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• How to Achieve Reliable and Reproducible ELISA Results

ELISA (enzyme-linked immunosorbent assay) is one of the most widely used methods for quantifying analytes in biological samples. In addition to its high sensitivity and specificity, ELISA is valued for its relative simplicity and cost-effectiveness compared with many other analytical techniques. However, while the procedure may appear straightforward, accurate measurement of biological samples can involve important technical considerations.

How to Achieve Reliable and Reproducible ELISA Results

Concept of a Sandwich ELISA Assay

In a typical sandwich ELISA, a 96-well microtiter plate is pre-coated with a target-specific capture antibody, which may be monoclonal or polyclonal. The sample is then added to the wells and incubated, allowing the protein of interest to bind to the immobilized capture antibody.

Next, a detection antibody is added. This antibody binds to a separate site on the target antigen, forming an antibody–antigen–antibody complex: capture antibody–target antigen–detection antibody.

 

 

Quantification of the results is achieved by introducing an enzyme-conjugated antibody that binds specifically to the detection antibody, catalyzing a colorimetric enzymatic reaction. After a brief incubation with an appropriate substrate, the amount of enzyme conjugate bound in the well can be detected. The resulting color change in the well is then measurable using a standard microtiter plate ELISA reader, which records the absorbance (optical density). A higher signal indicates a higher concentration of the analyte in the sample, corresponding to the range established by the standard curve.

 

 

How to Achieve Reliable and Reproducible ELISA Results

 

To obtain reliable results it is recommended to choose an ELISA Assay that has gone through a full validation protocol. Results (validation data) must be provided that include data on specificity, sensitivity (LOD, LLOQ), accuracy/recovery, parallelism and dilution linearity, precision (within-run and in-between run), calibration, stability, and lot-to-lot consistency.

 

 

How to Achieve Reliable and Reproducible ELISA Results

 

 Key Elements of ELISA Assay Validation

 1. Specificity

Specificity ensures accurate measurement of the target protein or biomarker.The performance of an ELISA assay depends largely on the quality of the antibody pair used to detect the analyte of interest.

To achieve high specificity, the assay developer should:

-Select antibody pairs with high affinity and specificity, ideally with well-characterized binding sites.

-Optimize the ELISA kit to accurately quantify biomarkers in both healthy and disease-state samples.

2. Sensitivity

 Sensitivity describes an ELISA assay’s ability to detect very low concentrations of the target analyte.

In an ELISA, sensitivity is determined by the lowest amount of protein that can be detected using the antibody pair included in the kit. It depends largely on the affinity of the solid-phase, or coating, antibody. Using a higher-affinity antibody can therefore improve assay sensitivity.

-Analytical sensitivity / Limit of Detection (LOD): The lowest analyte concentration that can be detected with statistical significance using a specific analytical method. It is typically calculated as the background signal plus or minus two standard deviations.

-Functional sensitivity / Lower Limit of Quantification (LLOQ): The lowest analyte concentration that can be reliably detected and quantified.

3. Accuracy / Recovery

Accuracy evaluates whether an ELISA assay correctly detects the presence or absence of the target protein or antigen in different sample matrices, such as serum and plasma. It also helps identify potential matrix effects that could interfere with accurate measurement of the analyte.

Ideally, accuracy should be assessed in every sample type in which the analyte will be measured, including serum, EDTA plasma, and heparin plasma. To evaluate recovery, each matrix is spiked with known concentrations of recombinant analyte. The samples are then measured against the assay’s standard curve, and the observed concentrations are compared with the expected, or nominal, values.

4. Parallelism / Dilution Linearity

Parallelism and dilution linearity confirm that samples can be measured accurately and reliably across different dilution levels.

-Parallelism assesses whether samples containing high endogenous concentrations of the analyte produce results that remain consistent with the assay’s standard curve after serial dilution. This evaluation can reveal differences in antibody binding affinity between the endogenous analyte in real samples and the recombinant analyte used to calibrate the ELISA. Parallelism should always be evaluated during assay validation using samples with naturally occurring analyte levels.

-Dilution linearity evaluates analyte recovery in samples spiked with the recombinant analyte used to generate the assay standards. It determines whether measured concentrations remain proportional and accurate following serial dilution.

5. Precision

Precision assesses an ELISA assay’s ability to produce consistent and reliable results both within a single run and across different kit lots.

-Within-run precision (repeatability): Evaluates variation among multiple measurements of the same sample performed during a single assay run.

-Between-run precision: Evaluates the consistency of results when samples are tested repeatedly in separate assay runs, including runs performed with different ELISA kit lots. This confirms that the assay provides accurate and reproducible results over time and across lot-to-lot variations.

6. Calibration

Calibration enables accurate quantification of the target protein.

-Accurate measurement depends on the linearity and reproducibility of the assay’s standard curve. During ELISA kit optimization, variability among calibrator results should be minimized. When available, standards traceable to NIBSC or WHO reference materials should be used to support harmonized assay standardization.

7. Stability

Stability evaluates both the integrity of the target analyte in sample matrices and the stability of ELISA kit reagents.

During assay development, all assay components should be assessed for stability, along with the analyte in relevant sample types, such as serum and plasma.

-Analyte stability: This can be evaluated by exposing samples to repeated freeze–thaw cycles or storing them at room temperature for a defined period before analysis.

-Kit reagent stability: ELISA reagents should be tested under different temperature conditions for specified time periods to confirm their stability.

-Shelf-life: Real-time stability testing should be performed throughout the intended shelf-life of the kit. For example, reagents stored at 4°C may be evaluated after 6, 12, and 18 months.

8. Lot-to-Lot Consistency

Lot-to-lot consistency ensures that different ELISA kit batches provide comparable and reliable results.

-To assess consistency, each kit lot is tested using in-house control samples, including serum and plasma samples containing endogenous analyte as well as samples spiked with recombinant analyte. Results are evaluated to confirm that they fall within established quality-control ranges.

 

 

Achieving Reproducible ELISA Assay Results

BIOMEDICA ELISA kits undergo comprehensive validation in accordance with international quality guidelines. This helps ensure that your valuable samples are measured accurately and that the assay specifically detects the analyte of interest.

Learn more about achieving reproducible ELISA assay results on our website : QUALITY 

 

Why Choose BIOMEDICA ELISA Kits?

 

-Specific: Accurate biomarker detection using well-characterized antibodies.

-Reliable: Validated using clinical samples.

-Reproducible: Consistent performance across ELISA kit lots.

 

 

 

Further reading 

A Practical Guide to Immunoassay Method Validation.

Andreasson U, Perret-Liaudet A, van Waalwijk van Doorn LJ, Blennow K, Chiasserini D, Engelborghs S, Fladby T, Genc S, Kruse N, Kuiperij HB, Kulic L, Lewczuk P, Mollenhauer B, Mroczko B, Parnetti L, Vanmechelen E, Verbeek MM, Winblad B, Zetterberg H, Koel-Simmelink M, Teunissen CE.Front Neurol. 2015 Aug 19;6:179. doi: 10.3389/fneur.2015.00179. PMID: 26347708; PMCID: PMC4541289.

Pulmonary arterial hypertension (PAH), also known as World Health Organization (WHO) Group 1 pulmonary hypertension, is a rare and worsening condition (1). It is a disease characterized by increased blood pressure in the arteries of the lungs, which can lead to heart failure if left untreated.

It involves damage to the lining of the blood vessels in the lungs and changes in the vessel structure. These changes cause increased pressure in the pulmonary arteries, higher resistance in the blood vessels, and eventually lead to failure of the right side of the heart (2).

NPPB (Natriuretic Peptide Precursor B) is the gene that encodes the precursor protein for B-type natriuretic peptide (BNP). It is an early-response gene that is activated in cardiac myocytes, particularly in the ventricles, in response to mechanical stress, volume overload, or hormonal and sympathetic stimuli (3). When NPPB is transcribed and translated, it produces a 134-amino acid preproBNP, which undergoes further processing to generate BNP and NT-proBNP, both important biomarkers used in diagnosing and managing heart failure and other cardiovascular conditions (2). NT-proBNP has no known biological function but, due to its longer half-life compared to BNP (70 minutes versus 22 minutes) (4) and greater stability during storage (5), it offers potential advantages for use as a biomarker in clinical settings (4, 5).

NT-proBNP – A Potential Biomarker of Pulmonary Hypertension

A recent study explored the pathophysiological changes in patients during hemodialysis and blood reinfusion in patients with kidney disease.

The NT-proBNP ELISA from BIOMEDICA was used to measure NT-proBNP plasma levels for the noninvasive estimation of pulmonary arterial pressure (PAP) patients with chronic kidney failure:

Pathophysiological changes in patients during hemodialysis and blood reinfusion predict potential development of hemodialysis reactions. Pethő ÁG et al., Ren Fail. 2025.

Abstract

Hemodialysis reactions (HDRs) are a type of hypersensitivity reactions (HSRs), such as complement activation-related pseudoallergy (CARPA) observed during nanoparticle infusions. Our study aimed to elucidate the mechanisms of human HDRs by focusing on hemodynamic and clinical chemistry changes of HSR-related or biocompatibility issues during human hemodialysis (HD) and the reinfusion of blood. Based on our recent animal experiments, we hypothesize that increased pulmonary arterial pressure (PAP), and increases in thromboxane B2 (TXB2) and complement 3a (C3a) plasma concentrations will likely manifest in, or at least predict, human HDRs during HD and blood reinfusion. To verify our hypothesis, we measured these parameters during high-flux HD in patients. Since direct PAP measurement was not possible, the plasma concentration of the N-terminal fragment of the brain natriuretic peptide (NT-proBNP) was determined for the noninvasive estimation of PAP. Our results show an increase in NT-proBNP and TXB2 during the reinfusion of extracorporeal blood. The plasma concentration of C3a increased in early HD already and remained elevated up to blood reinfusion. In conclusion, the observed changes in HSR-related parameters or biocompatibility issues in otherwise asymptomatic patients may suggest that a greater activation of these mechanisms could explain the development of human hemodialysis reactions.

NT-proBNP ELISA | SK-1204 – HIGHLIGHTS

• Convenient – ready -to-use reagents
• Flexible – can be run in every lab
• Two controls included
• TRUSTED – widely cited in over 140 publications
• REPRODICIBLE – rigorously validated following international quality guidelines
• Assay independently validated in saliva samples link

 

DISCOVER MORE:  Protocol Booklet, Validation data file

 

Literature

1. Rare but serious: pulmonary vascular disease around the world. Hjalmarsson C, Jose A, Poor H, Loureiro CMC, Stosor V, Pulido T, Krishnan M. JHLT Open. 2025 Jul 18;9:100327. doi: 10.1016/j.jhlto.2025.100327. PMID: 40808822; PMCID: PMC12345328.
2. BNP/NT-proBNP in pulmonary arterial hypertension: time for point-of-care testing? Lewis RA, Durrington C, Condliffe R, Kiely DG. Eur Respir Rev. 2020 May 15;29(156):200009. doi: 10.1183/16000617.0009-2020. PMID: 32414745; PMCID: PMC9488846
3. Biochemistry of the human B-type natriuretic peptide precursor and molecular aspects of its processing. Semenov AG, Seferian KR. Clin Chim Acta. 2011 May 12;412(11-12):850-60. doi: 10.1016/j.cca.2011.03.006. Epub 2011 Mar 21. PMID: 21396929.
4. Synthesis, secretion, function, metabolism and application of natriuretic peptides in heart failure. Fu S, Ping P, Wang F, Luo L. J Biol Eng. 2018 Jan 12;12:2. doi: 10.1186/s13036-017-0093-0. PMID: 29344085; PMCID: PMC5766980.
5. Amino-terminal pro-B-type natriuretic peptide: analytic considerations. Ordonez-Llanos J, Collinson PO, Christenson RH. Am J Cardiol. 2008 Feb 4;101(3A):9-15. doi: 10.1016/j.amjcard.2007.11.013. PMID: 18243867.
6. Pathophysiological changes in patients during hemodialysis and blood reinfusion predict potential development of hemodialysis reactions. Pethő ÁG, Révész C, Mészáros T, Sáfár O, Rosivall L, Domán J, Szénási G, Gigacz T, Dézsi L. Ren Fail. 2025 Dec;47(1):2500662. doi: 10.1080/0886022X.2025.2500662. Epub 2025 May 6. PMID: 40328739; PMCID: PMC12057777.

