Coexisting renal artery stenosis and primary aldosteronism

Chowdhury, Tumul; Lasker, Shoumen

doi:10.1093/ndt/12.12.2735

Cited by 12 publications

(6 citation statements)

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“…Spironolactone therapy resulted in marked reductions in blood pressure and normalisation of serum potassium levels. Our two cases and previous reports [7][8][9][10][11][12][13][14] suggest that clinicians should be aware that the two conditions may coexist in the same patient and that primary hyperaldosteronism may be an aetiology of resistant hypertension and/or hypokalaemia after revascularisation of renal artery stenosis.…”

Section: Introductionsupporting

confidence: 53%

“…[7][8][9][10][11][12][13][14] However, most of the cases have described the coexistence of an aldosteronoma with renovascular hypertension; only one case described unilateral adrenal hyperplasia. Complete exclusion of a small adrenal adenoma (Ͻ1.0 cm) in our two patients is not possible because they both refused adrenal vein sampling and computerised axial tomography of the adrenal glands only has about an 80% sensitivity for adenomas.…”

Section: Discussionmentioning

confidence: 99%

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Coexistence of atherosclerotic renal artery stenosis with primary hyperaldosteronism

Tendler

Anwar

et al. 2000

J Hum Hypertens

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The discovery of two forms of secondary hypertension in the same patient is unusual and suggests similar pathophysiological mechanisms, a predisposition to one type in the presence of the other or a chance occurrence. We describe two patients with renal artery stenosis who after successful correction of the stenotic lesions were discovered to have primary hyperaldosteronism associated with bilateral adrenal hyperplasia. Initially prior to revascularisation of the renal artery stenosis, the diagnosis of primary hyperaldosteronism was not evident. Both patients were subjected to further

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Section: Introductionsupporting

confidence: 53%

Section: Discussionmentioning

confidence: 99%

Coexistence of atherosclerotic renal artery stenosis with primary hyperaldosteronism

Tendler

Anwar

et al. 2000

J Hum Hypertens

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“…Indeed, activation of the renin-angiotensin system is a major stimulus for the expansion of the zona glomerulosa 58 , 59 . Such a mechanism is supported by previous results in healthy volunteers carrying hypomorphic alleles of the mineralocorticoid receptor (MR, encoded by NR3C2 ) 60 and by the description of APA in patients with a chronically activated renin angiotensin system due to renal artery stenosis 61 , 62 . Under ad libitum sodium and potassium diet, healthy volunteers with different NR3C2 rs2070951 alleles show plasma renin and aldosterone levels within the normal range, which do not differ across genotypes.…”

Section: Discussionmentioning

confidence: 64%

Identification of risk loci for primary aldosteronism in genome-wide association studies

et al. 2022

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Primary aldosteronism affects up to 10% of hypertensive patients and is responsible for treatment resistance and increased cardiovascular risk. Here we perform a genome-wide association study in a discovery cohort of 562 cases and 950 controls and identify three main loci on chromosomes 1, 13 and X; associations on chromosome 1 and 13 are replicated in a second cohort and confirmed by a meta-analysis involving 1162 cases and 3296 controls. The association on chromosome 13 is specific to men and stronger in bilateral adrenal hyperplasia than aldosterone producing adenoma. Candidate genes located within the two loci, CASZ1 and RXFP2, are expressed in human and mouse adrenals in different cell clusters. Their overexpression in adrenocortical cells suppresses mineralocorticoid output under basal and stimulated conditions, without affecting cortisol biosynthesis. Our study identifies the first risk loci for primary aldosteronism and highlights new mechanisms for the development of aldosterone excess.

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“…Primary hyperaldosteronism may coexist with renal artery stenosis (8,9). As renal angiograms were normal in our patients, we assume they had renal arteriolosclerosis induced by arterial hypertension.…”

Section: Discussionmentioning

confidence: 51%

Primary Hyperaldosteronism without Suppressed Renin Due to Secondary Hypertensive Kidney Damage

Oelkers

Diederich

Bähr

2000

The Journal of Clinical Endocrinology &Amp; Metabolism

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Primary hyperaldosteronism is characterized by high plasma and urinary aldosterone and suppressed PRA. Renin suppression is due to aldosterone-dependent sodium retention and mild extracellular volume expansion. We observed three patients with primary hyperaldosteronism, severe refractory hypertension, and normal to high normal PRA levels whose aldosterone/renin ratios were still elevated because of disproportionately high aldosterone levels. All available medical data on the patients as well as publications on the aldosterone/renin relationship in primary hyperaldosteronism were reviewed to explain the unusual findings.In one patient, histologically proven renal arteriolosclerosis was the probable cause of the escape of PRA from suppression by an aldosterone-producing adenoma. In the other two patients, hypertensive kidney damage due to primary hyperaldosteronism was the most likely explanation for the inappropriately high PRA, as in patient 1. All patients had high normal or slightly elevated serum creatinine levels and responded to 200 mg spironolactone/day with increased serum creatinine and hyperkalemia. Hyperkalemia was probably due to a decreased filtered load of sodium and a spironolactone-induced decrease in mineralocorticoid function. Two patients were cured of hyperaldosteronism by unilateral adrenalectomy but still need some antihypertensive therapy, whereas one patient has probable bilateral adrenal disease, with normal blood pressure on a low dose of spironolactone.In patients with severe hypertension due to primary hyperaldosteronism, PRA can escape suppression if hypertensive kidney damage supervenes. An increased aldosterone/PRA ratio is still useful in screening for primary hyperaldosteronism. These patients may respond to spironolactone therapy with a strong increase in serum creatinine and potassium. Early specific treatment of primary hyperaldosteronism is therefore indicated, and even a patient with advanced hypertension will profit from adrenalectomy or cautious spironolactone treatment. (J Clin Endocrinol Metab 85: 3266 -3270, 2000) T HE CLINICAL course of primary hyperaldosteronism can be extremely variable. A typical clinical constellation that raises suspicion of hyperaldosteronism is arterial hypertension plus hypokalemia. In early stages of the disease, serum potassium may still be in the normal range, and hypertension may be mild or very severe (1-4). Even in normotensive patients, hypokalemia may be due to primary hyperaldosteronism (5). As renin via angiotensin II is the most important regulator of aldosterone secretion, increased or high normal plasma and urinary aldosterone and suppressed renin activity (PRA) or renin concentration are the typical hormonal findings that establish the diagnosis of primary hyperaldosteronism. As aldosterone is increased and renin suppressed, the aldosterone/renin ratio is increased. A plasma aldosterone (nanograms per dL) to PRA (nanograms per mL/h) ratio of more than 20 in conjunction with a plasma aldosterone level greater than 15 ng/...

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Coexisting renal artery stenosis and primary aldosteronism

Cited by 12 publications

References 0 publications

Coexistence of atherosclerotic renal artery stenosis with primary hyperaldosteronism

Coexistence of atherosclerotic renal artery stenosis with primary hyperaldosteronism

Identification of risk loci for primary aldosteronism in genome-wide association studies

Primary Hyperaldosteronism without Suppressed Renin Due to Secondary Hypertensive Kidney Damage

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