Bilateral Aldosteronoma Associated with Secondary Aldosteronism in a Chronic Hemodialysis Subject

Abstract

We demonstrated a rare case of bilateral aldosteronoma accompanied by secondary aldosteronism in a 37-year-old

HSD2 neurons are evolutionarily conserved and required for aldosterone-induced salt appetite

“…We next characterized the effect of peripheral aldosterone infusion. We tested a range of infusion rates to reproduce plasma aldosterone levels spanning the full range of aldosterone levels reported after dietary sodium deprivation and across a variety of pathophysiologic states in humans, including dietary sodium deprivation, hyperkalemia, kidney disease, and aldosterone-secreting adenomas (34, 55, 61, 62). We again found dose-dependent effects on saline intake.…”

“…Like mice and rats, healthy human subjects generate circulating aldosterone levels upwards of 300 mg/dL if they are fed a low-sodium, high-potassium diet (55). Even higher aldosterone levels -more than three times this high -have been found in patients with aldosterone-secreting adenomas or chronic kidney disease (61,62). However, besides tribes outside contemporary civilization (78) and individuals who deliberately abstain from sodium (80), most people alive today consume more than enough sodium and probably will never generate such high aldosterone levels.…”

Bilateral Nephrectomy for Resistant Hypertension and Secondary Aldosteronism in a Hemodialysis Patient: A Case Report

“…This finding suggests that the cause of hyperaldosteronism in this patient was not an aldosterone-producing tumor but rather diffuse hyperplasia of the outer part of the cortex (zona glomerulosa) ( 23 ). While the success of unilateral adrenalectomy for unilateral PA in controlling blood pressure in dialysis patients has been reported ( 24 ), a previous study described a dialysis patient diagnosed with bilateral adrenocortical hyperplasia who underwent unilateral adrenalectomy and achieved a transient decrease in renin and aldosterone levels but subsequently experienced a re-elevation in PAC and PRA values ( 25 ).…”

Extraordinarily high aldosterone, 901.0 ng/dL, in a patient with primary aldosteronism: an insight into the underlying mechanism

“…hydroxy-delta-5-steroid dehydrogenase, 3 beta-and steroid delta-isomerase 1 (HSD3B1) C. cytochrome P450, family 11, subfamily B, polypeptide 2 (CYP11B2, aldosterone synthase) dialysis [9,10], in whom mechanism of extraordinarily high PAC remained unclear.…”