 

Further reading

• NT-proBNP Levels in Hemodialysis Patients: Unrelated to Interdialytic Weight Gain, Limited in Detecting Left Ventricular Systolic Dysfunction, but May Identify Atrial Fibrillation. Divani M, Katsanaki K, Tziastoudi M, Makri P, Poulianiti C, Lykotsetas E, Balatsouka A, Stefanidis I, Eleftheriadis Kidney and Dialysis. 2026; 6(2):42.  
• Dialysis for Chronic Kidney Failure: A Review. Flythe JE, Watnick S. JAMA. 2024 Nov 12;332(18):1559-1573. doi: 10.1001/jama.2024.16338. PMID: 39356511.

 

C4d Immunostaining and Molecular Tools for Heart Transplant Rejection – Heart transplantation is currently the most effective treatment option for patients with end-stage heart failure unresponsive to optimal medical therapy (1-3). Despite significant advancements in immunosuppressive therapies and transplant management, acute and chronic rejection-related allograft injuries remain among the leading causes of death and morbidity post-transplant, thereby limiting patient longevity. Improving rejection management remains an unmet medical need (5). Currently, the diagnosis of cardiac rejection predominantly depends on the pathological evaluation of endomyocardial biopsies (EMBs), which involves detecting and grading cellular infiltrates and myocardial injury (1, 6, 7).

C4d Immunostaining and Molecular Tools for Heart Transplant Rejection

In a recent study “Heart allograft rejection: molecular diagnosis using intra-graft targeted gene expression profiling” by Giarraputo A and colleagues explore the use of targeted gene expression analysis within cardiac graft tissue to improve the molecular diagnosis of heart transplant rejection. The research aims to identify specific gene expression patterns associated with rejection episodes, providing a potentially more precise and early detection method compared to traditional histopathological assessment. This approach could enhance rejection monitoring and guide more tailored therapeutic interventions in heart transplant recipients.

The study showed that a novel molecular diagnostic system based on formalin-fixed, paraffin-embedded (FFPE) tissue accurately detects cardiac allograft rejection. A tool that could be easily applicable in clinical settings alongside pathology and has the potential to improve the precision of rejection diagnosis.

> C4d antibodies by BIOMEDICA – for the identification of human complement split product C4d in paraffin and frozen sections as well as by flow cytometry. 

Anti-C4dAntibody | BI-RC4D

• widely cited in over 100 publications 

• for immunohistochemistry on paraffin embedded tissue and frozen sections 

• use in kidney, heart, liver and other transplants 

 

Anti-C4d Antibody (FITC) | BI-RC4D-FITC 

• protocol for cell- or solid-phase bound C4 and C4d split product by flow cytometry 

• for kidney, heart, liver and other transplants 

 

 

Literature:

1. 2016 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure: The Task Force for the diagnosis and treatment of acute and chronic heart failure of the European Society of Cardiology (ESC)Developed with the special contribution of the Heart Failure Association (HFA) of the ESC. Ponikowski P, Voors AA, Anker SD, Bueno H, Cleland JGF, Coats AJS, Falk V, González-Juanatey JR, Harjola VP, Jankowska EA, Jessup M, Linde C, Nihoyannopoulos P, Parissis JT, Pieske B, Riley JP, Rosano GMC, Ruilope LM, Ruschitzka F, Rutten FH, van der Meer P; ESC Scientific Document Group. Eur Heart J. 2016 Jul 14;37(27):2129-2200. PMID: 27206819.
2. 2017 ACC/AHA/HFSA Focused Update of the 2013 ACCF/AHA Guideline for the Management of Heart Failure: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Failure Society of America. Yancy CW, Jessup M, Bozkurt B, Butler J, Casey DE Jr, Colvin MM, Drazner MH, Filippatos GS, Fonarow GC, Givertz MM, Hollenberg SM, Lindenfeld J, Masoudi FA, McBride PE, Peterson PN, Stevenson LW, Westlake C. Circulation. 2017 Aug 8;136(6):e137-e161. PMID: 28455343.
3. Molecular Diagnosis of Heart Allograft Rejection Using Intra-Graft Targeted Gene Expression Profiling: the heart HistoMX system. Alessia Giarraputo, Guillaume Coutance, JigneshK. Patel, Marny Fedrigo, Olivier Aubert, Jessy Dagobert, Fariza Mezine, Blaise Robin, Philippe Rouvier, Shaida Varnous, Jean Paul Duong Van Huyen, Patrick Bruneval, Annalisa Angelini, Jon Kobashigawa, Alexandre Loupy.
4. Heart allograft rejection: molecular diagnosis using intra-graft targeted gene expression profiling. Giarraputo A, Coutance G, Patel JK, Fedrigo M, Aubert O, Varnous S, Barison I, Castellani C, Duong Van Huyen JP, Dagobert J, Mezine F, Robin B, Zielinski D, Rouvier P, Leprince P, Achouh P, Gerosa G, Verkarre V, Jouven X, Bruneval P, Angelini A, Kobashigawa J, Loupy A. Eur Heart J. 2026 Feb 23;47(8):956-970. PMID: 41342627.
5. The management of antibodies in heart transplantation: An ISHLT consensus document. Kobashigawa J, Colvin M, Potena L, Dragun D, Crespo-Leiro MG, Delgado JF, Olymbios M, Parameshwar J, Patel J, Reed E, Reinsmoen N, Rodriguez ER, Ross H, Starling RC, Tyan D, Urschel S, Zuckermann A. J Heart Lung Transplant. 2018 May;37(5):537-547. doi: 10.1016/j.healun.2018.01.1291. Epub 2018 Jan 31. PMID: 29452978.
6. Heart Transplant Rejection: From the Endomyocardial Biopsy to Gene Expression Profiling. Biomedicines. Farcas AO, Stoica MC, Maier IM, Maier AC, Sin AI.2024 Aug 22;12(8):1926. doi: 10.3390/biomedicines12081926. PMID: 39200392; PMCID: PMC11351478.
7. A Review of Biomarkers of Cardiac Allograft Rejection: Toward an Integrated Diagnosis of Rejection. Coutance G, Desiré E, Duong Van Huyen JP.Biomolecules. 2022 Aug 18;12(8):1135. doi: 10.3390/biom12081135. PMID: 36009029; PMCID: PMC9405997.

Quality IL-6 ELISA Kit – Cost-Effective and Efficient for Your Research!

Interleukin-6 (IL-6) is a multifunctional cytokine involved in regulating immune responses, inflammation, and hematopoiesis (1). It is produced by numerous cell types, including T cells, B cells, macrophages, and fibroblasts. IL-6 plays a crucial role in mediating the body’s response to infections and tissue damage. It promotes the activation of immune cells, stimulates the production of acute-phase proteins, and influences metabolic and regenerative processes (1). Elevated levels of IL-6 are associated with chronic inflammatory diseases, autoimmune disorders, and certain cancers, making it an important biomarker for disease diagnosis and monitoring. Due to its pivotal role in immune regulation, IL-6 is a key target for therapeutic interventions in inflammatory conditions.

In addition to its general functions, IL-6 is implicated in the pathogenesis of several diseases. In cardiovascular diseases (CVD), elevated IL-6 levels contribute to atherosclerosis by promoting inflammation within arterial walls, leading to plaque formation and instability, which can result in heart attacks and strokes. Additionally, elevated IL-6 levels, commonly detected in various neurodegenerative disorders, suggest its potential utility as a biomarker for disease progression and prognosis (3, 4).

Discover BIOMEDICA´s Quality Human Interleukin-6 (IL-6) ELISA Kit (cat. no. BI-IL6)

developed and manufactured by Biomedica

• SENSITIVE – detects IL-6 in serum and plasma samples
• HIGHLY SPECIFIC – characterized recombinant epitope-mapped antibodies
• STANDARDIZED – calibrated with WHO standards for accuracy
• QUALITY ASSURED – validated in accordance with international guidelines
• USER-FRIENDLY – includes ready-to-use, color-coded, prediluted standards and controls 

 

Elevate your research with reliable and easy-to-use IL-6 detection!

Biomedica´s Human IL-6 ELISA ASSAY CHARACTERISTICS (#BI-IL6)

-Method: Sandwich ELISA using HRP/TMB detection with 12×8-well detachable strips 

-Sample types: Plasma (EDTA, citrate, heparin), serum, cell culture, urine 

-Sample volume per well: 100 µl 

-Incubation times: 2 hours / 1 hour / 1 hour / 30 minutes 

-Sensitivity: 0.28 pg/ml (LLOQ: 0.78 pg/ml; capable of measuring concentrations in serum and plasma samples) 

-Assay range: 0 – 200 pg/ml, with standard concentrations at 0 / 3.12 / 6.25 / 12.5 / 25 / 50 / 100 / 200 pg/ml 

-Precision: Intra-assay CV ≤ 6%; Inter-assay CV ≤ 7% (n=3) 

-Specificity: Recognizes both recombinant and endogenous human IL-6 

-Validation data: Includes assessments of precision, accuracy, dilution linearity, and parallelism; healthy donor values are provided

-Use: For research purposes only

Quality IL-6 ELISA Kit – Cost-Effective and Efficient for Your Research!

 

 

Literature

1. IL-6 in inflammation, immunity, and disease. Tanaka T, Narazaki M, Kishimoto T. Cold Spring Harb Perspect Biol. 2014 Sep 4;6(10):a016295. doi: 10.1101/cshperspect.a016295. PMID: 25190079; PMCID: PMC4176007.
2. IL-6 in the spotlight: From cardiovascular pathophysiology to therapy. Preda A, Tirandi A, Leo G, Di Vece D, Vilahur G, Bonaventura A, Osto E, Ministrini S, Kraler S, Kleinbogard P, Camici G, Carbone F, Montecucco F, Liberale L.Eur J Clin Invest. 2026 Jan;56(1):e70161. doi: 10.1111/eci.70161. Epub 2025 Dec 3. PMID: 41340186.
3. The Role of IL-6 in Neurodegenerative Disorders. Shan C, Zhang C, Zhang C. Neurochem Res. 2024 Apr;49(4):834-846. doi: 10.1007/s11064-023-04085-6. Epub 2024 Jan 16. PMID: 38227113.
4. IL-6, IL-8 and IL-10 polymorphisms may impact predisposition of Alzheimer’s disease: a meta-analysis. Yang R, Duan J, Luo F, Tao P, Hu C.Acta Neurol Belg. 2021 Dec;121(6):1505-1512. doi: 10.1007/s13760-020-01369-4. Epub 2020 May 12. PMID: 32399737.

