Mineralocorticoid hypertension

Abstract

Hypertension affects about 10 – 25% of the population and is an important risk factor for cardiovascular and renal disease. The renin-angiotensin system is frequently implicated in the pathophysiology of hypertension, be it primary or secondary. The prevalence of primary aldosteronism increases with the severity of hypertension, from 2% in patients with grade 1 hypertension to 20% among resistant hypertensives. Mineralcorticoid hypertension includes a spectrum of disorders ranging from renin-producing pathologies (renin-secreting tumors, malignant hypertension, coarctation of aorta), aldosterone-producing pathologies (primary aldosteronism – Conns syndrome, familial hyperaldosteronism 1, 2, and 3), non-aldosterone mineralocorticoid producing pathologies (apparent mineralocorticoid excess syndrome, Liddle syndrome, deoxycorticosterone-secreting tumors, ectopic adrenocorticotropic hormones (ACTH) syndrome, congenitalvadrenal hyperplasia), and drugs with mineraocorticoid activity (locorice, carbenoxole therapy) to glucocorticoid receptor resistance syndromes. Clinical presentation includes hypertension with varying severity, hypokalemia, and alkalosis. Ratio of plasma aldosterone concentraion to plasma renin activity remains the best screening tool. Bilateral adrenal venous sampling is the best diagnostic test coupled with a CT scan. Treatment is either surgical (adrenelectomy) for unilateral adrenal disease versus medical therapy for idiopathic, ambiguous, or bilateral disease. Medical therapy focuses on blood pressure control and correction of hypokalemia using a combination of anti-hypertensives (calcium channel blockers, angiotensin converting enzyme inhibitors, or angiotensin receptor blockers) and potassium-raising therapies (mineralcorticoid receptor antagonist or potassium sparing diuretics). Direct aldosterone synthetase antagonists represent a promising future therapy.

Tumor de células yuxtaglomerulares (reninoma) como causa de hipertensión arterial en la adolescencia. A propósito de un caso

“…Los valores elevados de ARP y de AP permiten el diagnóstico diferencial entre el hiperaldosteronismo primario y secundario. 11,12 Ante la presencia de hiperaldosteronismo, hiperreninémico y HTA, debe realizarse el diagnóstico diferencial entre estenosis de arteria renal, coartación de aorta y tumor secretor de renina. 12 La producción de renina y aldosterona puede estar influenciada por muchos factores.…”

“…11,12 Ante la presencia de hiperaldosteronismo, hiperreninémico y HTA, debe realizarse el diagnóstico diferencial entre estenosis de arteria renal, coartación de aorta y tumor secretor de renina. 12 La producción de renina y aldosterona puede estar influenciada por muchos factores. 13 Los niveles de estas hormonas pueden fluctuar con el tiempo, pero la elevación por encima del límite superior del rango suele ser sostenida.…”

Juxtaglomerular cell tumor (reninoma) as a cause of arterial hypertension in adolescents. A case report

“…High PRA and BP values allow to make a differential diagnosis between primary and secondary hyperaldosteronism. 11,12 In the presence of hyperaldosteronism, elevated blood renin levels, and HTN, a differential diagnosis among renal artery stenosis, coarctation of the aorta, and renin-secreting tumor should be made. 12 Renin and aldosterone production may be affected by many factors.…”

An integrative review of the methods used for cortisol assessment in clinical studies investigating the association between Blood Pressure and Cortisol Hormone

“…However, it remains underdiagnosed and poorly controlled, with high rates of morbidity and mortality being an important risk factor for heart and / or kidney diseases and stroke. [1][2][3][4] The Renin-Angiotensin-Aldosterone System (RAAS) and the Hypothalamic-Hypophysis -Adrenal (HPA) axis, responsible for the regulation of blood pressure (BP), were reported to play an important role in the pathophysiology of SAH, and the glucocorticoid (cortisol) and mineralocorticoid (aldosterone) hormones are the respective effectors of these pathways. 5,6 In fact, increased circulating or intracellular glucocorticoids levels are common and frequently associated with SAH.…”