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At least 19 recordsLinked to original sources
PubMed1976

Renal abnormalities and vascular complications in primary hyperaldosteronism. Evidence on tertiary hyperaldosteronism.

The frequency of underlying renal or renal artery disease, and the incidence of vascular complications were reviewed in a series of 136 cases of primary hyperaldosteronism. This was in order to investigate the possible existence of 'tertiary' hyperaldosteronism, and to examine the commonly held view that primary hyperaldosteronism is a relatively benign form of hypertension. Ten cases (7-4 per cent) had evidence of renal artery stenosis and eleven (8-1 per cent) parenchymatous renal disease. In comparison with the reported frequency in large general series of hypertensives, these data show no evidence of an excess of underlying renal disease. It is unlikely, therefore, that autonomous aldosterone secreting adenomata occur commonly as a consequence of prolonged secondary hyperaldosteronism. Four cases (2-9 per cent) had evidence of the malignant-phase of hypertension, and over a mean observation time of 5-9 years, 31 cases (22-8 per cent) developed 39 vascular complications. It appears, therefore, that vascular complications are not rare in primary hyperaldosteronism, and early and effective treatment is thus necessary.

Adenoma↗
PubMed1978

Increased adrenal sensitivity to angiotensin II in idiopathic hyperaldosteronism.

Plasma aldosterone increases briskly during upright posture in patients with idiopathic hyperaldosteronism, despite only small increases in PRA and presumably small increases in angiotensin II. To examine the postulate that small increments in angiotensin II mediate these brisk increases in aldosterone, we infused graded doses of angiotensin II into normal subjects and patients with idiopathic hyperaldosteronism and compared the changes in levels of plasma aldosterone in the two groups. Supplemental sodium and dexamethasone were given before the infusion to minimize the influence of endogenous angiotensin II and ACTH. In response to the infusion of angiotensin II, increases in the levels of plasma aldosterone of patients with idiopathic hyperaldosteronism were significantly greater than those of normal subjects. In addition, levels of plasma aldosterone increased at a lower rate of infusion of angiotensin II in patients than in normal subjects. It is concluded that patients with idiopathic hyperaldosteronism have increased adrenal sensitivity to angiotensin II. This increased sensitivity may explain the brisk increases in aldosterone that occur during upright posture in these patients.

Adrenal Glands↗
PubMed1976

[Rectal electrical potential difference and plasma aldosterone in hyperaldosteronism and low-, normal- and high-renin hypertension].

Rectal electrical potential difference (P.D.), plasma aldosterone and plasma renin activity were measured in 25 normal subjects, 80 patients with untreated essential hypertension, 4 patients with primary and 9 patients with secondary hyperaldosteronism. In normal subjects the rectal P.D. was 26 +/- 10 mV (+/- S.D.); in patients with hyperaldosteronism it was 51 +/- 7 mV. Plasma aldosterone and rectal P.D. were correlated significantly (r = 0.84, p less than 0.001) in these two groups combined. In 29% of patients with low-renin hypertension, in 9% of patients with normal-renin hypertension and in 3 out of 8 patients with high-renin hypertension, rectal P.D. was found to be elevated in the presence of normal plasma and urinary aldosterone and no correlation was observed between plasma aldosterone and rectal P.D. (r = --0.09, n.s.). In 3 out of 7 patients with low-renin hypertension and high rectal P.D., plasma and urinary aldosterone were consistently suppressed. Since patients with low renin and high rectal P.D. responded favourably to spironolactone therapy it is suggested that mineralocorticoids other than aldosterone may contribute to the pathogenesis of the hypertension in these cases. The aetiology of raised rectal P.D. in normal and high-renin hypertension is not clear, but both catecholamines and angiotensin II may be involved. The measurement of rectal P.D. alone is of limited value as a screening test for primary hyperaldosteronism in hypertensive patients, but combined with renin measurements it is a valuable tool for further investigation of patients with suspected mineralocorticoid excess syndromes, as well as for adjusting therapy with competitive aldosterone antagonists in patients with proven primary or secondary hyperaldosteronism.

Action Potentials↗
PubMed1976

Elevation of serum creatine kinase in severe hypokalemic hyperaldosteronism.

The association between hypokalemia and increased serum creatine kinase has been investigated. Two patients were found who had severe hypokalemic hyperaldosteronism who had elevation of serum creatine kinase activity. The CPK activity returned to normal values after fluid and potassium replacement. In a prospective study of 129 patients with hypokalemia which did not include any patients with hyperaldosteronism, 12 were found to have increased CPK activity but each of these had some other severe disease process which could account for the increased CPK. Three other patients with K+ (2.2 MEq/1 did not have increased CPK. It is concluded that patients with severe hypokalemia such as that occurring in hyperaldosteronism with muscle weakness may have elevated CPK directly related to their hypokalemia. In other patients with hypokalemia, 10% may have increased CPK but this is related to other disease processes.