 

 

 

Glaucoma is one of the leading causes of blindness worldwide, characterized by the loss of retinal ganglion cells (RGCs). Since vision loss from glaucoma is irreversible, early therapeutic intervention is critically important. However, due to current limitations in assessing glaucomatous neurodegeneration, it remains challenging to objectively monitor disease severity and progression, hindering the development of targeted treatment strategies (1, 2).

Glaucoma Research with EZ4U Cell Viability Assay

Our EZ4U (easy for you) cell proliferation and cytotoxicity assay was highlighted in a recent study that explored the critical involvement of PEDF in zinc-related pathways contributing to neurodegeneration in glaucoma : A role of pigment epithelium-derived factor in zinc-mediated mechanism of neurodegeneration in glaucoma. Insights from this research could pave the way for novel therapeutic strategies

EZ4U Kit (cat.no. BI-5000)

– Non-radioactive & non-toxic assay

– Reliable & sensitive

– Convenient single-step incubation-for use on living cells

– Widely cited in more than 294 citations

 

Glaucoma Research with EZ4U Cell Viability Assay

A role of pigment epithelium-derived factor in zinc-mediated mechanism of neurodegeneration in glaucoma. Chistyakov DV et al., Commun Biol. 2025 Jul 1;8(1):965. PMID: 40596696.

Abstract

Glaucoma is a neurodegenerative condition involving optic nerve damage and retinal ganglion cells death. Animal studies suggested that the pathway linking these events can be mediated by mobile zinc secreted into the intraretinal space and exerting cytotoxic effects. Whether this mechanism is relevant for human glaucoma and what are the targets of extracellular zinc is unknown. We report that increased zinc content in the aqueous humor and retina is indeed a characteristic of glaucomatous neuropathy, and excess extracellular zinc may be recognized by the key retinal neurotrophic factor PEDF. Biophysical and X-ray crystallographic studies show that PEDF coordinates zinc ions in five types of intermolecular high-affinity sites, leading to a decrease in negative surface charge and reversible oligomerization of the protein, thereby masking the target recognition sites responsible for its neurotrophic and antiangiogenic activities and collagen binding. Notably, PEDF secretion is enhanced in both glaucoma and retinal cell models in response to zinc stress; however, zinc binding negatively affects axogenic, differentiative and prosurvival functions of PEDF by suppressing its ability to activate receptor PEDF-R/PNPLA2. We suggest that glaucomatous neurodegeneration is associated with direct inhibition of PEDF signaling by extracellular zinc, making their complex a promising target for neuroprotective therapy.

 

Literature:

1. Glaucoma: now and beyond. Lancet. Jayaram H, Kolko M, Friedman DS, Gazzard G. 2023 Nov 11;402(10414):1788-1801. doi: 10.1016/S0140-6736(23)01289-8. Epub 2023 Sep 21. PMID: 37742700.
2. Glaucoma in Adults-Screening, Diagnosis, and Management: A Review. Stein JD, Khawaja AP, Weizer JS. JAMA. 2021 Jan 12;325(2):164-174. doi: 10.1001/jama.2020.21899. PMID: 33433580.

Study Reveals Reliable Measurement of NT-proBNP in Rats Using Biomedica ELISA Assay in Cardiac Overload Model

We are pleased to share insights from a recent publication: ” Platelet transfusion induces transfusion-associated circulatory overload in rats with myocardial infarction.” (1). This study provides valuable understanding of transfusion-related complications in cardiac injury models, with a particular focus on monitoring cardiac stress and overload.

Key Highlight: Reliable detection of rat NT-proBNP in a TACO rat model in anemic Wistar rats with myocardial infarction using the Biomedica ELISA.

Accurate Detection of NT-proBNP in Rats – A Cardiac Safety Biomarker

A key tool in this research was the accurate quantification of NT-proBNP, a well-established biomarker for cardiac stress and heart failure. The researchers employed the Biomedica ELISA assay, renowned for its sensitivity and specificity, to measure NT-proBNP levels in rat plasma samples.

Rat NT-proBNP ELISA (cat. no. BI-1204R)

• CONVENIENT: Low sample volume (10 µL/well), kit control included
• HIGHLY SENSITIVE: Limit of detection (LOD) 21 pg/mL 
• QUICK RESULTS: Assay time 3.5 hours 
• TRUSTWORTHY RESULTS: Reference values provided, click here

 

The use of the Biomedica ELISA assay enabled precise detection of NT-proBNP levels, providing robust data on cardiac function and overload following platelet transfusion.

• Citations
• Testimonials

 

Implications for Future Research

The successful application of the Biomedica Rat NT-proBNP ELISA assay in this context demonstrates its suitability for preclinical cardiac studies involving small animals. Researchers aiming to explore cardiac biomarkers in rat models can confidently utilize this assay to obtain reliable and meaningful data.

Interested in measuring NT-proBNP in your research?

• Explore the Biomedica ELISA assay and enhance your data accuracy today!
• Contact us (info@bmgrp.com  or +43 1 29107 54 ) ) for your evaluation kit!

 

Accurate Detection of NT-proBNP in Rats – A Cardiac Safety Biomarker

 

 

Related Products:

NT-proANP ELISA assay (cat. no. BI-20892)  

• CONVENIENT – 10 µl / well, serum or plasma, kit control included
• TRUSTED – widely cited as cardiovascular safety biomarker in rats
• MULTI-USE – for human and non-human samples (high cross-reactivity between species)

 

BIOMEDICA’s NT-proANP ELISA kit (BI-20892) has been independently validated through preclinical toxicology testing in rats. Click here to view citations

Cross-laboratory analytical validation of the cardiac biomarker NT-proANP in rat

Specifically, a cross-laboratory analytical validation of the cardiac biomarker NT-proANP in rats was conducted.

Briefly, the assay was evaluated by the Predictive Safety Testing Consortium’s Cardiac Hypertrophy Working Group (PSTC—CHWG) across five laboratories in a comprehensive analytical assessment for rat samples. The results demonstrated that the assay is robust and technically suitable for detecting NT-proANP serum levels in Sprague-Dawley rats.

 

Related Publications:

Evaluation of Cardiac Toxicity Biomarkers in Rats from Different Laboratories. Kim, K., Chini, N., Fairchild, D.G., Engle, S.K., Reagan, W.J., Summers, S.D., Mirsalis, J.C., 2016. Toxicol Pathol 44, 1072–1083. PMID: 27638646.

Serum Natriuretic Peptides as Differential Biomarkers Allowing for the Distinction between Physiologic and Pathologic Left Ventricular Hypertrophy . Dunn, M.E., Manfredi, T.G., Agostinucci, K., Engle, S.K., Powe J., King, N.M.P., Rodriguez, L.A, Gropp, K.E., Gallacher, M., Vetter, F.J., More, V., Shimpi, P., Serra, D., Colton, H.M., for The Cardiac Hypertrophy Working Group of the Predictive Safety Testing Consortium . 2017. Toxicol Pathol 45(2): 334-352. PMID: 27102652.

Natriuretic Peptides as Cardiovascular Safety Biomarkers in Rats: Comparison With Blood Pressure, Heart Rate, and Heart Weight . Engle, S.K., and Watson, D.E. 2016. Toxicol Sci 149: 458 – 472. PMID: 26609138.

2-Deoxy-d-Glucose (2-DG)-Induced Cardiac Toxicity in Rat: NT-proBNP and BNP as Potential Early Cardiac Safety Biomarkers. Terse PS, Joshi PS, Bordelon NR, Brys AM, Patton KM, Arndt TP, Sutula TP. Int J Toxicol. 2016 May;35(3):284-93. doi: 10.1177/1091581815624397. Epub 2016 Feb 2. PMID: 26838190; PMCID: PMC4864115.

also available: NT-proBNP ELISA (cat.no. SK-1204)

• Proficiency testing 
• For human serum and plasma samples  – saliva protocol
• Widely cited

The link between type 2 diabetes mellitus (T2DM) and bone fragility is complex. While individuals with type 2 diabetes often have normal to elevated bone mineral density, their risk of fractures is up to three times higher (1, 2).

Understanding Bone Health in Type 2 Diabetes

Recent research has shed new light on the complex relationship between Type 2 diabetes mellitus (T2DM) and bone health. The study, titled “Profiling bone status indices reveals evidence of a low-turnover bone phenotype in type 2 diabetes: findings from the DiaFALL cohort. Rasmussen NH et al., Osteoporos Int. 2026, provides valuable insights into how diabetes affects bone metabolism and fracture risk.

In this matched cross-sectional study, the researchers profiled Bone Status Indices (BSIs), which are biochemical markers of bone remodeling, in individuals with type 2 diabetes (T2D).

The BIOMEDICA assays bioactive Sclerostin and intact FGF23 were included in the study.

Bioactive Sclerostin ELISA (cat. no. BI-20472)

• Characterized antibodies that target the Sclerostin receptor binding region
• The assay is  validated for clinical samples  (validation data file)
• Only  20µl sample /well (protocol booklet)
• Widely cited

 

 FGF23 intact ELISA (cat. no. BI-20700)

• Extensively validated according to international quality guidelines
• Correlates with existing methods (validation data file)
• One-step ELISA  (protocol booklet)
• Cited in top-tier journals

 

Key findings:

-Individuals with T2D have an increased risk of #fractures compared to those without diabetes.

-The elevated fracture risk persists even when bone mineral density (BMD) is normal or only slightly reduced.

-The researchers uncovered an altered bone remodeling processes in T2D, which could impact fracture risk and treatment strategies. 

Profiling bone status indices reveals evidence of a low-turnover bone phenotype in type 2 diabetes: findings from the DiaFALL cohort. Rasmussen NH, Kvist AV, Bech AA, Lykkeboe S, Starup-Linde J, Handberg A, van den Bergh JP, Vestergaard P. Osteoporos Int. 2026 Mar;37(3):703-716. doi: 10.1007/s00198-026-07850-9. Epub 2026 Jan 21. PMID: 41563408; PMCID: PMC13083425.

Abstract

People with type 2 diabetes have increased fracture risk despite preserved bone density. In this matched cross-sectional study, suppressed Bone Status Indices and exploratory sex-related hormonal associations were observed in T2D, indicating altered bone remodeling that is not captured by aBMD alone. These findings support the need for fracture risk assessment approaches that incorporate biochemical markers and potential sex-related differences.

Introduction/aim: People with type 2 diabetes (T2D) experience increased fracture risk despite preserved or higher areal bone mineral density (aBMD). We evaluated Bone Status Indices (BSIs) and their relationships with aBMD in T2D, with exploratory evaluation of sex-related hormonal influences.

Methods: In this matched cross-sectional study from the DiaFALL cohort, 105 adults with T2D were compared 1:1 with age- and sex-matched controls. aBMD was assessed at lumbar spine, femoral neck, arms, and legs using DXA. BSIs included intact PINP (i-PINP), β-CTX-I, osteocalcin (OCN), sclerostin, TRACP5b, IGF-1, OPN, PTH, and vitamin-D metabolites. Group differences and associations with aBMD were evaluated using multivariable regression and Spearman correlations, with exploratory sex-stratified analyses.

