Aldosterone ELISA Kit

Name: Aldosterone ELISA Kit
SKU: DEIA4996
Rating: 5 (1 reviews)

Regulatory status: For research use only, not for use in diagnostic procedures.

COA

SDS

Datasheet

Summary

Sample

serum, plasma, urine, other sample matrices

Species Reactivity

Human

Intended Use

CD's Aldosterone ELISA Kit is a competitive assay that can be used for quantification of aldosterone in serum, plasma, urine, and other sample matrices. The assay has a range from 15.6-2,000 pg/ml and a sensitivity (80% B/B0) of approximately 30 pg/ml.

Storage

This kit will perform as specified if stored as directed at -20°C and used before the expiration date indicated on the outside of the box.

Performance Characteristics

##Sample Data##
The standard curve presented here is an example of the data typically produced with this kit; however, your results will not be identical to these. You must run a new standard curve. Do not use the data below to determine the values of your samples. Your results could differ substantially.
Raw Data Average Corrected
Total Activity 0.499 0.533 0.516
NSB 0.007 0.007 0.007
B0 1.224 1.254
1.258 1.179 1.237 1.230

Typical results

Typical standard curve
Assay Range = 15.6-2,000 pg/ml
Sensitivity (defined as 80% B/B0) = 30 pg/ml Mid-point (defined as 50% B/B0) = 100-180 pg/ml
The sensitivity and mid-point were derived from the standard curve shown above. The standard was diluted with ELISA Buffer.

##Precision##:
The intra-assay CVs have been determined at multiple points on the standard curve.

Intra-assay variation
*%CV represents the variation in concentration (not absorbance) as determined using a reference standard curve.

Sample Inter-assay variation for plasma, serum, and urine
Plasma, serum and urine samples from different individuals containing high, medium, or low level of aldosterone were measured eight times on four different days using a different set of reagents each time. The calculated %CV is reported as inter-assay variance.

##Cross Reactivity##:

Cross Reactivity of the Aldosterone ELISA

General Description

Aldosterone, a steroid hormone secreted by the adrenal cortex, is the principle mineralocorticoid controlling sodium and potassium balance.1,2 The primary role of aldosterone is to promote unidirectional salt reabsorption in a variety of epithelial tissues, the salivary gland, intestine, sweat glands, and the kidney. Aldosterone is synthesized from cholesterol in the zona glomerulosa of the adrenal cortex. Secretion of aldosterone is complex, being regulated by both hormones and electrolytes. However, the renin-angiotensin system (RAS) is the primary regulator of aldosterone secretion.3 Angiotensin II and potassium stimulate secretion of aldosterone by increasing the rate of synthesis of the hormone. Serum aldosterone levels vary depending on age and body posture, i.e., supine versus upright. In normal upright adult individuals, serum aldosterone concentrations are generally less than 300 pg/ml. Only a fraction of urinary aldosterone is excreted intact, with larger percentages excreted as aldosterone- 18-glucuronide and tetrahydroaldosterone-3-glucuronide.4 Urinary excretion of aldosterone in normal adults, assessed as a combination of free aldosterone and aldosterone-18-glucuronide, is generally less than 20 μg/24 hr.5,6 The average reported level of tetrahydroaldosterone in urine is 103 nmol/L (37 ng/ml) or less than 70 μg/24 hr.5,6

Citations

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Documents

pdf COA

pdf SDS

pdf Datasheet

QA & Reviews

Customer Reviews

References

Relationship between parathyroid hormone and renin-angiotensin-aldosterone system in hemodialysis patients with secondary hyperparathyroidism

JOURNAL OF BONE AND MINERAL METABOLISM

Authors: Kono, Keiji; Fujii, Hideki; Watanabe, Kentaro; Goto, Shunsuke; Nishi, Shinichi

Abstract

Introduction Hyperparathyroidism (HPT) is associated with mortality and cardiovascular disease (CVD) in dialysis patients. However, its mechanism is still unclear. It is suspected that parathyroid hormone (PTH) is associated with the renin-angiotensin-aldosterone system (RAAS) as a possible mechanism. Thus, we examined their hormonal interaction in hemodialysis patients with secondary HPT. Materials and methods Seventeen hemodialysis patients with HPT were included. All patients underwent total parathyroidectomy (PTx). Serum intact PTH (iPTH), calcium and phosphate levels, plasma renin activity (PRA), and plasma aldosterone levels (ALD) were measured pre- and post-PTx. Results Pre-serum iPTH tended to be correlated with pre-PRA and were significantly correlated with pre-ALD (pre-PRA:r = 0.44,p = 0.07, pre-ALD:r = 0.49,p < 0.05). With the reduction in serum iPTH after PTx, PRA and ALD significantly decreased after PTx. Additionally, the change in serum iPTH tended to be correlated with the changes in PRA and ALD (PRA;r = 0.46,p = 0.05, ALD;r = 0.45,p = 0.06). Conclusion Our results suggest that PTH could be interrelated with RAAS in hemodialysis patients with secondary HPT.

Pathogenesis and treatment of primary aldosteronism

NATURE REVIEWS ENDOCRINOLOGY

Authors: Zennaro, Maria-Christina; Boulkroun, Sheerazed; Fernandes-Rosa, Fabio L.

Abstract

Early diagnosis and appropriate treatment of primary aldosteronism, the most frequent cause of secondary hypertension, are crucial to prevent deleterious cardiovascular outcomes. In the past decade, the discovery of genetic abnormalities responsible for sporadic and familial forms of primary aldosteronism has improved the knowledge of the pathogenesis of this disorder. Mutations in genes encoding ion channels and pumps lead to increased cytosolic concentrations of calcium in zona glomerulosa cells, which triggersCYP11B2expression and autonomous aldosterone production. Improved understanding of the mechanisms underlying the disease is key to improving diagnostics and to developing and implementing targeted treatments. This Review provides an update on the genetic abnormalities associated with sporadic and familial forms of primary aldosteronism, their frequency among different populations and the mechanisms explaining excessive aldosterone production and adrenal nodule development. The possible effects and uses of these findings for improving the diagnostics for primary aldosteronism are discussed. Furthermore, current treatment options of primary aldosteronism are reviewed, with particular attention to the latest studies on blood pressure and cardiovascular outcomes following medical or surgical treatment. The new perspectives regarding the use of targeted drug therapy for aldosterone-producing adenomas with specific somatic mutations are also addressed. This Review outlines the latest understanding of the pathogenesis of primary aldosteronism. Current treatment options are also discussed, including the potential for targeted therapies.