Adult↗
PubMedDate not supplied

[Post-operative hyperaldosteronism and related endocrine perturbations (author's transl)].

Electrolytes disturbances during operative period are believed to be related to an hyperaldosteronism produced by anaesthetic management and surgery. Effects of ethrane anaesthesia and surgery on hydroelectrolytic metabolism and endocrin function were investigated in 11 patients submitted to an abdominal surgery. Plasma and urinary levels of aldosterone were increased (x3) significantly (p less than or equal to 0.001) during operation, then decreased gradually in post-operative period, and return to normal values when Na/K ratio is reversed in urines. Relationship between hyperaldosteronism and other changes in endocrine function are established by determination of following hormones: A.C.T.H., cortisol, plasma renin activity (P.R.A.) catecholamines in plasma and urinary levels of 17-ceto, 17-hydroxysteroids and catecholamines. Ethrane anesthesia give a good neurovegetative stability since plasma catecholamines levels are not affected significatively. Plasma aldosterone level is correlated with urinary aldosterone and plasma renin activity. Plasma A.C.T.H. is much more increased at the operative time and decreases rapidly instead of plasma cortisol which decreases more slowly. Relationship of this hyperaldosteronism with anesthetic management, surgical stress intestinal transit disturbances, other endocrine function changes is discussed.

17-Hydroxycorticosteroids↗
PubMedDate not supplied

[Primary hyperaldosteronism. Diagnostic procedure useful in hospital routine].

Personal experience in the management of three cases of primary hyperaldosteronism, in which a cure was obtained by surgical removal of an adrenocortical adenoma, is was used in the elaboration of a diagnostic procedure requiring hospitalisation for 12 days. During 6 days, the patient is kept on a diet containing 100 mEq Na and K, and blood potassium values are repeatedly determined. Other causes of hypertension are ruled out. On the 6th day, baselines for blood renin and urinary aldosterone are calculated. Next, a hyposodic diet is given for 4 days, and a diuretic is administered on the last of these days, after which renin is determined "in response to stimulation". Lastly, two days of i.v. NaCl loading are followed by the determination of urinary aldosterone "during inhibition". If the picture is positive for hyperaldosteronism, the patient is discharged and followed during treatment with spironolactone, and eventually subjected to renal and adrenal arteriography to determine the site of the adenoma. Division of the procedure into increasingly complex steps enables the examination to be halted at any point when evidence in support of the suspected diagnosis fails to appear. This feature, coupled with the simplicity of the procedures adopted, enables all young subjects admitted for unexplained hypertension to be screened for hyperaldosteronism, with the assurance of obtaining certain diagnosis without an excessively long stay in hospital.

Adenoma↗
PubMed1979

Hyperaldosteronism in the sodium-depleted rat: mode of aldosterone-stimulating action of frusemide.

The mechanism of diuretic-induced hyperaldosteronism was examined in dexamethasone-pretreated rats. The diuretic drug frusemide brought about a rapid increase in plasma renin activity and aldosterone concentration in serum. Half an hour after the administration of frusemide the mean concentration of aldosterone was 25 times higher than in vehicle-treated control animals. Administration of SQ 20,881, an inhibitor of angiotensin converting enzyme, prevented the adrenal response to frusemide. The response of aldosterone was completely blocked by indomethacin. This drug reduced renin release and probably also inhibited the effect on the adrenal glands of angiotensin, released in response to frusemide. Our results indicate that the effects of diuretics on the adrenal glomerulosa cells are mediated by the renin-angiotensin system also in the rat. Hyperaldosteronism is dependent on the maintenance of prostaglandin synthesis. ACTH has no essential role in this response.

Adrenal Glands↗
PubMed1976

Radiology in primary hyperaldosteronism.