Results: Femoral-neck aBMD was higher in people with T2D (men: + 0.070 g/cm², 95%CI + 0.026 to + 0.114, p = 0.002; women: + 0.089, 95%CI + 0.039 to + 0.139, p = 0.001) and lumbar-spine aBMD was higher in women (+ 0.137 g/cm², 95%CI + 0.072 to + 0.202, p < 0.001). In contrast, multiple BSIs were suppressed in T2D, including i-PINP (men: Δ-12.8 µg/L, 95%CI -19.4 to -6.2, p = 0.002; women: Δ-13.6 µg/L, 95%CI -25.9 to -1.3, p = 0.002), osteocalcin (men: Δ-6.36 µg/L, 95%CI -9.15 to -3.57, p < 0.001; women: Δ-6.66 µg/L, 95%CI -11.0 to -2.20, p < 0.001), and β-CTX-I (men: Δ-40.5 ng/L, 95%CI -62 to -18, p = 0.012; women: Δ-110 ng/L, 95%CI -180 to -44, p = 0.014). Sclerostin was higher in men with T2D (Δ + 24.6 pmol/L, 95%CI + 1.5 to + 47.7, p = 0.019) and correlated positively with lumbar-spine aBMD (r = 0.411; p = 0.007). Furthermore, 1,25(OH)₂D (men p = 0.013; women p = 0.001) and magnesium (p = 0.002 both sexes) were lower in T2D despite similar PTH. No significant T2D-sex interactions were observed for any BSI (all p > 0.05).

Conclusion: T2D was characterized by higher aBMD together with broadly suppressed BSIs, consistent with a low-turnover skeletal phenotype not captured by DXA alone. Osteocalcin og sclerostin appeared most informative. These findings support longitudinal studies to determine whether BSIs can enhance identification of skeletal fragility in T2D.

 

Literature

1. Update on the impact of type 2 diabetes mellitus on bone metabolism and material properties. Picke AK, Campbell G, Napoli N, Hofbauer LC, Rauner M. Endocr Connect. 2019 Mar 1;8(3):R55-R70. doi: 10.1530/EC-18-0456. PMID: 30772871; PMCID: PMC6391903.
2. Bone Health in Patients With Type 2 Diabetes. Forner P, Sheu A. J Endocr Soc. 2024 Jun 6;8(7):bvae112. doi: 10.1210/jendso/bvae112. PMID: 38887632; PMCID: PMC11181004.

 

Related Reviews

Bone fragility in diabetes: novel concepts and clinical implications. Hofbauer LC, Busse B, Eastell R, Ferrari S, Frost M, Müller R, Burden AM, Rivadeneira F, Napoli N, Rauner M.Lancet Diabetes Endocrinol. 2022 Mar;10(3):207-220. doi: 10.1016/S2213-8587(21)00347-8. Epub 2022 Jan 31. PMID: 35101185.

Contributors to impaired bone health in type 2 diabetes. Sheu A, Greenfield JR, White CP, Center JR. Trends Endocrinol Metab. 2023 Jan;34(1):34-48. doi: 10.1016/j.tem.2022.11.003. Epub 2022 Nov 23. PMID: 36435679.

CNP mainly operates through autocrine and paracrine mechanisms and is crucial for promoting bone growth (1). Recent studies have deepened our understanding of CNP’s role in cardiovascular regulation (2). It exhibits antifibrotic effects across various organs (3), induces vasodilation in microcirculations, improves myocardial relaxation, and has anti-inflammatory properties (4). These benefits have shown therapeutic potential in experimental models of pulmonary hypertension, myocardial infarction, and organ fibrosis (4).

CNP Preserves Cardiac and Vascular Function in Sepsis – A Promising Therapeutic Target

About NT-proCNP

NT-proCNP is generated through the cleavage of a 103-amino acid prohormone called proCNP, resulting in the production of the amino-terminal fragment (NT-proCNP) and the biologically active CNP peptides (5) . NTproCNP has a longer half-life and is present in the blood at higher concentrations than biologically active CNP (6, 7). 

CNP Preserves Cardiac and Vascular Function in Sepsis – A Promising Therapeutic Target

Our NT-proCNP ELISA was a key tool in a recent study (8) examining the potential of C-Type Natriuretic Peptide (CNP) in sepsis treatment. The study demonstrates that CNP helps preserve both vascular and cardiac function during sepsis, offering promising insights into improving patient outcomes.

C-Type Natriuretic Peptide Preserves Vascular and Cardiac Function in Sepsis, Moyes AJ et al., Hypertension, 2026.

Key findings:

• Genetic deletion of #CNP worsens disease severity in experimental sepsis.
• CNP levels increase in sepsis and correlate with lung hypoxemia.
• Therapeutic administration of CNP significantly reduces sepsis progression.

Abstract

Background: Sepsis is a life-threatening condition and a major cause of mortality in intensive care units worldwide, a clear unmet medical need. CNP (C-type natriuretic peptide) regulates inflammation and cardiovascular homeostasis, but its involvement in sepsis pathogenesis is not fully elucidated. This study investigated the intrinsic role of CNP, and therapeutic potential of the peptide, in offsetting the pathogenesis of sepsis.

Methods: Plasma concentrations of CNP, and its N-terminal cleavage product NT-proCNP (N-terminal pro-CNP), were measured in sepsis patients. Cardiac function, vascular hemodynamics, endothelial integrity, and biomarkers of inflammation were analyzed in wild-type, endothelium-restricted (ecCNP^-/-), or cardiomyocyte-restricted (cmCNP^-/-) CNP knockout animals, or global NPR (natriuretic peptide receptor)-C^-/- deficient mice, in etiologically distinct models of sepsis. CNP (0.2 mg/kg per d) was infused to rescue any adverse phenotype and probe therapeutic potential.

Results: Circulating [NT-proCNP] increased in sepsis patients and was associated with reduced disease severity. ecCNP^-/- mice exhibited an aggravated phenotype compared with wild-type mice in experimental sepsis, exemplified by impaired microcirculatory flow, edema, and increased expression of inflammatory biomarkers. In addition, cmCNP^-/- animals showed overt cardiac dysfunction following lipopolysaccharide treatment. This worsened phenotype was mirrored in NPR-C^-/- mice, implying that this cognate NPR subtype underpins the salutary actions of endogenous CNP. Pharmacological CNP administration improved microvascular perfusion, cardiac output, and inflammation in wild-type and ecCNP^-/-, but not NPR-C^-/-, mice.

Conclusions: Endogenous CNP plays a protective role in sepsis by preserving microvascular perfusion, reducing inflammation, maintaining endothelial integrity, and sustaining cardiac function via NPR-C. Pharmacologically targeting CNP signaling warrants further evaluation as a potential therapeutic opportunity in sepsis.

NT-proCNP #ELISA kit  (cat.no. BI-20812)

TRUSTED – widely cited

RELIABLE – full validation package

FLEXIBEL – for serum and plasma samples, protocols available for urine, cell culture and non-human samples

Literature

1. CNP-related Short and Tall Stature: A Close-knit Family of Growth Disorders. Lui JC, Baron J. J Endocr Soc. 2022 Apr 16;6(6):bvac064. doi: 10.1210/jendso/bvac064. PMID: 35528827; PMCID: PMC9070793.
2. C-type natriuretic peptide (CNP): The cardiovascular system and beyond. Dickinson YA, Moyes AJ, Hobbs AJ.Pharmacol Ther. 2024 Oct;262:108708. doi: 10.1016/j.pharmthera.2024.108708. Epub 2024 Aug 21. PMID: 39154787.
3. Pathophysiological and therapeutic implications of C-type natriuretic peptide/cyclic GMP signaling in pulmonary fibrosis. Weyer R, Völker K, Potapenko T, Krebes L, Abeßer M, Friedrich AL, Lessmann E, Khadim A, Ruppert C, El Agha E, Sheta D, Beilhack A, Santi DV, Schneider EL, Kuhn M, Dabral S. JCI Insight. 2026 Jan 6;11(4):e196812. doi: 10.1172/jci.insight.196812. PMID: 41499484; PMCID: PMC12956015.
4. C-Type Natriuretic Peptide and Cardiovascular-Renal Protection in Sepsis. Sangaralingham SJ, Burnett JC Jr. Hypertension. 2026 Jun;83(6):e26731. doi: 10.1161/HYPERTENSIONAHA.126.26731. Epub 2026 May 20. PMID: 42160495.
5. Endothelial C-type natriuretic peptide/guanylyl cyclase-B signaling prevents pulmonary arterial hypertension. Yanagisawa H, Kuwahara K, Nakagawa Y, Moriuchi K, Kinoshita H, Inazumi H, Kanamori T, Nishikimi T, Oya M, Nakao K, Ueda Y, Nakamura D, Shimizu K, Yoshie K, Tanaka S, Nakajima D, Sakanoue I, Yasoda A, Nakao K, Kimura T, Ono K. Nat Commun. 2026 Mar 17;17(1):2331. doi: 10.1038/s41467-026-70139-2. PMID: 41844596; PMCID: PMC12996325.
6. Emerging Roles of Natriuretic Peptides and their Receptors in Pathophysiology of Hypertension and Cardiovascular Regulation. Pandey KN. J Am Soc Hypertens. 2008 Jul-Aug;2(4):210-26. doi: 10.1016/j.jash.2008.02.001. PMID: 19746200; PMCID: PMC2739409.
7. N-Terminal pro C-Type Natriuretic Peptide (NTproCNP) and myocardial function in ageing. Keng BMH, Gao F, Tan RS, Ewe SH, Teo LLY, Xie BQ, Goh GBB, Koh WP, Koh AS. PLoS One. 2018 Dec 19;13(12):e0209517. doi: 10.1371/journal.pone.0209517. PMID: 30566484; PMCID: PMC6300279.
8. C-Type Natriuretic Peptide Preserves Vascular and Cardiac Function in Sepsis. Moyes AJ, Sand C, Young L, Pérez-Ternero C, Salam AT, Baliga RS, Mohammad S, Antcliffe DB, Gordon AC, Aubdool AA, Hobbs AJ.Hypertension. 2026 Jun;83(6):e25938. doi: 10.1161/HYPERTENSIONAHA.125.25938. Epub 2026 Feb 4. PMID: 41636071; PMCID: PMC13189390.

 

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Currently, kidney transplantation (KT) is the optimal treatment option for patients with end-stage kidney disease (ESKD), providing improved survival rates, enhanced quality of life, and greater cost-effectiveness compared to all forms of dialysis (1). However, despite successful transplantation, kidney transplant recipients (KTR) still remain susceptible to graft failure, especially in the long-term period (2).

Tubular injury, plays a significant role in graft failure. Biomarkers indicating tubular injury may offer insights into risk assessment following kidney transplantation.

About Vanin-1

 -Urinary vanin-1 levels increase prior to serum creatinine and other tubular injury markers in acute kidney injury, as shown by experimental and observational studies (3). 

-Urinary vanin-1 is associated with estimated glomerular filtration rate (eGFR) and kidney function decline in hypertensive patients (3). 

