Captopril Suppression for Diagnosis of Primary Aldosteronism

12/03/02 (Dronavalli)

Question: is there an alternative to salt loading as a diagnostic tool in the diagnosis of primary aldosteronism?

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Unique Identifier:12003708

Authors: Racine MC. Douville P. Lebel M.

Institution: CHUQ, L'Hotel-Dieu de Quebec Hospital, 11 Cote du Palais, Quebec, (QC), G1R 2J6, Canada.

Title: Functional tests for primary aldosteronism: value of captopril suppression. [Review] [27 refs]

Source: Current Hypertension Reports. 4(3):245-9, 2002 Jun.

Abstract: With the introduction of more simple screening tests such as the aldosterone/renin ratio, the detection rate of primary aldosteronism has increased considerably. Until now, no reference values have been available for reporting the aldosterone/renin ratio using plasma aldosterone values expressed in SI units (pmol/L) and plasma active renin (ng/L) measured by immunoradiometric assay. We studied 153 subjects who had either normal blood pressure, essential hypertension, or primary aldosteronism. Essential hypertensive patients usually have aldosterone/renin (pmol/L/ng/L) ratios below 100, whereas ratios for patients with primary aldosteronism are above 140. Results that fall between 100 and 140 suggest a need for repeat testing. Patients with elevated aldosterone/renin ratios require confirmatory testing to demonstrate nonsuppressive autonomous aldosterone production. To this end, salt loading is widely used, but this approach may be contraindicated in patients with severe hypertension. The captopril suppression test appears as effective as salt loading in confirming a diagnosis of primary aldosteronism. In addition, the captopril test is safe, well tolerated, and cost-effective. [References: 27] CAS Registry/EC Number 52-39-1 (Aldosterone). 62571-86-2 (Captopril). EC 3-4-23-15 (Renin).

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Unique Identifier:11791034

Authors: Schlaich MP. Klingbeil AU. Jacobi J. Delles C. Schneider MP. Schmidt BM. Schmieder RE.

Institution: Department of Medicine IV/Nephrology, University of Erlangen-Nurnberg, Breslauer Strasse 201, D-90471 Nurnberg, Germany.

Title: Altered aldosterone response to salt intake and angiotensin II infusion in young normotensive men with parental history of arterial hypertension.

Source: Journal of Hypertension. 20(1):117-24, 2002 Jan.

Abstract: OBJECTIVE: An increased sensitivity to angiotensin II (Ang II) has been observed in patients with established hypertension. In the current study we tested whether young normotensive subjects with positive family history of arterial hypertension exhibit an increased sensitivity to Ang II, thereby potentially contributing to the pathogenesis of essential hypertension in these subjects. METHODS AND DESIGN: Normotensive young men (25 +/- 2 years) with positive family history (PFH) (n = 28) and negative family history (NFH) (n = 60) of arterial hypertension were investigated to study aldosterone response, and systemic and renal haemodynamic changes (p-aminohippurate- and inulin-clearance) to Ang II infusion (0.5 and 3.0 ng/min per kg). In addition, aldosterone response to salt loading (5 g/day for 1 week) was analysed. RESULTS: Ambulatory blood pressure (ABP) (mean: 84 +/- 4 versus 83 +/- 4 mmHg; NS), body mass index (23.5 +/- 2.5 versus 24.1 +/- 2.4 kg/m(2); NS), and urinary sodium excretion (191 +/- 55 versus 170 +/- 73 mmol/24 h; NS) did not differ between PFH and NFH at baseline. Changes in BP, urinary sodium and potassium excretion were similar between PFH and NFH in response to salt loading. However, salt loading did not result in an adequate suppression of aldosterone in PFH compared with NFH (8 +/- 62 versus -32 +/- 39 pg/ml; P < 0.001). Baseline values and changes in mean arterial BP (NFH: +13.4 +/- 7.6; PFH: +14.4 +/- 5.3 mmHg; NS), renal plasma flow (NFH: - 113 +/- 68; PFH: - 122 +/- 64 ml/min; NS) and glomerular filtration rate (NFH: +5.0 +/- 5.3; PFH: +4.2 +/- 8.3 ml/min; NS) in response to Ang II (3.0 ng/min per kg) were similar between the two groups. In contrast, the increases in serum aldosterone (PFH: 63.6 +/- 70.1 versus NFH: 37.7 +/- 46.8 pg/ml; P < 0.05) and urinary potassium excretion (PFH: 0.05 +/- 0.1 versus NFH: -0.01 +/- 0.07 mmol/min; P < 0.05) 30 min after stopping Ang II infusion were more pronounced and prolonged in PFH than in NFH. CONCLUSIONS: Our findings suggest that young normotensive subjects with parental history of arterial hypertension are characterized by an inadequate suppression of aldosterone production in response to salt loading and an exaggerated and prolonged hyper-responsiveness of aldosterone secretion in response to Ang II. This might contribute to the increased risk for the development of essential hypertension in subjects with positive family history of arterial hypertension. CAS Registry/EC Number 0 (Sodium, Dietary). 11128-99-7 (Angiotensin II). 52-39-1 (Aldosterone). 7440-09-7 (Potassium). EC 3-4-23-15 (Renin).

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Unique Identifier:11408392

Authors: Agharazii M. Douville P. Grose JH. Lebel M.

Institution: CHUQ, L'Hotel-Dieu de Quebec Hospital, and Department of Medicine, Faculty of Medicine, Laval University, Quebec, Canada.

Title: Captopril suppression versus salt loading in confirming primary aldosteronism.

Source: Hypertension. 37(6):1440-3, 2001 Jun.

Abstract: This prospective study was designed to compare the captopril suppression test with the salt-loading approach to confirm the diagnosis of primary aldosteronism. A total of 49 patients were referred with a presumed diagnosis of primary aldosteronism. The captopril test was performed in the morning with patients in the seated position after overnight fasting. Blood samples for plasma aldosterone were obtained before captopril administration (25 mg PO) and again 2 hours later. Patients were then subjected to a high salt diet (300 mmol sodium per day for 3 days). On the third day, urinary sodium (24 hours) was measured, and plasma aldosterone levels were measured at 8:00 AM (recumbent) and at noon (standing). Of the 49 patients, 44 had nonsuppressible aldosterone concentrations with all the clinical characteristics of primary aldosteronism: 22 patients had surgically confirmed unique adenoma, and 22 patients had presumed bilateral hyperplasia. There was a significant correlation between plasma aldosterone values of salt-loaded patients (mean of 8:00 AM and noon results) and the values 2 hours after captopril administration (r=0.8, P<0.01). Plasma aldosterone cumulative distribution curves in primary aldosteronism patients (adenoma and hyperplasia) were not significantly different between the 2 suppression tests. Our results showed that the captopril suppression test is as effective as sodium loading in confirming the diagnosis of primary aldosteronism. CAS Registry/EC Number 0 (Angiotensin-Converting Enzyme Inhibitors). 52-39-1 (Aldosterone). 62571-86-2 (Captopril). 7440-23-5 (Sodium).