A new diagnostic test for primary aldosteronism

Isotonic-isooncotic central volume expansion by head-out water immersion was induced in six aldosterone-producing adenoma subjects and in six patients with idiopathic hyperaldosteronism. Plasma renin activity and plasma aldosterone levels did not significantly change during water immersion while serum cortisol was significantly suppressed (P less than .001) and the aldosterone-cortisol ratio increased (P less than .02) in aldosterone-producing adenoma patients. Water immersion also revealed the failure of plasma aldosterone levels to decrease below 10 ng/dL in these subjects, thus confirming previous results obtained during isotonic saline infusion. Otherwise, plasma renin activity and plasma aldosterone were significantly reduced (P less than .05 and P less than .01 respectively) by water immersion and plasma aldosterone invariably fell below 10 ng/dL in patients with idiopathic aldosteronism. In view of the diagnostic reliability of such a suppression test we conclude that water immersion is suitable for discriminating between the two forms of primary aldosteronism. We therefore suggest its use for assessing renin-aldosterone responsiveness in primary aldosteronism.     

Single dose captopril as a diagnostic test for primary aldosteronism

Most diagnostic tests for primary aldosteronism use maneuvers to expand the extracellular fluid volume, thereby suppressing the renin-angiotensin system. This results in a decline in plasma aldosterone concentrations in normal subjects and essential hypertension (EH) patients, but not in patients with primary aldosteronism. Captopril blocks angiotensin II synthesis and might be used as a diagnostic test for primary aldosteronism. We have measured plasma aldosterone concentrations 2 h after the administration of 25 mg captopril in 9 normotensive subjects, 10 patients with EH, and 12 patients with primary aldosteronism while they were ingesting an unrestricted diet. The plasma aldosterone concentration decreased to less than 15 ng/dl in all normotensive subjects and in 9 of 10 patients with EH, but remained greater than 15 ng/dl in 4 of 5 patients with idiopathic hyperaldosteronism and in all patients with an aldosterone-producing adenoma. The aldosterone to renin ratio was greater than 50 in 4 of 5 patients with idiopathic hyperaldosteronism and in all adenoma patients, but less than 50 in all normotensive subjects and EH patients. A nomogram comparing the plasma aldosterone concentration with the aldosterone to renin ratio clearly separated primary aldosteronism patients from EH patients.     

Screening for primary aldosteronism

A serum potassium determination is usually recommended for new hypertensive patients as a screening test for primary aldosteronism and as a baseline for drug therapy. Since hypokalemia is not specific for aldosteronism, the authors assessed its use and limitations as a screening test in nine reported studies of 303 patients with aldosterone-producing adenomas (n=252) or adrenal hyperplasia (n=51). The optimal potassium cutoff level and the predictive ability of hypokalemia to detect aldosteronism were analyzed in a primary care setting with different diseases, test characteristics, and prevalences. Optimal screening for primary aldosteronism occurred at serum potassium <3.2 mEq/l in a primary care, low-prevalence population, and at higher potassium levels in higher-prevalence populations. Other screening tests, such as urinary aldoster-one levels and plasma renin activity, showed lower individual test performance characteristics, but when combined were similar in performance to serum potassium measurement. Received from the General Internal Medicine Division, Department of Medicine, Wright State University School of Medicine, Miami Valley Hospital, and Veteran’s Administration Medical Center, Dayton, Ohio. Dr. Snyder is presently a fellow in the Endocrinology Division, Department of Medicine, University of North Carolina School of Medicine, Chapel Hill, North Carolina. Presented in part at the Seventh Annual Meeting of the Society for Research and Education in Primary Care Internal Medicine, Microcomputer Users Group, Washington, D.C., May 3, 1984.     