-Elevated urinary vanin-1 has been observed in patients with obstructive nephropathy and IgA nephropathy, suggesting its potential as a biomarker (4).

Vanin-1 tubular injury and graft failure in kidney transplant recipients

The BIOMEDICA  Vanin-1 ELISA was utilized in a study investigating whether urinary vascular non-inflammatory molecule-1 (Vanin-1), a promising early marker of tubular injury, correlates with other established tubular injury indicators and is linked to graft failure in kidney transplant recipients (KTR). Urinary Vanin-1 was measured in 656 kidney transplant recipients (KTR) more than 1-year post-transplant.

Key findings:

-First study to investigate 24-hour urinary vanin-1 excretion in a cohort of stable, outpatient kidney transplant recipients.

-Week but significant correlation with other tubular injury markers.

-No association between urinary Vanin-1 levels and risk of graft failure.

The findings do not support 24-hour urinary vanin-1 excretion as a useful biomarker for predicting the risk of death-censored graft failure.

Human Vanin-1 (urine) ELISA | BI-VAN1U

• Optimized for human urine samples
• Rigorously validated according to quality guidelines
• One-step ELISA (protocol booklet)

 

Urinary vanin-1, tubular injury, and graft failure in kidney transplant recipients.

Abstract

We investigated whether urinary vascular non-inflammatory molecule-1 (vanin-1), a promising early-onset tubular injury marker, correlates with other established tubular injury markers and is associated with graft failure in kidney transplant recipients (KTR). We measured 24 h urinary vanin-1 excretion in 656 KTR (age 53 ± 13 years, 43% female, estimated glomerular filtration rate (eGFR) 53 ± 21 mL/min/1.73 m²) who had undergone kidney transplantation ≥ 1 year. The median 24 h urinary vanin-1 excretion was 145 [51–331] pmol/24 h. 24 h urinary vanin-1 excretion correlated weakly but significantly with other tubular injury markers (ρ = 0.14, p < 0.001 with urinary liver-type fatty acid binding protein, ρ = 0.13, p = 0.001 with urinary post-translationally modified fetuin-A protein, and ρ = 0.10, p = 0.011 with plasma neutrophil gelatinase-associated lipocalin) and with eGFR (ρ = − 0.13, p = 0.001). During a median follow-up of 7.4 [4.9–8.0] years, 94 (14%) KTR developed death-censored graft failure. In multivariable Cox regression analyses, 24 h urinary vanin-1 excretion was not associated with an increased risk of death-censored graft failure (adjusted hazard ratio [95% confidence interval] = 0.96 [0.86–1.07], p = 0.5). In conclusion, our findings do not support the role of urinary vanin-1 as a biomarker of graft failure after kidney transplantation.

Literature

1. Life and expectations post-kidney transplant: a qualitative analysis of patient responses. Tucker EL, Smith AR, Daskin MS, Schapiro H, Cottrell SM, Gendron ES, Hill-Callahan P, Leichtman AB, Merion RM, Gill SJ, Maass KL. BMC Nephrol. 2019 May 16;20(1):175. doi: 10.1186/s12882-019-1368-0. PMID: 31096942; PMCID: PMC6524208.
2. Long-Term Survival after Kidney Transplantation. Hariharan S, Israni AK, Danovitch G. N Engl J Med. 2021 Aug 19;385(8):729-743. doi: 10.1056/NEJMra2014530. PMID: 34407344.
3. Urinary vanin-1, tubular injury, and graft failure in kidney transplant recipients. Alkaff FF, Kremer D, Niekolaas TM, van den Born J, Rimbach G, Tseng TL, Berger SP, Bakker SJL, de Borst MH. Sci Rep. 2024 Jan 27;14(1):2283. doi: 10.1038/s41598-024-52635-x. PMID: 38280883; PMCID: PMC10821939.
4. The Usefulness of Vanin-1 and Periostin as Markers of an Active Autoimmune Process or Renal Fibrosis in Children with IgA Nephropathy and IgA Vasculitis with Nephritis-A Pilot Study. Mizerska-Wasiak M, Płatos E, Cichoń-Kawa K, Demkow U, Pańczyk-Tomaszewska M. J Clin Med. 2022 Feb 25;11(5):1265. doi: 10.3390/jcm11051265. PMID: 35268356; PMCID: PMC8911128.

 

 

Fetal growth restriction (FGR) is believed to occur in about 3–7% of pregnancies (1), making it a relatively common complication in pregnancy. FGR is linked to higher rates of perinatal morbidity and mortality. Early prenatal detection and appropriate intervention can enhance outcomes (2).

Understanding Fetal Growth Retardation

Osteoprotegerin – Fetal Growth Retardation and Atherosclerosis in Newborns

Fetal Growth Retardation (FGR) is a condition characterized by the inadequate growth of the fetus in utero, typically resulting from placental insufficiency, maternal health factors, or fetal anomalies. It is diagnosed when the fetus exhibits a growth trajectory below the 10th percentile for gestational age, often associated with compromised nutrient and oxygen delivery. FGR has been linked to adverse perinatal outcomes and may have long-term implications for cardiovascular and metabolic health, potentially mediated by alterations in vascular structure and function established during fetal development.

The Role of Osteoprotegerin

Osteoprotegerin (OPG) is a protein involved in bone metabolism and vascular health. Elevated levels of OPG have been associated with various cardiovascular conditions, including atherosclerosis and arterial stiffness (3, 4).

Exploring the Link Between Fetal Growth Retardation, Postnatal Osteoprotegerin Levels, and Aortic Health

A recent study titled “Association of Fetal Growth Retardation with Postnatal Osteoprotegerin Concentrations and Aortic Intima-Media Thickness.” sheds light on how early-life growth issues might influence cardiovascular health later in life.

Osteoprotegerin – Fetal Growth Retardation and Atherosclerosis in Newborns

Using the Biomedica Osteoprotegerin (OPG) ELISA assay (cat. no. BI-20403), scientists investigated how fetal growth issues might influence postnatal OPG serum levels and aortic intima-media thickness.

Key findings:

• The study examined the association between FGR and postnatal cardiovascular markers.
• Increased postnatal OPG levels were linked to FGR.
• FGR was also associated with increased Aortic Intima-Media Thickness, indicating early vascular changes.

The findings suggest that fetal growth issues might play a role in future cardiovascular health, highlighting the potential benefits of early detection and monitoring of at-risk infants for better long-term outcomes.

Osteoprotegerin (OPG) can reliably be measured with a conventional ELISA assay

 Biomedica OPG ELISA (cat. no. BI-20403)

-TRUSTED – Widely cited in over 280 publications!

-CONVENIENT – 20 µl sample / well

-EASY – ready to use prediluted standards

-RELIABLE – full validation according to international quality guidelines

Association of Fetal Growth Retardation with Postnatal Osteoprotegerin Concentrations and Aortic Intima-Media Thickness. Diseases. Karatza AA, Kostopoulou E, Fouzas S, Antonakopoulos N, Sinopidis X, Kritikou D, Efthymiadou A, Dimitriou G, Chrysis D. 2026 Mar 8;14(3):100. doi: 10.3390/diseases14030100. PMID: 41892001; PMCID: PMC13025314.

Abstract

Background: Fetal Growth Retardation (FGR) is considered a risk factor for atherosclerosis and coronary artery disease in adulthood. Osteoprotegerin (OPG), a member of the tumor necrosis factor receptor superfamily, is reported to be elevated in atherosclerosis.

Objectives: In this case-control study, we investigated whether FGR affects postnatal OPG serum concentrations and the possible association between OPG levels and aortic intima-media thickness (aIMT), an index of preclinical atherosclerosis.

Methods: We studied 30 infants with FGR and 30 appropriate for gestational age (AGA) infants matched for gestational age and sex. Quantitative determination of plasma OPG was performed via enzyme immunoassay on the second (DOL2) and fifth (DOL5) day of life. aIMT was measured in the distal abdominal aorta and adjusted for aortic lumen diameter.

Results: Infants with FGR had significantly higher OPG levels on both DOL2 and DOL5 as compared to controls (DOL2: 5.4 ± 1.0 pmol/L vs. 4.6 ± 1.0 pmol/L, p = 0.002 and DOL5: 5.1 ± 0.8 pmol/L vs. 3.9 ± 0.7 pmol/L, p < 0.001). Between DOL2 and DOL5, OPG concentrations did not change significantly in infants with FGR (difference 0.3 ± 0.2 pmol/L, p = 0.087) but decreased slightly in controls (difference 0.7 ± 0.3 pmol/L, p = 0.003). FGR was also associated with increased aIMT (0.11 ± 0.03 vs. 0.06 ± 0.02, p < 0.001). There was a positive correlation between OPG and aIMT on DOL2 (r = 0.494, p < 0.001), which became stronger on DOL5 (r = 0.791, p < 0.001).

Conclusions: We report significantly increased concentrations of OPG in infants with FGR and a positive correlation with aIMT. Follow-up studies with repeat OPG and aIMT measurements may be indicated to evaluate whether these findings represent a permanent effect of FGR on the offspring.

Literature

1. Genetic Background of Fetal Growth Restriction. Nowakowska BA, Pankiewicz K, Nowacka U, Niemiec M, Kozłowski S, Issat T. Int J Mol Sci. 2021 Dec 21;23(1):36. doi: 10.3390/ijms23010036. PMID: 35008459; PMCID: PMC8744929.
2. Clinical practice guidance for the management of fetal growth restriction: an expert review. Villalaín C, Herraiz I, Akolekar R, Figueras F, Crispi F, Rizzo G, Mappa I, Mendoza M, Del Moral T, Stampalija T, Ghi T, Galindo A. J Matern Fetal Neonatal Med. 2025 Dec;38(1):2526111. doi: 10.1080/14767058.2025.2526111. Epub 2025 Jul 7. PMID: 40623849.
3. Association of bone biomarkers with advanced atherosclerotic disease in people with overweight/obesity. Del Toro R, Cavallari I, Tramontana F, Park K, Strollo R, Valente L, De Pascalis M, Grigioni F, Pozzilli P, Buzzetti R, Napoli N, Maddaloni E. Endocrine. 2021 Aug;73(2):339-346. doi: 10.1007/s12020-021-02736-8. Epub 2021 May 4. PMID: 33948786.
4. Atherosclerosis and Bone Loss in Humans-Results From Deceased Donors and From Patients Submitted to Carotid Endarterectomy. Carmona-Fernandes D, Barreira SC, Leonardo N, Casimiro RI, Castro AM, Santos PO, Fernandes AN, Cortes-Figueiredo F, Gonçalves CA, Cruz R, Fernandes ML, Ivo M, Pedro LM, Canhão H, Fonseca JE, Santos MJ.Front Med (Lausanne). 2021 May 20;8:672496. doi: 10.3389/fmed.2021.672496. PMID: 34095177.

Big ET-1 is a promising cardiotoxicity marker in childhood cancer survivors

Advancements in oncological therapies have resulted in a childhood cancer survivor (CCS) long-term survival rate exceeding 80%.  However, up to 60% of CCS are exposed to cardiotoxic treatments, significantly increasing their risk of congestive heart failure (CHF). CHF is a leading cause of long-term morbidity and mortality, with CCS facing a 15-fold higher incidence of CHF and a 7-fold greater risk of premature cardiac death compared to the general population (1).

