Primary aldosteronism (PA) is a state of renin-independent aldosterone secretion that can range from subclinical to overt. Some normotensive individuals for whom PA screening is not routinely recommended are reported to fulfill the loading test criterion used for the diagnosis of PA. Multiple endocrine neoplasia type 1 (MEN1) is an autosomal dominant disorder characterized by the development of various endocrine tumors. Cases of PA associated with MEN1 have been reported; however, there has been no previous report on renin-independent aldosterone secretion within a family with MEN1. Herein, we present the case of a normotensive family presenting with both MEN1 and renin-independent aldosterone secretion. A 49-year-old man was admitted to our hospital for PA evaluation owing to the plasma aldosterone concentration/plasma renin activity ratio being greater than the screening cut-off value; the patient was normotensive.
The patient had a history of left nephrectomy and adrenalectomy for left renal carcinoma and adrenal tumor at the age of 39 years. Subsequently, he was diagnosed with MEN1 concurrent with primary hyperparathyroidism, insulinoma, and novel MEN1 gene mutations (c.655-5_655-4insC and c.818delC). The loading tests for PA confirmation, including saline infusion, and furosemide upright and captopril challenge tests, yielded positive findings, confirming a case of renin-independent aldosterone secretion. The patient’s mother, brother, and sister were also genetically or clinically diagnosed with MEN1. All of them were also normotensive and confirmed to have renin-independent aldosterone secretion. The coexistence of renin-independent aldosterone secretion and MEN1 within this family suggests a relationship between the 2 entities.
Compromised blood flow in the optic nerve head after systemic administration of 2 aldosterone in rats: A possible rat model of retinal ganglion cell loss
Purpose: To investigate the optic nerve head (ONH) blood flow, retinal vessel diameters, and retinal ganglion cell (RGC) loss after systemic administration of aldosterone in rats.
Methods: Aldosterone (80 μg/kg/day) or vehicle was administered using an osmotic minipump in Brown Norway rats. The mean blur rate in the vessel (MV) and tissue (MT) regions and retinal vessel diameters in the ONH were measured by laser speckle flowgraphy before and 1, 2, and 4 weeks after administration of aldosterone or vehicle. Intraocular pressure (IOP), blood pressure, and heart rate were recorded. The retrogradely labeled RGCs were counted in the retinal flatmounts prepared 5 weeks after treatment.
Results: The MV and MT in the aldosterone group significantly decreased at 2 and 4 weeks (MV: 2 weeks, P = 0.001, 4 weeks, P < 0.001; MT: 2 weeks, P = 0.02, 4 weeks, P = 0.03). The artery and vein diameters significantly decreased at 1, 2, and 4 weeks in the aldosterone group (all P < 0.001). The MV, MT, and vessel diameters remained unchanged in the vehicle group. Other parameters did not change over time in either group. RGC counts were significantly lower in the aldosterone group than in the vehicle group (P < 0.001).
Conclusions: ONH blood flow decreased following retinal vessel constriction without changes in IOP or blood pressure in a possible rat model of RGC loss by systemic administration of aldosterone.
Ocular Distribution of the Renin-Angiotensin-Aldosterone System in the Context of the SARS-CoV-2 Pandemic
The COVID-19 pandemic has resulted in an unprecedented impact on global health, economy, and way of life. SARS-CoV-2, the virus responsible for the disease, utilizes the ACE2 receptor found on host cells to mediate entry, replication, and infection. Numerous studies have elucidated the presence of many components of the renin-angiotensin-aldosterone system (RAAS) in the eye, including the ACE2 receptor. Considering this, and the anatomical vulnerability that the exposed ocular surface offers with its interconnectedness to the respiratory system, there is a theoretical risk of pathogen entry from the ocular route as well as the development of COVID-19-associated eye disease.
Despite this, the actual epidemiological data demonstrates low ocular symptoms, possibly due to differing ACE2 receptor expression across age, ethnicity, and sex coupled with the protective properties of tears. We summarize the current literature on ocular RAAS with specific focus on the ACE2 receptor and its interplay with the SARS-CoV-2 virus.
Report from the HarmoSter study: impact of calibration on comparability of LC-MS/MS measurement of circulating cortisol, 17OH-progesterone and aldosterone
Objectives: Liquid chromatography-tandem mass spectrometry (LC-MS/MS) is recommended for measuring circulating steroids. However, assays display technical heterogeneity. So far, reproducibility of corticosteroid LC-MS/MS measurements has received scant attention. The aim of the study was to compare LC-MS/MS measurements of cortisol, 17OH-progesterone and aldosterone from nine European centers and assess performance according to external quality assessment (EQA) materials and calibration.
Methods: Seventy-eight patient samples, EQA materials and two commercial calibration sets were measured twice by laboratory-specific procedures. Results were obtained by in-house (CAL1) and external calibrations (CAL2 and CAL3). We evaluated intra and inter-laboratory imprecision, correlation and agreement in patient samples, and trueness, bias and commutability in EQA materials.
