our patients 2 and 3 demonstrate functional evidence thereof.…”

Section: Renal Hemodynamicssupporting

confidence: 51%

“…The same was true of Conn's patient (1) and of the patient of Chalmers and his associates (11). This, like the defect in water reabsorption, might represent renal injury with a defect of the mechanism of urinary acidification, notably the renal carbonic anhydrase system.…”

Section: Acidification and Aldosteronismmentioning

confidence: 77%

Renal Function in Primary Aldosteronism 1

Dustan¹,

Corcoran²,

Page³

1956

J. Clin. Invest.

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“…Early attempts at imaging APAs involved relatively insensitive and invasive procedures such as abdominal X-ray/tomography with presacral gas insufflation (86) and adrenal venography (99), which carried with it a significant risk of contrast extravasation and adrenal hemorrhage (254,369).…”

Section: E Imaging 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

124

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 diagnosis is strengthened by fi nding excessive potassium in the urine and is proven by the presence of excessive aldosterone in the urine. The hypertension may sometimes be very severe and mimic hypertension of any other cause (40). Surgical removal of the tumor cures the hypertension.…”

Section: Hypertensionmentioning

confidence: 99%