Big Endothelin-1 (Big ET-1) is the inactive precursor of Endothelin-1 (ET-1), a 21-amino acid peptide that functions as one of the most potent vasoconstrictors in the human cardiovascular system. Under physiological conditions, Big ET-1 is cleaved by endothelin-converting enzyme (ECE) to generate active ET-1, which exerts its effects primarily through endothelin receptor type A (ETA) and type B (ETB) on vascular smooth muscle cells and endothelial cells (2).

Endothelial damage is characterized by dysfunction of the vascular endothelium, leading to increased permeability, pro-inflammatory and pro-thrombotic states, and impaired vasodilatory responses (3). Elevated circulating levels of Big ET-1 serve as a biomarker for endothelial cell activation and injury because increased production or impaired processing of Big ET-1 reflects endothelial cell distress (4). This dysfunction is a central mechanism in the pathogenesis of various cardiovascular diseases, including hypertension, atherosclerosis, and cardiomyopathy.

Big ET-1 is a promising cardiotoxicity marker in childhood cancer survivors

A recent study published in Cardiovascular Toxicology, investigated the long-term cardiotoxic effects of cancer therapy in CCS through a dual approach combining CMR imaging and blood biomarkers (5).

Big Endothelin-1 was measured in blood samples with an ELISA assay from BIOMEDICA.

 Big-ET-1 ELISA kit highlights (BI-20082H)

 – HIGH SENSITIVITY – direct measurement

– RELIABLE – Fully validated according to international guidelines

– Published cut-off values

– TRUSTED – widely cited in over 90 publications

 

 

Big ET-1 is a stable marker for investigating endothelial damage in cardiovascular diseases.

Long-term Subclinical Cardiotoxicity of Modern Cardiotoxic Treatment Protocols in Childhood Cancer Survivors Assessed by Cardiovascular Magnetic Resonance T1 Mapping and Circulatory Biomarkers

Key Findings

• CMR imaging revealed differences between CCS and control subjects
• In CCS, biomarkers indicating endothelial activation (Big ET-1) and oxidative stress (MPO, IMA) were elevated
• Blood biomarkers can enhance early detection and risk assessment of myocardial abnormalities

 

Monitoring Big ET-1 alongside imaging may improve long-term cardiac outcomes in childhood cancer survivors.

Long-term Subclinical Cardiotoxicity of Modern Cardiotoxic Treatment Protocols in Childhood Cancer Survivors Assessed by Cardiovascular Magnetic Resonance T1 Mapping and Circulatory Biomarkers. Panovský R, Tomandlová M, Mojica-Pisciotti ML, Kepák T, Máchal J, Feitová V, Frič J, Hortová-Kohoutková M, Holeček T, Tomandl J, Opatřil L, Kincl V.Cardiovasc Toxicol. 2026 Jan 28;26(2):23. doi: 10.1007/s12012-026-10098-8. PMID: 41604073; PMCID: PMC12852242.

Abstract

Childhood cancer survivors (CCS) are at increased risk of developing heart disease due to the cardiotoxic effects of oncological treatment. This study aimed to investigate the long-term cardiotoxic effects of cancer therapy in CCS using a multimodal approach combining cardiac magnetic resonance (CMR) imaging and circulating blood biomarkers. A total of 117 CCS (mean age 24.7 ± 5.2 years), at least five years post-treatment and in complete remission, were prospectively enrolled. All participants underwent CMR, including T1 mapping, and blood analysis for biomarkers of endothelial damage and oxidative stress. Parameters were compared with sex- and age-matched healthy control groups. Anthracycline treatment was administered in 82.9% of CCS (mean cumulative doxorubicin equivalent dose 231.7 ± 92.0 mg/m²). Left ventricular ejection fraction and mitral annular plane systolic excursion were significantly reduced in CCS compared to controls (59.0 ± 5.5% vs. 67.2 ± 6.9%, p < 0.001; 12.5 ± 1.7 mm vs. 13.9 ± 2.2 mm, p = 0.001). Late gadolinium enhancement was detected in four CCS. No significant differences in global native T1 relaxation time or extracellular volume were observed. N-terminal pro-B-type natriuretic peptide (NT-proBNP) levels remained within normal limits but correlated with native T1, ECV, and MAPSE. Levels of myeloperoxidase, big endothelin-1, and ischemia-modified albumin were significantly higher than in controls. Subclinical myocardial changes were detected in long-term CCS using CMR and circulating biomarkers. These findings support the utility of a multimodal approach for the early identification of individuals at increased cardiovascular risk after childhood cancer treatment.

 

Literature

1. Long-term Subclinical Cardiotoxicity of Modern Cardiotoxic Treatment Protocols in Childhood Cancer Survivors Assessed by Cardiovascular Magnetic Resonance T1 Mapping and Circulatory Biomarkers. Panovský R, Tomandlová M, Mojica-Pisciotti ML, Kepák T, Máchal J, Feitová V, Frič J, Hortová-Kohoutková M, Holeček T, Tomandl J, Opatřil L, Kincl V.Cardiovasc Toxicol. 2026 Jan 28;26(2):23. doi: 10.1007/s12012-026-10098-8. PMID: 41604073; PMCID: PMC12852242.
2. Endothelin and the Cardiovascular System: The Long Journey and Where We Are Going. Haryono A, Ramadhiani R, Ryanto GRT, Emoto N. Biology (Basel). 2022 May 16;11(5):759. doi: 10.3390/biology11050759. PMID: 35625487; PMCID: PMC9138590.
3. Endothelial Dysfunction, Inflammation and Coronary Artery Disease: Potential Biomarkers and Promising Therapeutical Approaches. Medina-Leyte DJ, Zepeda-García O, Domínguez-Pérez M, González-Garrido A, Villarreal-Molina T, Jacobo-Albavera L. Int J Mol Sci. 2021 Apr 8;22(8):3850. doi: 10.3390/ijms22083850. PMID: 33917744; PMCID: PMC8068178.
4. Plasma big endothelin-1 levels at admission and future cardiovascular outcomes: A cohort study in patients with stable coronary artery disease. Zhou BY, Guo YL, Wu NQ, Zhu CG, Gao Y, Qing P, Li XL, Wang Y, Dong Q, Liu G, Xu RX, Cui CJ, Sun J, Li JJ. Int J Cardiol. 2017 Mar 1;230:76-79. doi: 10.1016/j.ijcard.2016.12.082. Epub 2016 Dec 21. PMID: 28038820.
5. Long-term Subclinical Cardiotoxicity of Modern Cardiotoxic Treatment Protocols in Childhood Cancer Survivors Assessed by Cardiovascular Magnetic Resonance T1 Mapping and Circulatory Biomarkers. Panovský R, Tomandlová M, Mojica-Pisciotti ML, Kepák T, Máchal J, Feitová V, Frič J, Hortová-Kohoutková M, Holeček T, Tomandl J, Opatřil L, Kincl V. Cardiovasc Toxicol. 2026 Jan 28;26(2):23. doi: 10.1007/s12012-026-10098-8. PMID: 41604073; PMCID: PMC12852242.

Interleukin-6 (IL-6) is a cytokine involved in immune responses, inflammation, and metabolism. It is produced by various cells, including immune cells, adipocytes, and muscle tissue (1). In the context of cancer, IL-6 can function both as a promoter and an inhibitor of tumor growth.

Skeletal muscle is a significant source of circulating IL-6 in individuals who participate in exercise training (2). Research has shown that engaging in 150–300 minutes of exercise weekly can reduce the risk of several cancers, such as breast, colon, endometrial, kidney, and liver cancers, as well as myeloma and non-Hodgkin’s lymphoma (3, 4).

Paradoxical role of IL-6 in cancer

A recent study published in Trends Endocrinol Metab (Orange ST et al., 2023) (6) investigates the complex role of IL-6 in cancer development and explores how physical activity influences this cytokine.

Highlights:

• IL-6 can either inhibit or promote cancer, depending on the specific context. 
• It is released from skeletal muscles during exercise and by immune cells at inflammation sites and within the tumor microenvironment.
• Muscle-derived IL-6 improves insulin sensitivity, boosts anti-inflammatory cytokines, enhances immune response, and may protect against cancer progression.
• Conversely, prolonged IL-6 signaling in inflammation and tumors can promote chronic inflammation and tumor growth.         

 

Looking to accurately measure IL-6 levels in your research?

The BIOMEDICA IL-6 ELISA assay is designed to provide reliable and precise results in serum and plasma samples.

Key benefits:  Human IL-6 ELISA Kit | BI-IL6 | Biomedica

-High Sensitivity and Specificity: designed to accurately detect and quantify IL-6 levels in serum, plasma, and cell culture supernatants.

-Quantitative Measurement: provides precise and reproducible measurements of IL-6 concentrations.

-User-friendly: ready to use calibrators & controls included

 

Literature:

1. IL-6 Signaling in Immunopathology: From Basic Biology to Selective Therapeutic Intervention. Schumertl T, Lokau J, Garbers C. Immunotargets Ther. 2025 Jul 5;14:681-695. doi: 10.2147/ITT.S485684. PMID: 40636466; PMCID: PMC12239904.
2. Exercise as an anti-inflammatory therapy for cancer cachexia: a focus on interleukin-6 regulation. Daou HN. Am J Physiol Regul Integr Comp Physiol. 2020 Feb 1;318(2):R296-R310. doi: 10.1152/ajpregu.00147.2019. Epub 2019 Dec 11. PMID: 31823669.
3. Amount and Intensity of Leisure-Time Physical Activity and Lower Cancer Risk. Matthews CE, Moore SC, Arem H, Cook MB, Trabert B, Håkansson N, Larsson SC, Wolk A, Gapstur SM, Lynch BM, Milne RL, Freedman ND, Huang WY, Berrington de Gonzalez A, Kitahara CM, Linet MS, Shiroma EJ, Sandin S, Patel AV, Lee IM. J Clin Oncol. 2020 Mar 1;38(7):686-697. doi: 10.1200/JCO.19.02407. Epub 2019 Dec 26. PMID: 31877085; PMCID: PMC7048166.
4. The Impact of Exercise on Cancer Mortality, Recurrence, and Treatment-Related Adverse Effects. Cormie P, Zopf EM, Zhang X, Schmitz KH. Epidemiol Rev. 2017 Jan 1;39(1):71-92. doi: 10.1093/epirev/mxx007. PMID: 28453622.
5. American College of Sports Medicine Roundtable Report on Physical Activity, Sedentary Behavior, and Cancer Prevention and Control. Patel AV, Friedenreich CM, Moore SC, Hayes SC, Silver JK, Campbell KL, Winters-Stone K, Gerber LH, George SM, Fulton JE, Denlinger C, Morris GS, Hue T, Schmitz KH, Matthews CE.Med Sci Sports Exerc. 2019 Nov;51(11):2391-2402. doi: 10.1249/MSS.0000000000002117. PMID: 31626056; PMCID: PMC6814265.
6. The exercise IL-6 enigma in cancer. Orange ST, Leslie J, Ross M, Mann DA, Wackerhage H. Trends Endocrinol Metab. 2023 Nov;34(11):749-763. doi: 10.1016/j.tem.2023.08.001. Epub 2023 Aug 24. PMID: 37633799.

Simplify Your Testing Process

We at Biomedica provide tailored analytical testing services for ELISA Kits, Luminex Assays, and microRNA Analysis.

