Aldosterone to Renin Ratio as Screening Tool in Primary Aldosteronism

Schilbach, Katharina; Junnila, Riia K.; Bidlingmaier, Martin

doi:10.1055/a-0672-0836

Cited by 23 publications

(22 citation statements)

References 83 publications

(111 reference statements)

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“…In addition, hypokalemia is known to promote the pro-arrhythmic effects of class III antiarrhythmic drugs. Ultimately, it is worth mentioning that hypokalemia can also be a pitfall in the diagnosis of PA: A low potassium value results in a reduced secretion of aldosterone and therefore potentially a false negative calculation of the ARR [50,51]. Thus pre-analytics is of particular importance in the setting of hypokalemia.…”

Section: Reviewmentioning

confidence: 99%

Hypokalemia and the Prevalence of Primary Aldosteronism

Gruber

Beuschlein

2020

Horm Metab Res

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Hypokalemia is closely linked with the pathophysiology of primary aldosteronism (PA). Although hypokalemic PA is less common than the normokalemic course of the disease, hypokalemia is of particular importance for the manifestation and development of comorbidities. Specifically, a growing body of evidence demonstrates that hypokalemia in PA patients is associated with a more severe disease course regarding cardiovascular and metabolic morbidity and mortality. It is also well appreciated that low potassium levels per se can promote or exacerbate hypertension. The spectrum of hypokalemia-related symptoms ranges from asymptomatic courses to life-threatening conditions. Hypokalemia is found in 9–37% of all cases of PA with a predominance in patients with aldosterone producing adenoma. Conversely, hypokalemia resolves in almost 100% of cases after both, specific medical or surgical treatment of the disease. However, to date, high-level evidence about the prevalence of primary aldosteronism in a hypokalemic population is missing. Epidemiological data are expected from the recently launched IPAHK+study (“Incidence of Primary Aldosteronism in Patients with Hypokalemia”).

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Section: Reviewmentioning

confidence: 99%

Hypokalemia and the Prevalence of Primary Aldosteronism

Gruber

Beuschlein

2020

Horm Metab Res

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“…The following biochemical profile confirmed the diagnosis since there was spontaneous hypokalemia, undetectable renin, and a PAC above 20 ng/dL [20][21][22][23][24]. • To confirm successful catheterization; the adrenal vein cortisol-to-inferior vena cava cortisol ratio's cut off is greater than a ratio of 5:1.…”

Section: Discussionmentioning

confidence: 89%

“…The following biochemical profile confirmed the diagnosis since there was spontaneous hypokalemia, undetectable renin, and a PAC above 20 ng/dL [ 20 – 24 ].…”

Section: Discussionmentioning

confidence: 99%

Seizure and coma secondary to Conn’s syndrome: a case report

2020

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Background: Conn's syndrome is a curable condition if identified properly. It is characterized by autonomous secretion of aldosterone from the adrenal gland cortex. Its morbidity is related to the increased risk of cardiovascular diseases. Case presentation: We report the case of a 48-year-old man of African descent presenting with generalized tonicclonic seizure and coma secondary to hypertensive encephalopathy. A biochemical evaluation revealed a very high aldosterone level and an undetectable renin level, both are compatible with primary aldosteronism. The presentation of the following confirms the diagnosis of primary aldosteronism: spontaneous hypokalemia, an undetectable renin level, and a high aldosterone level. Abdominal computed tomography revealed a left adrenal adenoma. Adrenal venous sampling confirmed lateralization of aldosterone excretion from the left adrenal gland. Our patient underwent left laparoscopic adrenalectomy that confirmed a left functional adrenal adenoma. After 12 months of follow up, his hypertension was controlled on only one antihypertensive drug which was down from four drugs preoperatively. Conclusion: Conn's syndrome, in this case, was complicated by coma secondary to seizure. Adrenalectomy normalized the hypokalemia and improved resistant hypertension. Potassium supplementation and several antihypertensives were discontinued as our patient became normokalemic and normotensive on one antihypertensive agent.

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“…Measurement of serum cortisol was conducted using an immunochemiluminescence assay (Liaison; DiaSorin, Saluggia, Italy). Within and between intra-assay and interassay variability was < 10 %, with a lower limit of quantification at 0.2 μg/dl as previously described [13,14,17]. Urinary cortisol measurement was performed with chemiluminescence immunoassay (ADVIA Centaur, Siemens) with within-and between-assay coefficients variations below 7 %.…”

Section: Definitions and Laboratory Measurementsmentioning

confidence: 99%

The Impact of Glucocorticoid Co-Secretion in Primary Aldosteronism on Thyroid Autoantibody Titers During the Course of Disease

et al. 2020

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Excess aldosterone is associated with the increased risk of cardio-/cerebrovascular events as well as metabolic comorbidities not only due to its hypertensive effect but also due to its proinflammatory action. Autonomous cortisol secretion (ACS) in the setting of primary aldosteronism (PA) is known to worsen cardiovascular outcome and potentially exhibit immunosuppressive effects. The aim of this study was to determine the impact of ACS status in patients with PA on kinetics of thyroid autoantibodies (anti-TPO, anti-TG) pre and post therapy initiation. Ninety-seven PA patients (43 unilateral, 54 with bilateral PA) from the database of the German Conn’s Registry were included. Anti-TPO and anti-TG levels were measured pre and 6–12 months post therapeutic intervention. Patients were assessed for ACS according to their 24- hour urinary cortisol excretion, late night salivary cortisol and low-dose dexamethasone suppression test. Abnormal test results in line with ACS were identified in 74.2% of patients with PA. Following adrenalectomy, significant increases in anti-TPO levels were observed in patients with at least one abnormal test (p = 0.049), adrenalectomized patients with at least two pathological ACS tests (p = 0.015) and adrenalectomized patients with pathologic dexamethasone suppression tests (p = 0.018). No antibody increases were observed in unilateral PA patients without ACS and in patients with bilateral PA receiving mineralocorticoid antagonist therapy (MRA). Our data are in line with an immunosuppressive effect of mild glucocorticoid excess in PA on thyroid autoantibody titers. This effect is uncovered by adrenalectomy, but not by MRA treatment.

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Aldosterone to Renin Ratio as Screening Tool in Primary Aldosteronism

Cited by 23 publications

References 83 publications

Hypokalemia and the Prevalence of Primary Aldosteronism

Hypokalemia and the Prevalence of Primary Aldosteronism

Seizure and coma secondary to Conn’s syndrome: a case report

The Impact of Glucocorticoid Co-Secretion in Primary Aldosteronism on Thyroid Autoantibody Titers During the Course of Disease

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