Screening for primary aldosteronism

Normokalaemic manifestation of primary aldosteronism is a frequent cause of secondary hypertension. It occurs in approximately 5-12% of all patients with hypertension, primarily patients with severe and uncontrolled blood pressure. Main causes are bilateral adrenal hyperplasia (2/3 of cases) and aldosterone-producing adenoma (1/3 of cases). Screening is performed by measurement of the aldosterone/renin ratio, which is raised in affected patients. Suspicion of primary aldosteronism due to a pathological ratio requires confirmatory testing e.g. by saline infusion test or fludrocortisone suppression test. If the diagnosis is confirmed, the underlying cause of aldosterone excess needs to be identified because therapy differs. First, adrenal imaging (CT/MRI) is performed, which is followed by postural testing in cases with a unilateral lesion. Concordant results confirm the diagnosis of an aldosterone-producing adenoma and allow treatment to proceed to adrenalectomy. In cases of equivocal results or normal/bilaterally enlarged adrenal glands on imaging, adrenal venous sampling must be performed for subtype differentiation.     

坐位盐水试验对原发性醛固酮增多症的诊断价值及切点探究

目的 评估坐位盐水试验(SSST)对原发性醛固酮增多症(PA)的诊断价值及适宜切点.方法 分析2018年9月至2019年9月就诊于重庆医科大学附属第一医院内分泌科的242例PA高危的高血压患者的临床资料,所有患者均接受SSST和氟氢可的松试验(FST).以FST作为PA的诊断标准,利用受试者工作特征(ROC)曲线评价S...     

Detecting and treating primary aldosteronism: primary aldosteronism.

Primary aldosteronism (PA) is the most common cause of mineralocorticoid hypertension. Different studies, using the plasma aldosterone concentration to plasma renin activity ratio (PAC/PRA) for the screening of patients with hypertension, have shown a marked increase in the detection rate of PA. Idiopathic bilateral adrenal hyperplasia (IHA) and aldosterone-producing adrenal adenoma (APA), are the leading causes of primary aldosteronism. Glucocorticoid-remediable aldosteronism (GRA), also called familial hyperaldosteronism type I, familial hyperaldosteronism type II and carcinomas are rare causes of PA. Patients with hypertension and hypokalemia, those with a family history of hypertension and stroke at an early age, or patients with medication-resistant hypertension should be screened for PA using the PAC/PRA ratio. If a high ratio is found, a sodium loading test or a captopril test is warranted to confirm the diagnosis. Adrenal gland imaging is important in subtype differentiation (APA vs IHA). Adrenal venous sampling should be used when other tests prove inconclusive. Genetic testing has facilitated detection of GRA. Surgery is considered the treatment of choice for patients with APA, while bilateral hyperplasia subtypes are treated medically. Normalization of aldosterone levels or aldosterone receptor blockade are necessary to prevent the morbidity and mortality associated with hypertension, hypokalemia, and cardiovascular damage.     

Normotensive primary aldosteronism

A very unusual case of normotensive primary aldosteronism is described. A 25 year old woman first noticed numbness of both hands followed by a typical tetany attack. The blood pressure was within normal ranges. The results of other physical examinations were negative except for the findings of Trousseau's sign. Hypokalemia, increased potassium clearance, disturbed urine concentration and increased circulating plasma volume were noticeable. Diagnosis was established by (1) increased levels of plasma aldosterone, (2) low plasma renin activity, (3) normal adrenocortical function and (4) typical aldosterone-producing adenoma. After removal of the adenoma, the abnormalities subsided.The lack of hypertension in primary aldosteronism is a rare condition. Several possible causes of normotension must be considered, such as the early phase of primary aldosteronism, essential hypotension associated with primary aldosteronism and lack of concomitant secretion of other mineralocorticoids from the adenoma, but these were all negligible. As blood pressure response to the administration of angiotensin II was lower than is typical for primary aldosteronism, and the patient transiently suffered from frequent attacks of blackouts soon after the operation, the cause of normotension was thought to be due to the existence of a hypotensive mechanism which counteracts the increase in blood pressure in primary aldosteronism.