MicroVue™ Ba EIA

The MicroVue Ba Enzyme Immunoassay Kit measures the amount of the complement fragment Ba in human urine, plasma or serum.


Product Specifications

Citations 31
Specimen

Serum 10 μL, EDTA Plasma 25 μL, Urine 10 μL

LLOQ 0.033 ng/mL
ULOQ 3.239 ng/mL
Assay Time 2.5 hours
Cross Reactivity

African Green Monkey, Cynomolgous monkey, Dog, Rhesus monkey

Ordering Information

For Research Use Only in the United States. Not for use in diagnostic procedures.
Catalog Number A033
Catalog Number (CE) A034
Size 96 wells/test
Price (USD) $725.00
Price (EURO) 640,00 €

Contact us

US Phone+1 (858) 552 1100
EU Phone+353 (91) 412 474
US Emailcontact-us@quidelortho.com
EU Emailcontact-emea@quidelortho.com

Specifications

Description

The MicroVue Ba Enzyme Immunoassay Kit measures the amount of the complement fragment Ba in human urine, plasma or serum.

Size 96 wells/test
Form

96 well plate with 12 eight-well strips in a resealable foil pouch

Specimen Serum 10 μL, EDTA Plasma 25 μL, Urine 10 μL
Limit of Detection (LOD) 0.011 ng/mL
Lower Limit of Quantitation (LLOQ) 0.033 ng/mL
Upper Limit of Quantitation (ULOQ) 3.239 ng/mL
Intra Assay 2.2–3.3%
Inter Assay 2.4–8.1%
Standards 5
Controls 2
Sample Values

Serum 436–3362 ng/mL, EDTA Plasma 226–2153 ng/mL, Urine 0.6–27.0 ng/mL

Assay Time 2.5 hours
Cross Reactivity

African Green Monkey, Cynomolgous monkey, Dog, Rhesus monkey

Storage

Store the unopened kit at 2°C to 8°C. Refer to Product Insert for additional storage details.

Background

Measurement of Ba in human urine, plasma or serum provides evidence of the involvement of the alternative pathway of complement. The alternative complement pathway provides innate protection against microbial agents in the absence of specific antibody. The activation of this complement pathway can be triggered by a variety of substances including microbial polysaccharides or lipids, gram-negative bacterial lipopolysaccharides, and surface determinants present on some viruses, parasites, virally infected mammalian cells, and cancer cells. In autoimmune diseases, the alternative complement pathway may contribute directly to tissue damage. A centrally important reaction that occurs during alternative pathway activation is the conversion of the 93 Kd molecular weight Factor B zymogen to an active proteolytic enzyme. This is accomplished in a two-step reaction. During the first reaction step the Factor B forms a magnesium-dependent complex with C3(H20) or C3b. The C3(H20),B complex is formed only in fluid-phase while the C3b,B complex can be formed either in fluid-phase or on a target surface. Factor B, which is present in the C3(H20),B or the C3b,B complex, is cleaved into the Ba (33 Kd) and Bb (60 Kd) fragments in the second reaction step by the alternative pathway enzyme, Factor D. Although alternative pathway activation is thought to occur primarily in the absence of specific antibody, many situations arise in which alternative pathway activation can occur as the result of classical pathway activation. For example, immune complexes that are present in autoimmune disease patients can trigger classical complement pathway activation with resultant production of C3b fragments. As described above, these C3b molecules are capable of binding Factor B and initiating its cleavage into the Ba and Bb fragments. Thus, alternative pathway activation can occur in antibody-mediated autoimmune disease states and may contribute significantly to enhanced complement activation and concomitant tissue destruction. By assessing Factor B cleavage products in test specimens, one can estimate the extent of alternative pathway utilization occurring at the time of sample collection in the disease state under investigation. The MicroVue Ba EIA provides a simple, rapid, non-radioactive, highly specific, and quantitative procedure for measuring Factor B activation. It is ideal for investigations involving the role or status of the alternative complement pathway in numerous research and clinical settings and for monitoring the generation of Ba in vitro.

Citations

Title Year Applications Sample Species Sample Sample Details

TNF Regulates Essential Alternative Complement Pathway Components and Impairs Activation of Protein C in Human Glomerular Endothelial Cells.

2015

ELISA

Human

GMVEC cells, HUVEC cells

Brain microvascular endothelial cells exhibit lower activation of the alternative complement pathway than glomerular microvascular endothelial cells.

2018

ELISA

Human

GMVEC cells, BMVEC cells

Intravascular hemolysis activates complement via cell-free heme and heme-loaded microvesicles.