Customized Testing Solutions for ELISA, Luminex, and microRNA

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Discover more about the Biomedica Service Measurements  here  

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We provide services for our proprietary Biomedica ELISA kits (refer to our product list), as well as for ELISA assays from other suppliers.

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We employ Luminex xMAP® (multiple analyte profiling) technology to perform immunoassays that allow for the concurrent detection and measurement of multiple biomarkers.

For additional details, please view our workflow chart or contact us (info@bmgrp.com) directly to discuss how we can assist with your specific research needs.

NEXT-GENERATION SEQUENCING & RT-qPCR MICRORNA SERVICES

We offer a comprehensive suite of high-quality RNA services, including RNA extraction, next-generation sequencing (NGS), RT-qPCR, and customized microRNA signature analysis, all carried out by our skilled laboratory team. Our services include:

• RNA extraction from biofluids (such as serum, plasma, extracellular vesicles), cells, and tissues, with quality control of total RNA using Bioanalyzer chips
• Next-generation sequencing (NGS)
• RT-qPCRCell-type specific microRNA and mRNA analysis within complex tissues, along with tailored microRNA signature analysis   

 

For more information about our microRNA services, please visit our website or contact us directly (info@bmgrp.com).

Literature

Gyöngyösi M, Guthrie J, Hasimbegovic E, Han E, Riesenhuber M, Hamzaraj K, Bergler-Klein J, Traxler D, Emmert MY, Hackl M, Derdak S, Lukovic D. Critical analysis of descriptive microRNA data in the translational research on cardioprotection and cardiac repair: lost in the complexity of bioinformatics. Basic Res Cardiol. 2025 Jun;120(3):443-472. doi: 10.1007/s00395-025-01104-1. Epub 2025 Apr 9. PMID: 40205177; PMCID: PMC12159128.

Abstract

Krammer TL, Mayr M, Hackl M. microRNAs as promising biomarkers of platelet activity in antiplatelet therapy monitoring. Int J Mol Sci. 2020 May 14;21(10):3477. doi: 10.3390/ijms21103477. PMID: 32423125; PMCID: PMC7278969.

Abstract

Given the high morbidity and mortality of cardiovascular diseases (CVDs), novel biomarkers for platelet reactivity are urgently needed. Ischemic events in CVDs are causally linked to platelets, small anucleate cells important for hemostasis. The major side-effect of antiplatelet therapy are life-threatening bleeding events. Current platelet function tests are not sufficient in guiding treatment decisions. Platelets host a broad spectrum of microRNAs (miRNAs) and are a major source of cell-free miRNAs in the blood stream. Platelet-related miRNAs have been suggested as biomarkers of platelet activation and assessment of antiplatelet therapy responsiveness. Platelets release miRNAs upon activation, possibly leading to alterations of plasma miRNA levels in conjunction with CVD or inadequate platelet inhibition. Unlike current platelet function tests, which measure platelet activation ex vivo, signatures of platelet-related miRNAs potentially enable the assessment of in vivo platelet reactivity. Evidence suggests that some miRNAs are responsive to platelet inhibition, making them promising biomarker candidates. In this review, we explain the secretion of miRNAs upon platelet activation and discuss the potential use of platelet-related miRNAs as biomarkers for CVD and antiplatelet therapy monitoring, but also highlight remaining gaps in our knowledge and uncertainties regarding clinical utility. We also elaborate on technical issues and limitations concerning plasma miRNA quantification.

 

 

 

 

FGF23 Reveals Mineral Imbalance in Hypoparathyroidism – Hypoparathyroidism (HypoPT) is a rare endocrine condition marked by inadequate or absent production of parathyroid hormone (PTH), leading to low calcium levels (hypocalcemia), elevated phosphate levels (hyperphosphatemia), and disturbed calcium-phosphate balance (1, 2). When this deficiency persists over the long term, it is referred to as chronic hypoparathyroidism, which is characterized by a sustained lack of PTH that results in ongoing hypocalcemia and often hyperphosphatemia.

Patients with chronic hypoparathyroidism may experience symptoms such as muscle cramps, fatigue, difficulty thinking clearly (“brain fog”), anxiety, depression, and reduced physical ability, and in severe cases, seizures or cardiac issues. The most common cause is surgery on the neck, like thyroid or parathyroid surgery. Less often, causes include autoimmune conditions, inherited syndromes, or genetic issues affecting the parathyroid glands (2). Chronic hypoparathyroidism is also associated with cardiovascular complications and an increased risk of developing kidney disease (3, 4).

FGF23 Reveals Mineral Imbalance in Hypoparathyroidism

In a recent study, researchers examined FGF23 levels in patients with chronic hypoparathyroidism (5). The results showed that, despite maintaining normal serum calcium and other biochemical markers, these patients often exhibited elevated FGF23 levels. This finding indicates the presence of subclinical disturbances in mineral metabolism that are not detected through standard biochemical assessments. Elevated FGF23 may reflect underlying dysregulation of mineral homeostasis, which could have implications for bone health and long-term mineral balance. The study underscores the potential value of monitoring FGF23 as a biomarker for ongoing mineral disturbances in the management of chronic hypoparathyroidism.

The BIOMEDICA FGF23 intact and FGF23 C-terminal ELISA kits were used in this study (5).

 FGF23 intact ELISA (cat. no.BI-20700) and FGF23 (C-terminal) (cat. no. BI-20702)   

• RELIABLE – Validated following international quality guidelines
• TRUSTED – Cited in over 90 publications
• EASY – 8 standards and 2 controls included
• FLEXIBLE – For SERUM & PLASMA samples

 

 

Elevated FGF23 Despite Biochemical Control Reveals Hidden Mineral Dysregulation in Chronic Hypoparathyroidism. Malagrinò M, Piazza A, Bisceglia N, Capra S, Cantone C, Pagotto U, Zavatta G. J Endocr Soc. 2025 Dec 20;10(2):bvaf217. doi: 10.1210/jendso/bvaf217. PMID: 41623900; PMCID: PMC12853065.

Abstract

Background: Fibroblast growth factor (FGF23) is a phosphate-regulating hormone and might be a biomarker of cardiorenal comorbidities in the general population. Its role in hypoparathyroidism is unclear.

Objective: To assess the prevalence of abnormal FGF23 concentrations in patients with chronic hypoparathyroidism and explore their associations with mineral metabolism and renal phosphate handling.

Design: Cross-sectional, observational study complemented by a retrospective longitudinal analysis of biochemical parameters over a median follow-up of 5 years.

Patients: Forty-eight consecutive patients with chronic hypoparathyroidism (mean age 60.6 ± 16.3 years; 85% women; 87.5% postsurgical) evaluated at an academic medical center between January 2023 and December 2024.

Measurements: Serum intact FGF23 levels, serum calcium (Ca) and phosphate (P), Ca × P product, PTH, 1,25-dihydroxyvitamin D [1,25(OH)₂D], estimated glomerular filtration rate (eGFR), and renal phosphate reabsorption [maximum rate of renal tubular reabsorption of phosphate/glomerular filtration rate (TmPO₄/GFR)].

Results: Elevated FGF23 levels were found in 71% of patients (mean 157.9 ± 92.4 pg/mL; reference range 23.2-95.4), despite adequate biochemical control (calcium 8.7 ± 0.8 mg/dL; phosphate 4.5 ± 0.8 mg/dL; Ca × P product 39.2 ± 6.8 mg²/dL²). FGF23 was associated with longer disease duration (P = .004), lower eGFR (P = .008), lower PTH (P = .03), reduced 1,25(OH)₂D (P = .016), and elevated Ca × P product (P = .036). Despite elevated FGF23, TmPO₄/GFR was paradoxically increased, suggesting impaired renal responsiveness. Female sex and Ca × P product were independent predictors of FGF23 levels.

Conclusion: FGF23 is frequently elevated in chronic hypoparathyroidism, indicating a disrupted phosphate metabolism, and its increase seems to be ineffective in promoting phosphate excretion, probably due to renal resistance mechanisms. Further studies are needed to clarify the role of FGF23 as a clinical biomarker, risk factor, and potential therapeutic target in this population.

Literature

1. Chronic Hypoparathyroidism-Current and Emerging Therapies. Khan S, Khan AA.Endocr Pract. 2025 Nov;31(11):1478-1487. doi: 10.1016/j.eprac.2025.07.011. Epub 2025 Jul 16. PMID: 40680836.
2. Unveiling the complexities of hypoparathyroidism: a comprehensive review of clinical manifestations, diagnosis, and novel therapies. Cetani F, Bertoldo F, Bononi M, Tarallo M, Camozzi V, Cipriani C, Palermo A, Pasquali D, Zavatta G. J Endocrinol Invest. 2026 Apr;49(4):725-746. doi: 10.1007/s40618-025-02760-9. Epub 2025 Dec 3. PMID: 41335198; PMCID: PMC13053346.
3. Skeletal and nonskeletal consequences of hypoparathyroidism. Silva BC. Arch Endocrinol Metab. 2022 Nov 11;66(5):642-650. doi: 10.20945/2359-3997000000553. PMID: 36382753; PMCID: PMC10118831.
4. Renal complications in patients with chronic hypoparathyroidism on conventional therapy: a systematic literature review : Renal disease in chronic hypoparathyroidism. Gosmanova EO, Houillier P, Rejnmark L, Marelli C, Bilezikian JP.Rev Endocr Metab Disord. 2021 Jun;22(2):297-316. doi: 10.1007/s11154-020-09613-1. Epub 2021 Feb 18. PMID: 33599907; PMCID: PMC8087595.
5. Elevated FGF23 Despite Biochemical Control Reveals Hidden Mineral Dysregulation in Chronic Hypoparathyroidism. Malagrinò M, Piazza A, Bisceglia N, Capra S, Cantone C, Pagotto U, Zavatta G. J Endocr Soc. 2025 Dec 20;10(2):bvaf217. doi: 10.1210/jendso/bvaf217. PMID: 41623900; PMCID: PMC12853065.

 

Discover BIOMEDICA FGF23 (Fibroblast Growth Factor) ELISA Assay Kits

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Biomarkers in Clinical Nephrology

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Periostin – A Serum Biomarker for Osteogenesis Imperfecta Progression

Osteogenesis Imperfecta (OI), also known as brittle bone disease, is a genetic disorder characterized by fragile bones that break easily, often with little or no apparent cause. It is caused by mutations in the genes responsible for producing collagen, a vital protein for bone strength and structure. Symptoms can vary widely, from mild bone fragility to frequent fractures, joint laxity, hearing loss, dental issues, and skeletal deformities. There are several types of OI, ranging from mild to severe, with the most common being Type I (1, 2).

Management of OI focuses on strengthening bones, reducing fracture risk, and improving quality of life through medications, physical therapy, and sometimes surgical interventions (3, 4). Advances in research, including biomarkers like Periostin, are helping to better understand disease severity and develop targeted treatments.

Periostin – A Serum Biomarker for Osteogenesis Imperfecta Progression

In a first-time study, researchers investigated the relationship between serum Periostin levels and disease severity in adults with OA, highlighting its potential link with skeletal severity. Periostin was measured in serum samples using the Periostin ELISA from Biomedica (cat.no. BI-20433).