Autonomous hypersecretion of aldosterone (primary hyperaldosteronism) is caused by either hyperplasia (usually bilateral) or an adenoma (frequently unilateral) of the adrenal cortex. Systemic hypertension due to an aldosteronoma is a potentially curable condition through surgical extirpation of the offending organ. In our experience with 37 patients clinically suspected to have primary hyperaldosteronism, radiological methods contributed significantly in preoperative diagnosis. These included (1) selective bilateral adrenal vein catheterization and blood sample collection, (2) adrenal venography, and (3) radioisotope adrenal scan. Unilateral hyperfunction could be accurately detected by the aldosterone assays from the collected samples. When adrenal venography was technically satisfactory, a nodule or aggregate of nodules measuring at least 7 mm and located on the margin of the gland or 1.5 cm or more in diameter when located in the center of the gland were readily identified. Enlarged adrenal gland on venography, in itself, was not a dependable index of a hyperfunctioning gland. Presence of a higher uptake on one side on the radioisotope adrenal scan did not always indicate the hyperfunctioning gland, but lack of lateralization of adrenal hyperfunction was more accurately predicted on the radioisotope scan than by venography. Four histopathological patterns were recognized in the surgically removed adrenal glands, but no correlation between these patterns and clinical behavior or postoperative course was found.

Adenoma↗
PubMed1976

The role of ACTH in the episodic release of aldosterone in patients with idiopathic adrenal hyperplasia, hypertension, and hyperaldosteronism.

The relationship of plasma aldosterone concentration to its identified stimuli was examined in three patients with hypertension, hyperaldosteronism, and idiopathic adrenal hyperplasia. Four patients with hyperaldosteronism due to adrenal adenomas served as controls. Plasma aldosterone, cortisol, sodium, and potassium concentrations and renin activity were measured in blood samples taken at 20 minute intervals from 2 A.M. to 8 A.M. during recumbency and sleep. The tests were performed on all patients following a regular sodium diet both before and after short-term treatment with dexamethasone. Two of the three subjects with adrenal hyperplasia were re-examined after 2 weeks of dexamethasone therapy. All four control patients with adenomas had episodic increases of plasma aldosterone which were significantly correlated with those of plasma cortisol (r = +0.48 to +0.90). This confirms the previously reported relationship between aldosterone and ACTH in such patients. Two patients with idiopathic adrenal hyperplasia had a similar secretion pattern and a highly significant correlation of the two hormones (r = +0.76 and +0.77); one did not (r = 0.13). Short-term dexamethasone pretreatment attenuated the episodic release pattern and partially suppressed the mean plasma concentrations of aldosterone in the four patients with an adenoma and in the two patients with idiopathic hyperplasia whose plasma aldosterone and cortisol concentrations were positively correlated. There was no such effect in the third patient. The first two patients with idiopathic hyperplasia were subsequently retested following 2 weeks of dexamethasone treatment to determine if the episodic secretion pattern of plasma aldosterone would correlated with other stimuli following this period of ACTH suppression. One showed little change from the pattern observed after short-term glucocorticoid treatment. The second had a similarly blunted aldosterone response until ACTH secretion led to a resumption of episodic changes in plasma aldosteerone concentrations. These data indicate that ACTH frequently is the dominant stimulus of the episodic secretion of aldosterone in patients with either adrenal adenomas or hyperplasia. When ACTH is suppressed, the hypersecretion of aldosterone is presumably sustained by an intrinsic adrenal abnormality or by an as yet unidentified stimulus.

Adenoma↗
PubMed1979

[Secondary hyperaldosteronism in patients with liver cirrhosis, frequently caused by therapy].

Plasma angiotensin II and plasma aldosterone was measured by radioimmunoassay in 78 patients with cirrhosis of the liver (group I: untreated, without ascites, n = 21; group II:untreated, with ascites, n = 25; group III: with ascites, during saluretic therapy, n = 32). From the obtained results it was concluded: (1) Excluding any pretreatment on the outpatient basis in most cirrhotics with or without ascites unaltered plasma levels of angiotensin II and aldosterone were found. (2) In contrast to previous suggestion secondary aldosteronism seems to be a minor determinant of hepatic ascites formation. (3) In untreated patients the 24-h-urinary excretion of electrolytes (Na+/K+ less than 1) represents an insufficient index of hyperaldosteronism. Obviously the kidney retains considerable amounts of sodium independent of circulating aldosterone levels. (4) Far above other mechanism hyperaldosteronism is most often induced by saluretic treatment of ascites and edema. The increased aldosterone secretion might indicate an adaptation phenomenon to restore total body sodium content. Certainly, the established concept of ascites therapy remains unimpaired by this physiological reaction.

Aldosterone↗
PubMed1976

[Primary and idiopathic hyperaldosteronism. Course 1 year after operation. Apropos of 28 cases].

The course of mean arterial pressure was compared in two series concerning 18 primary or tumoral hyperaldosteronism and 8 idiopathic ones. Identification of the nature of the hyperaldosteronism should not yet motivate a decision on principle, surgical in case of tumor, medical in an idiopathic case. In the latter case cooperation and tolerance of medical treatment, severity of hypertension also come into consideration. A positive spirolactone test, a hypertension course of less than six years were in our experience a good indication of successful surgery, as opposed to a normal unilateral renal biopsy. In case of operation, the removal protocol should adapt to the peroperative findings; 80% adrenalectomy is the most common procedure, except in the case of isolated adenoma of more than 10 mm diameter.

