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Primary Aldosteronism: Present and Future.
Vitam Horm. 2019; 109:285-302.VH

Abstract

Primary aldosteronism (PA), currently recognized to be 5-10% of hypertension, has a cardiovascular risk profile double that in age-, sex-, and blood pressure-matched essential hypertensives. Screening for PA is by determining the plasma aldosterone to renin ratio (ARR), followed by one of half a dozen confirmatory/exclusion tests. Unilateral hyperaldosteronism normally reflects an aldosterone producing adenoma; bilateral disease is the more common form, and termed idiopathic hyperaldosteronism (IHA). Subjects confirmed undergo imaging, followed by adrenal venous sampling (AVS) for lateralization. Unilateral lesions undergo laparoscopic adrenalectomy, to normalize aldosterone levels, and in approximately half reduction of BP/antihypertensive use. Bilateral hyperaldosteronism is treated by low dose mineralocorticoid receptor antagonists MRAs, plus amiloride/conventional antihypertensives, if/as indicated.In the future, what is needed is recognition that inappropriate aldosterone levels for sodium status (i.e., PA) represents up to 50% of "essential" hypertensives; all hypertensive should thus be screened by a modified ARR, using 24-h urinary aldosterone rather than a single plasma aldosterone. The current reluctance to do so reflects the costs of AVS if PA is confirmed-optimally by a standard seated saline suppression test-followed by surgery or life-long MRAs. Increasingly AVS will be replaced by plasma steroid assays capable of discriminating APA from the far more common IAH. Third generation MRAs (as selective as eplerenone, as potent as spironolactone, non-steroidal) are in development; in the interim, to minimize side effects and maximize compliance, spironolactone dosage should be set at 12.5-25 mg/day.

Authors+Show Affiliations

Hudson Institute of Medical Research, Clayton, VIC, Australia; Monash University, Clayton, VIC, Australia. Electronic address: john.funder@hudson.org.au.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

30678860

Citation

Funder, John W.. "Primary Aldosteronism: Present and Future." Vitamins and Hormones, vol. 109, 2019, pp. 285-302.
Funder JW. Primary Aldosteronism: Present and Future. Vitam Horm. 2019;109:285-302.
Funder, J. W. (2019). Primary Aldosteronism: Present and Future. Vitamins and Hormones, 109, 285-302. https://doi.org/10.1016/bs.vh.2018.10.006
Funder JW. Primary Aldosteronism: Present and Future. Vitam Horm. 2019;109:285-302. PubMed PMID: 30678860.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Primary Aldosteronism: Present and Future. A1 - Funder,John W, Y1 - 2018/12/23/ PY - 2019/1/26/entrez PY - 2019/1/27/pubmed PY - 2019/4/23/medline KW - Aldosterone producing adenomas KW - Aldosterone producing cell clusters (APCC) KW - Hyperaldosteronism—a public health issue KW - Somatic mutations SP - 285 EP - 302 JF - Vitamins and hormones JO - Vitam Horm VL - 109 N2 - Primary aldosteronism (PA), currently recognized to be 5-10% of hypertension, has a cardiovascular risk profile double that in age-, sex-, and blood pressure-matched essential hypertensives. Screening for PA is by determining the plasma aldosterone to renin ratio (ARR), followed by one of half a dozen confirmatory/exclusion tests. Unilateral hyperaldosteronism normally reflects an aldosterone producing adenoma; bilateral disease is the more common form, and termed idiopathic hyperaldosteronism (IHA). Subjects confirmed undergo imaging, followed by adrenal venous sampling (AVS) for lateralization. Unilateral lesions undergo laparoscopic adrenalectomy, to normalize aldosterone levels, and in approximately half reduction of BP/antihypertensive use. Bilateral hyperaldosteronism is treated by low dose mineralocorticoid receptor antagonists MRAs, plus amiloride/conventional antihypertensives, if/as indicated.In the future, what is needed is recognition that inappropriate aldosterone levels for sodium status (i.e., PA) represents up to 50% of "essential" hypertensives; all hypertensive should thus be screened by a modified ARR, using 24-h urinary aldosterone rather than a single plasma aldosterone. The current reluctance to do so reflects the costs of AVS if PA is confirmed-optimally by a standard seated saline suppression test-followed by surgery or life-long MRAs. Increasingly AVS will be replaced by plasma steroid assays capable of discriminating APA from the far more common IAH. Third generation MRAs (as selective as eplerenone, as potent as spironolactone, non-steroidal) are in development; in the interim, to minimize side effects and maximize compliance, spironolactone dosage should be set at 12.5-25 mg/day. SN - 0083-6729 UR - https://www.unboundmedicine.com/medline/citation/30678860/Primary_Aldosteronism:_Present_and_Future_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0083-6729(18)30078-5 DB - PRIME DP - Unbound Medicine ER -