2018

ELISA

Human

Serum

Microvesicles with heme

Early local activation of complement in aqueous humour of patients with age-related macular degeneration.

2019

ELISA

Human

Aqueous humour

Age-Related Macular Degeneration

Complement fragments are biomarkers of antibody-mediated endothelial injury.

2019

ELISA

Human

Plasma

Antibody-mediated endothelial injury

Local complement activation is associated with primary graft dysfunction after lung transplantation.

2020

ELISA

Human

Bronchoalveolar lavage

Lung transplant

Complement Activation in the Vitreous of Patients With Proliferative Diabetic Retinopathy.

2020

ELISA

Human

Plasma, Vitreous Humor

Proliferative Diabetic Retinopathy

Alternative complement pathway activation in thrombotic microangiopathy associated with lupus nephritis.

2020

ELISA

Human

Serum

Lupus Nephritis, Thrombotic Microangiopathy

Alternative complement pathway activation in thrombotic microangiopathy associated with lupus nephritis.

2020

ELISA

Human

Urine

Lupus Nephritis, Thrombotic Microangiopathy

Complement Expression and Activation in Osteoarthritis Joint Compartments.

2020

ELISA

Human

Chondrocytes

Supernatent

Complement Expression and Activation in Osteoarthritis Joint Compartments.

2020

ELISA

Human

Synoviocytes

Supernatent

Establishing a Case for Anti-complement Therapy in Membranous Nephropathy.

2020

ELISA

Human

Urine

Membranous Nephropathy

Increased complement activation is a distinctive feature of severe SARS-CoV-2 infection

2021

ELISA

Human

Plasma

COVID-19

Alternative Complement Pathway Is Activated and Associated with Galactose-Deficient IgA 1 Antibody in IgA Nephropathy Patients

2021

ELISA

Human

Plasma

IgA Nephropathy

Early Elevation of Complement Factor Ba Is a Predictive Biomarker for Transplant-Associated Thrombotic Microangiopathy

2021

ELISA

Human

Plasma

Thrombotic Microangiopathy - TA

Increased complement activation is a distinctive feature of severe SARS-CoV-2 infection.

2021

ELISA

Human

Plasma

COVID-19

Persistently elevated complement alternative pathway biomarkers in COVID-19 correlate with hypoxemia and predict in-hospital mortality.

2022

ELISA

Human

Plasma

COVID-19

Persistently elevated complement alternative pathway biomarkers in COVID-19 correlate with hypoxemia and predict in-hospital mortality.

2022

ELISA

Human

Serum

COVID-19

Complement Activation in Patients With Heat-Related Illnesses: Soluble CD59 Is a Novel Biomarker Indicating Severity of Heat-Related Illnesses.

2022

ELISA

Human

Plasma

Heat-related illnesses

Mathematical Modeling of Complement Pathway Dynamics for Target Validation and Selection of Drug Modalities for Complement Therapies.

2022

ELISA

Human

Complement Proteins

Comparison of Complement Pathway Activation in Autoimmune Glomerulonephritis.

2022

ELISA

Human

Urine

AAV, FSGS, IgAN, MN, and LN

Sex and Age-Related Differences in Complement Factors Among Patients With Intermediate Age-Related Macular Degeneration.

2022

ELISA

Human

Plasma

Age-Related Macular Degeneration

Associations between Biomarkers of Complement Activation, Galactose-Deficient IgA1 Antibody and the Updated Oxford Pathology Classification of IgA Nephropathy.

2022

ELISA

Human

Plasma

IgA Nephropathy

Serum and plasma levels of Ba, but not those of soluble C5b-9, might be affected by renal function in chronic kidney disease patients.

2023

ELISA

Human

Plasma, Serum

Glomerulonephritis

Human factor H-related protein 2 (CFHR2) regulates complement activation

2013

ELISA

Human

Serum

Defining the complement biomarker profile of C3 glomerulopathy

2014

ELISA

Human

Plasma

C3G

Iron-induced Local Complement Component 3 (C3) Up-regulation via Non-canonical Transforming Growth Factor (TGF)-β Signaling in the Retinal Pigment Epithelium

2015

ELISA

Human

ARPE-19 Cells

Functional Characterization of Autoantibodies against Complement Component C3 in Patients with Lupus Nephritis

2015

ELISA

Human

Serum

Age-related macular degeneration associated polymorphism rs10490924 in ARMS2 results in deficiency of a complement activator.

2017

ELISA

Human

Serum

ARMS2 protein

Persistent complement dysregulation with signs of thromboinflammation in active Long Covid

2024

ELISA

Human

Serum

COVID-19