Adrenal Cortex Neoplasms↗
PubMed1977

[The renin-angiotensin-aldosterone system in hypertensive patients. II. Diagnosis of primary hyperaldosteronism].

Twenty patients suffering from primary hyperaldosteronism were studied. Sixteen had a single adenoma of the adrenal and four had bilateral hyperplasia affecting both adrenals. Cases of primary hyperaldosteronism due to a tumour were characterised by a higher degree of hypermineralocorticism than was seen in the patients with hyperplasia. Plasma aldosterone, after acute volaemic expansion, did not fall below 13 ng/100 ml in the adenoma patients whilst it was lower in the case of hyperplasia. Adrenal phlebography is a useful tool in preoperative diagnosis.

Adenoma↗
PubMed1978

Differentiation between subtypes of primary hyperaldosteronism by multiple steroid measurement after dexamethasone administration.

In 6 patients with primary hyperaldosteronism (P.H.) and a unilateral adrenal adenoma (A) and in 5 patients with P.H. obviously due to bilateral adrenal hyperplasia (H), multiple serum corticosteroids were measured after different dietary or drug regimens. After administration of dexamethasone on a normal sodium diet, serum levels of 11-deoxycorticosterone (DOC), corticosterone (B) and cortisol (F) were much lower in the H than in the A group. With respect to 11-deoxycorticosterone levels, there was no overlap between the two groups. Multiplication of individual serum DOC, B and F levels allowed a clearer separation of patients with A and H. This non-invasive method may offer an additional means in the differential diagnosis of P.H.

Adenoma↗
PubMed1979

Hyperreninemia and secondary hyperaldosteronism in pheochromocytomas.

Foremost in the differential diagnosis of hypertension is the identification of surgically correctable lesions. Increased plasma renin activity in a hypertensive patient suggests the presence of a renovascular or renal etiology. We have recently seen two adolescent patients whose hyperreninemia was cuased by a pheochromocytoma. Secondary hyperaldosteronism was an associated finding.

Adolescent↗
PubMed1977

Amiloride in the treatment of primary hyperaldosteronism and essential hypertension.

Amiloride (40 mg/day) was given to nineteen patients with primary hyperaldosteronism. There were significant falls in systolic and diastolic blood pressure, in total exchangeable sodium, and in serum sodium sodium and bicarbonate; while total exchangeable potassium, total body potassium, serum potassium, chloride and urea, and plasma renin, angiotensin II and aldosterone all increased significantly. Amiloride was effective in reducing blood pressure in patients with and without adrenocortical adenoma. No carry-over effect was seen on withdrawing amiloride. Similar changes were associated with amiloride treatment in five patients with essential hypertension; hyperkalaemia was not observed. Only negligible side-effects were encountered in the entire series of twenty-four patients.

Adult↗
PubMed1979

Hypokalemic periodic paralysis in primary hyperaldosteronism. Subclinical myopathy with atrophy of the type 2A muscle fibers.

A case of a patient suffering from primary hyperaldosteronism is reported. In this case the disease is manifested clinically by periodic paralysis and hypopotasemia without permanent myopathy. The morphological study of the muscle demonstrates selective atrophy of the type 2A fibers as the most pronounced alteration. These findings suggest a chronic myopathic process.

Aged↗
PubMed1979

Hyperaldosteronism in the sodium-depleted rat: mechanism of aldosterone stimulation by peritoneal dialysis with glucose solution.

Peritoneal dialysis with 5% glucose solution was carried out in dexamethasone-pretreated rats. Dialysis brought about a severe loss of sodium and a slight loss of potassium into the peritoneal fluid. This kind of sodium depletion took place without any decrease in total body-water space, thus it evoked a severe fall in plasma sodium concentration. Plasma renin activity and the serum concentration of aldosterone increased in response to dialysis. Peak values in renin activity were attained within 60 min, whereas aldosterone concentrations exhibited a continuous rise until at least 120 min. Despite the correlation of renin and aldosterone values, neither the administration of an angiotensin I converting enzyme inhibitor (SQ 20,881) nor the reduction of plasma renin activity by indomethacin could reduce hyperaldosteronism evoked by peritoneal dialysis. Therefore, it is assumed that there is no causal relationship between renin and aldosterone in this kind of acute, severe sodium depletion.

Aldosterone↗