Results: Using CAL1, intra-laboratory CVs ranged between 2.8-7.4%, 4.4-18.0% and 5.2-22.2%, for cortisol, 17OH-progesterone and aldosterone, respectively. Trueness and bias in EQA materials were mostly acceptable, however, inappropriate commutability and target value assignment were highlighted in some cases. CAL2 showed suboptimal accuracy. Median inter-laboratory CVs for cortisol, 17OH-progesterone and aldosterone were 4.9, 11.8 and 13.8% with CAL1 and 3.6, 10.3 and 8.6% with CAL3 (all p<0.001), respectively. Using CAL1, median bias vs. all laboratory-medians ranged from -6.6 to 6.9%, -17.2 to 7.8% and -12.0 to 16.8% for cortisol, 17OH-progesterone and aldosterone, respectively. Regression lines significantly deviated from the best fit for most laboratories. Using CAL3 improved cortisol and 17OH-progesterone between-method bias and correlation.
Conclusions: Intra-laboratory imprecision and performance with EQA materials were variable. Inter-laboratory performance was mostly within specifications. Although residual variability persists, adopting common traceable calibrators and RMP-determined EQA materials is beneficial for standardization of LC-MS/MS steroid measurements.
Aldosterone |
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| HY-113313 | MedChemExpress | 10mM/1mL | 524.4 EUR |
Aldosterone Antibody |
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| 10011-05011 | AssayPro | 150 ug | 260.4 EUR |
Aldosterone Antibody |
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| 10021-05011 | AssayPro | 150 ug | 260.4 EUR |
Aldosterone Antibody |
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| 41011-05011 | AssayPro | 150 ug | 260.4 EUR |
Aldosterone Antibody |
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| abx021121-02mg | Abbexa | 0.2 mg | 1011.6 EUR |
Aldosterone Antibody |
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| abx022859-1ml | Abbexa | 1 ml | 1028.4 EUR |
Aldosterone ELISA Kit |
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| E4342-100 | Biovision | each | 966 EUR |
Aldosterone 3 antibody |
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| 20-AR23 | Fitzgerald | 1 ml | 300 EUR |
Aldosterone (ALD) Antibody |
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| abx411014-02mg | Abbexa | 0.2 mg | 678 EUR |
Aldosterone (ALD) Antibody |
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| abx411018-02mg | Abbexa | 0.2 mg | 678 EUR |
Aldosterone (ALD) Antibody |
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| abx411019-02mg | Abbexa | 0.2 mg | 678 EUR |
Aldosterone (ALD) Antibody |
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| abx411068-1ml | Abbexa | 1 ml | 526.8 EUR |
Aldosterone (ALD) Antibody |
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| abx411069-01ml | Abbexa | 0.1 ml | 526.8 EUR |
Aldosterone (ALD) Antibody |
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| abx415727-1ml | Abbexa | 1 ml | 526.8 EUR |
Aldosterone (ALD) CLIA Kit |
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| 20-abx490318 | Abbexa |
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Aldosterone Standard, 125UL |
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| C182-125UL | Arbor Assays | 125UL | 85 EUR |
Aldosterone Standard, 625UL |
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| C182-625UL | Arbor Assays | 625UL | 207 EUR |
Aldosterone (ALD) ELISA Kit |
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| 20-abx150317 | Abbexa |
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Aldosterone (ALD) ELISA Kit |
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| abx514362-96tests | Abbexa | 96 tests | 801.6 EUR |
Aldosterone (ALD) ELISA Kit |
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| abx575139-96tests | Abbexa | 96 tests | 801.6 EUR |
Aldosterone (ALD) ELISA Kit |
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| DLR-ALD-Ge-48T | DL Develop | 48T | 681.6 EUR |
Aldosterone (ALD) ELISA Kit |
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| DLR-ALD-Ge-96T | DL Develop | 96T | 892.8 EUR |
ALD(Aldosterone) ELISA Kit |
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| EU2580 | FN Test | 96T | 571.5 EUR |
Rat Aldosterone ELISA kit |
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| E02A0774-192T | BlueGene | 192 tests | 1524 EUR |
Rat Aldosterone ELISA kit |
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| E02A0774-48 | BlueGene | 1 plate of 48 wells | 624 EUR |
Rat Aldosterone ELISA kit |
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| E02A0774-96 | BlueGene | 1 plate of 96 wells | 822 EUR |
High Prevalence of Autonomous Aldosterone Production in Hypertension: How to Identify and Treat It
Purpose of review: Primary aldosteronism (PA) affects millions of individuals worldwide. When unrecognized, PA leads to cardiovascular and renal complications via mechanisms independent from those mediated by hypertension. In this review, we emphasize the importance of PA screening in at-risk populations, and we provide options for customized PA therapy, with consideration for a variety of clinical care settings.
Recent findings: Compelling evidence puts PA at the forefront of secondary hypertension etiologies. Cardiovascular and renal damage likely begins in early stages of renin-independent aldosterone excess. PA must be considered not only in patients with resistant hypertension or hypokalemia, but also when hypertension is associated with obstructive sleep apnea or atrial fibrillation, or in those with early-onset hypertension. Screening with plasma aldosterone and renin is widely accessible, and targeted PA therapy can successfully circumvent the excess cardiorenal risk relative to equivalent primary hypertension. Identifying and treating PA in early stages provide opportunities for personalized hypertension therapy in a large number of patients. Additionally, early targeted therapy of PA is essential for pivoting the care of such patients from reactive to preventive of cardiovascular and renal morbidity and mortality.