Methodological simplifications in radioimmunoassay of urinary aldosterone

Malvano, R.; Orlandini, Serena; Cozzani, P.; Duranti, P.; Simonini, N.; Salvetti, Antonio

doi:10.1016/0009-8981(76)90232-1

Cited by 33 publications

(10 citation statements)

References 11 publications

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“…Serum calcitonin was determined by RIA (SRL, Tokyo). Urinary aldosterone was determined by RIA as the acid-labile conjugate of aldosterone (Malvano et al, 1976). Urinary 17-hydroxycortico-steroids (17-OHCS) (Silber and Porter, 1954) and 17-ketosteroids (17-KS) (Drekter et al, 1952) were estimated by conventional methods.…”

Section: Methodsmentioning

confidence: 99%

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Reversible hypertension caused by calcium overloading in a patient with postoperative hypoparathyroidism.

et al. 1982

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A 37-year-old woman with postoperative hypoparathyroidism had hypertension, and elevated plasma renin activity (PRA) and subsequent hyperaldosteronism during a twomonth hypercalcemic period caused by vitamin D and excessive calcium supplements. The hypertension with elevated PRA, however, was resistant to the angiotensin II (AII) analog [Sar1, Ile8] AII. PRA further increased and plasma aldosterone decreased in response to the [Sar1, Ile8] AII. When the patient became normocalcemic, normotensive and normoreninemic, calcium gluconate (5mg calcium/kg/h) was infused for one hour. The calcium infusion reproduced hypercalcemic hypertension mediated by an increase in total peripheral resistance.These observations suggest that the hypertension observed while taking vitamin D and excessive calcium supplements may be caused by a direct effect of calcium on peripheral blood vessels and the renin-angiotensin system may play a negligible role.Reversible hypertension has been reported to occur during a hypercalcemic period in many patients with or without hyperparathyroidism (Cope, 1960;Moore and Smith, 1963;Major et al., 1966;Weidmann et al., 1972;Brinton et al., 1975;Overbeck et al., 1975;Blum et al., 1977;Marone et al., 1980;Waeber et al., 1982). In these patients, the hypertension has been explained by a direct vasoconstrictor effect of calcium on peripheral blood vessels (Moore and Smith, 1963;Weidmann et al., 1972;Overbeck et al., 1975;Blum et al., 1977;Marone et al., 1980) or a change in the reninangiotensin system (Brinton et al., 1975;Waeber et al., 1982).Recently, we had a patient with postoperative hypoparathyroidism whose blood pressure and plasma renin activity (PRA) rose during The present report deals with this case and the investigation into the pathogenesis of this reversible hypertension. MethodsPRA was determined by the method of Skinner (1967), and plasma aldosterone and plasma cortisol were measured by RIA. The details of these methods are described elsewhere (Takeda et al., 1976). Serum parathyroid hormone levels were measured by RIA with carboxy-and amino-terminal specific antibodies (SRL, Tokyo). Serum calcitonin was determined by RIA (SRL, Tokyo). Urinary aldosterone was determined by RIA as the acid-labile conjugate of aldosterone (Malvano et al., 1976

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Section: Methodsmentioning

confidence: 99%

“…Serum calcitonin was determined by RIA (SRL, Tokyo). Urinary aldosterone was determined by RIA as the acid-labile conjugate of aldosterone (Malvano et al, 1976 …”

mentioning

confidence: 99%

Reversible hypertension caused by calcium overloading in a patient with postoperative hypoparathyroidism.

et al. 1982

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“…(Tokyo). Urinary aldosterone was determined by RIA as the acid-labile conjugate of aldosterone [14], Urinary 17-hydroxycorticosteroids (17-OHCS) [15] and 17-ketosteroids (17-KS) [16] were estimated by conventional methods. Plasma and urinary catecholamines were measured fluorometrically by HPLC (Kitazato Biochem.…”

Section: Methodsmentioning

confidence: 99%

Adrenal Adenoma with 18-Hydroxycorticosterone Excess and Hypertension: A Variant of Aldosteronomas

Kigoshi¹,

Imaizumi²,

Azukizawa³

et al. 1984

Horm Res

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A 46-year-old woman with hypertension, normokalemia, suppressed renin, normal catecholamines, and a left adrenal mass on the CT scan was found to have excessive 18-hydroxycorticosterone (18-OHB) and normal aldosterone levels in plasma, both of which responded poorly to sodium restriction and angiotension II, and supranormally to ACTH. Plasma 18-hydroxydeoxycorticosterone (18-OHDOC) was normal. After adrenalectomy, amelioration from hypertension occurred with a reduction in plasma 18-OHB and aldosterone. The plasma 18-OHDOC remained normal. The adrenal tumor was histologically an adenoma, containing a large amount of 18-OHB and a small amount of aldosterone. Thus, the present adenoma seems to be a variant of aldosteronomas.

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“…respectively). Urinary aldosterone [13] was 11 pg/24 h (normal 3.5-15 pg/ 24 h). Roentgenologic examination of the skull was normal.…”

Section: Case Reportmentioning

confidence: 99%

Cushing’s Syndrome due to Unilateral Adrenal Nodular Hyperplasia with Incomplete Inhibition of the Contralateral Gland

et al. 1986

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A 57-year-old woman was demonstrated to be affected by adrenocorticotropic hormone (ACTH)-independent Cushing’s syndrome. Computed-axial tomography of the abdomen demonstrated an expansion of the left adrenal. In apparent contrast with these findings, adrenal scintigraphy demonstrated radiocholesterol uptake also by the right gland. At surgery, the left adrenal was found to be hard and enlarged and was excised, while the right gland was found of normal appearance and left in place. Histologic examination of the excised gland demonstrated nodular hyperplasia. Early after surgery, plasma cortisol returned to normal values with a normal circadian rhythm and complete inhibition by low dose dexamethasone; the response of plasma cortisol to ACTH was normal. The patient represents a rare case of unilateral adrenal nodular hyperplasia. Radiocholesterol uptake by the contralateral gland and early recovery from adrenal atrophy after surgery are exceptional findings and suggest incomplete inhibition of endogenous ACTH.

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Methodological simplifications in radioimmunoassay of urinary aldosterone

Cited by 33 publications

References 11 publications

Reversible hypertension caused by calcium overloading in a patient with postoperative hypoparathyroidism.

Reversible hypertension caused by calcium overloading in a patient with postoperative hypoparathyroidism.

Adrenal Adenoma with 18-Hydroxycorticosterone Excess and Hypertension: A Variant of Aldosteronomas

Cushing’s Syndrome due to Unilateral Adrenal Nodular Hyperplasia with Incomplete Inhibition of the Contralateral Gland

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Methodological simplifications in radioimmunoassay of urinary aldosterone

Cited by 33 publications

References 11 publications

Reversible hypertension caused by calcium overloading in a patient with postoperative hypoparathyroidism.

Reversible hypertension caused by calcium overloading in a patient with postoperative hypoparathyroidism.

Adrenal Adenoma with 18-Hydroxycorticosterone Excess and Hypertension: A Variant of Aldosteronomas

Cushing&rsquo;s Syndrome due to Unilateral Adrenal Nodular Hyperplasia with Incomplete Inhibition of the Contralateral Gland

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Product

Resources

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Cushing’s Syndrome due to Unilateral Adrenal Nodular Hyperplasia with Incomplete Inhibition of the Contralateral Gland