Rastreamento, Comprovação e Diferenciação Laboratorial do Hiperaldosteronismo Primário

Primary aldosteronism (PA), previously considered a rare cause of hypertension, may be responsible in recent series for 5-10% of the hypertensive population. Although one might consider PA as the main cause of secondary hypertension, caution is recommended when interpreting this sudden epidemics. Be...

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Detalles Bibliográficos
Autor: Kater, Claudio Elias [UNIFESP]
Tipo de recurso: artículo
Estado:Versión publicada
Fecha de publicación:2002
País:Brasil
Institución:Universidade Federal de São Paulo (UNIFESP)
Repositorio:Repositório Institucional da UNIFESP
Idioma:portugués
OAI Identifier:oai:repositorio.unifesp.br:11600/1346
Acceso en línea:http://dx.doi.org/10.1590/S0004-27302002000100015
http://repositorio.unifesp.br/handle/11600/1346
Access Level:acceso abierto
Palabra clave:Hypertension
Mineralocorticoid excess
Hyperaldosteronism
Aldosterone
Plasma renin activity
Potassium
Hipertensão
Excesso mineralocorticóide
Hiperaldosteronismo
Aldosterona
Atividade plasmática de renina
Potássio
Descripción
Sumario:Primary aldosteronism (PA), previously considered a rare cause of hypertension, may be responsible in recent series for 5-10% of the hypertensive population. Although one might consider PA as the main cause of secondary hypertension, caution is recommended when interpreting this sudden epidemics. Because the classical manifestations of aldosterone excess are not always present, screening for PA must include determinations of random plasma aldosterone: renin ratios (ng/dl:ng/ml/h). Hypertensive patients with ratio> or =25 (and aldosterone >14ng/dl) must be further investigated with plasma/urine aldosterone suppression tests (IV saline infusion, oral fludrocortisone or high-sodium diets). Failure to suppress is typical of aldosterone autonomy in PA. Differentiation of the two main subgroups (aldosterone-producing adenoma - APA -, and bilateral adrenal hyperplasia or idiopathic hyperaldosteronism - IHA) is mandatory since therapeutic intervention varies. Distinction between APA and IHA is based on the absence of plasma aldosterone increases to renin stimulation (upright posture, diuretics or low-sodium diets) in the first, as opposed to exaggerated responses in the latter. The diagnostic workup must include an adrenal CT and, if necessary, bilateral adrenal vein catheterization and aldosterone measurement to ascertain the source of aldosterone excess.