Key findings

• Periostin serum levels are higher in adults with OI compared to healthy controls.
• Elevated circulating Periostin levels in adults with OI are associated with increased disease severity.
• Serum Periostin could potentially serve as a biomarker for assessing disease progression or severity in OI.

 

This research offers a new, non-invasive way to assess and track the progression of OI in adults.

Elevated periostin level in serum of adults with Osteogenesis Imperfecta is associated with disease severity. Mercier-Guery A, Auroux M, Gineyts E, Borel O, Szulc P, Sornay-Rendu E, Fontanges E, Croset M, Rousseau JC, Chapurlat R. J Clin Endocrinol Metab. 2026 Mar 17:dgag119. doi: 10.1210/clinem/dgag119. Epub ahead of print. PMID: 41841693.

Abstract

Objective: In Osteogenesis Imperfecta (OI), phenotypic variability and the limited predictive value of genotype-phenotype correlations underscore the need for reliable predictive marker of disease severity. Periostin is a matricellular protein involved in bone formation, remodeling, and response to mechanical stress. It interacts with type I collagen and modulates osteoblast activity via Wnt/β-catenin and TGF-β signaling. Given its established role in other bone disorders, we hypothesized that circulating periostin may be a relevant biomarker in OI.

Methods: We performed a matched case-control analysis of serum periostin levels in 61 adult patients with OI and 61 age-, sex-, and BMI-matched controls. Periostin was measured by ELISA. Associations between periostin levels and clinical variables were assessed using t-tests, Pearson correlations, and multivariable linear regression models.

Results: Mean periostin levels were significantly higher in OI patients than in controls (796.5 ± 209 vs. 713.6 ± 167 pmol/L, p = 0.017). Among OI patients, higher periostin level was associated with female sex (p = 0.01), presence of scoliosis (p = 0.01), and Sillence type III (p = 0.05). Positive correlations were observed between periostin and markers of axial skeletal severity as height-wingspan discrepancy (r = 0.30, p = 0.023). In multivariable analysis, the number of severe fractures (defined as femur/pelvis/humerus/vertebral fractures) was independently associated with higher periostin level (β = 25.6, p = 0.041), while smoking was negatively associated (β = -269.8, p = 0.012).

Conclusion: This study is the first to report the elevated circulating level of periostin in adults with OI and its association with disease severity.

Assay Highlights – PERIOSTIN ELISA (Cat. No. BI-20433)

• Only assay that detects all known Periostin isoforms
• Extensively validated according to international quality guidelines
• 7 human serum-based standards and 2 controls included
• Small sample volume – 10 µl / well
• Reliable – widely referenced 

 

Download our Periostin Flyer here

 

Literature

1. Comprehensive Review of Osteogenesis Imperfecta: Current Treatments and Future Innovations. Chaugule S, Constantinou CK, John AA, Micha D, Eekhoff M, Gravallese E, Gao G, Shim JH. Hum Gene Ther. 2025 Mar;36(5-6):597-617. doi: 10.1089/hum.2024.191. Epub 2025 Feb 11. PMID: 39932815; PMCID: PMC11971546.
2. Osteogenesis imperfecta. BJA Educ. Chan E, DeVile C, Ratnamma VS.2023 May;23(5):182-188. doi: 10.1016/j.bjae.2023.01.005. Epub 2023 Feb 24. PMID: 37124171; PMCID: PMC10140476.
3. Early Life Management of Osteogenesis Imperfecta. Arundel P, Borg SA.Curr Osteoporos Rep. 2023 Dec;21(6):779-786. doi: 10.1007/s11914-023-00823-5. Epub 2023 Sep 26. PMID: 37752354; PMCID: PMC10724332.
4. Medical Management for Fracture Prevention in Children with Osteogenesis Imperfecta. Arundel P, Bishop N. Calcif Tissue Int. 2024 Dec;115(6):812-827. doi: 10.1007/s00223-024-01202-7. Epub 2024 Mar 29. PMID: 38553634; PMCID: PMC11606989.
5. OI- Osteogenesis Imperfecta Foundation

Type 2 Diabetes Mellitus (T2DM) and Cardiovascular (CV) diseases

Patients with T2DM have an elevated risk of developing CV diseases due to multiple factors. Chronic hyperglycemia, or elevated blood sugar levels, can cause damage to blood vessels promoting the development of atherosclerosis (1). Insulin resistance, a hallmark of T2DM, contributes to abnormal lipid profiles, such as increased triglycerides and low HDL cholesterol, both of which are risk factors for cardiovascular disease. Additionally, high blood sugar levels impair endothelial function, reducing the blood vessels’ ability to dilate properly and increasing the likelihood of plaque formation. T2DM is also associated with increased systemic inflammation, which accelerates the process of atherosclerosis. Moreover, patients with T2DM often develop increased arterial stiffness, further elevating cardiovascular risk (2).

Measuring Arterial Stiffness

Arterial stiffness is commonly measured using several non-invasive techniques, including Pulse Wave Velocity (PWV). PWV it the most widely used and regarded as the gold standard. It measures the speed at which the blood pressure pulse propagates through the arteries. A higher PWV indicates increased arterial stiffness. In patients with T2DM, arterial stiffness has been demonstrated to predict cardiovascular events independently of traditional risk factors, including glycemic control and 24-hour ambulatory blood pressure (3).

Sclerostin – A Biomarker for Vascular Risk in Diabetes

Sclerostin and DKK-1 in Type 2 Diabetes Mellitus (T2DM)

Sclerostin and DKK-1 are proteins that act as inhibitors of the Wnt signaling pathway, which is crucial for bone formation and remodeling (4).

In cardiovascular diseases, elevated levels of these proteins are associated with increased vascular calcification and atherosclerosis (5, 6). They influence the functioning of vascular cells and contribute to the development and progression of vascular damage.

In a recent study, researchers investigated the relationship of the biomarkers Sclerostin and DKK-1with peripheral arterial stiffness in patients with Type 2 Diabetes Mellitus (T2DM) (7). Sclerostin and DKK-1 were both successfully measured in serum samples using the ELISA assays from BIOMEDICA.

Key findings:

• Sclerostin, but not DKK-1 is independently associated with increased arterial stiffness in T2DM patients. 
• Circulating sclerostin may represent a potential biomarker of arterial stiffness in this population

 

The study highlights the potential of sclerostin as a biomarker for arterial stiffness and cardiovascular risk in diabetes.

SCLEROSTIN ELISA Assay | BI-20492

• most referenced in over 340 publications
• full validation package
• 20µl sample/well – serum and plasma – sample volume: 20µl / well

 

DKK-1 ELISA Assay | BI-20413

• highly cited in over 180 publications 
• full validation package
• 20µl sample/well – for serum  – sample volume: 20µl / well
• no sample pre-dilution – direct measurment

 

 

Positive Correlates of Sclerostin and Association with Peripheral Arterial Stiffness in Patients with Type 2 Diabetes Mellitus. Hsu B-G et al., Medicina. 2026

Abstract

Background and Objectives: Sclerostin or dickkopf-1 (DKK1) inhibits the canonical Wnt/β-catenin signaling pathway, which regulates vascular calcification and may contribute to the development of arterial stiffness. The brachial–ankle pulse wave velocity (baPWV) measures peripheral arterial stiffness (PAS). This study aimed to investigate the correlation between sclerostin and DKK1 levels and PAS in patients with type 2 diabetes mellitus (T2DM). Materials and Methods: Biochemical data and sclerostin and DKK1 levels were analyzed in the fasting blood samples of 125 patients with T2DM. baPWV measurements using the VaSera VS-1000 automatic pulse wave analyzer classified patients with values > 18.0 m/s on either side into the PAS group. Results: Among patients with T2DM, 47 (37.6%) were classified as having PAS. These patients exhibited higher hypertension prevalence (p = 0.002); greater age (p < 0.001); elevated systolic (p < 0.001) and diastolic blood (p = 0.012) pressures; and increased fasting glucose (p = 0.001), glycated hemoglobin (p = 0.008), triglyceride (p = 0.001), blood urea nitrogen (p < 0.001), and creatinine (p = 0.001) levels, urine albumin-to-creatinine ratio (p = 0.039), and C-reactive protein (p = 0.024) and serum sclerostin (p < 0.001) levels, but decreased estimated glomerular filtration rate (p < 0.001). Multivariate logistic regression analysis identified serum sclerostin level (odds ratio, 1.127; 95% confidence interval, 1.058–1.200; p < 0.001) as an independent PAS predictor in patients with T2DM. Serum log-transformed sclerostin levels were positively correlated with left (p = 0.005) and right (p = 0.001) baPWV via Spearman’s rank-order correlation coefficient analysis. Conclusions: Serum sclerostin levels, but not DKK1 levels, are positively correlated with PAS in patients with T2DM.

Literature

1. 2-Fold More Cardiovascular Disease Events Decades Before Type 2 Diabetes Diagnosis: A Nationwide Registry Study. Gyldenkerne C, Kahlert J, Thrane PG, Olesen KKW, Mortensen MB, Sørensen HT, Thomsen RW, Maeng M.J Am Coll Cardiol. 2024 Dec 3;84(23):2251-2259. doi: 10.1016/j.jacc.2024.06.050. PMID: 39603746.
2. The Interplay Between Diabetes, Cardiovascular Disease, and Kidney Disease. Usman MS, Khan MS, Butler J. In: Chronic Kidney Disease and Type 2 Diabetes. Arlington (VA): American Diabetes
3. Association; 2021 Jun. PMID: 34279879.Prognostic impact of aortic stiffness in high-risk type 2 diabetic patients: the Rio deJaneiro Type 2 Diabetes Cohort Study. Diabetes Care. Cardoso CR, Ferreira MT, Leite NC, Salles GF. 2013 Nov;36(11):3772-8. doi: 10.2337/dc13-0506. Epub 2013 Jul 22. PMID: 23877987; PMCID: PMC3816863.
4. Wnt signaling pathway inhibitors, sclerostin and DKK-1, correlate with pain and bone pathology in patients with Gaucher disease. Ivanova MM, Dao J, Kasaci N, Friedman A, Noll L, Goker-Alpan O.Front Endocrinol (Lausanne). 2022 Nov 24;13:1029130. doi: 10.3389/fendo.2022.1029130. PMID: 36506070; PMCID: PMC9730525.
5. Sclerostin and Cardiovascular Disease. Tobias JH.Curr Osteoporos Rep. 2023 Oct;21(5):519-526. doi: 10.1007/s11914-023-00810-w. Epub 2023 Jul 25. PMID: 37490188; PMCID: PMC10543142.
6. Dickkopf-1, a potential target for heart disease. Xu P, Cao Y, Zhang S, Liu X, Zhang M, Zhang C.Int J Cardiol. 2024 Aug 1;408:132146. doi: 10.1016/j.ijcard.2024.132146. Epub 2024 May 9. PMID: 38729311.
7. Positive Correlates of Sclerostin and Association with Peripheral Arterial Stiffness in Patients with Type 2 Diabetes Mellitus. Hsu B-G, Li J-C, Wu D-A, Chen M-C. Medicina. 2026; 62(4):643.

 

 

 

Monitoring inflammatory responses with serum marker LRG

Inflammatory Bowel Diseases (IBD) are chronic conditions characterized by inflammation of the gastrointestinal tract. The main types are Crohn’s disease and ulcerative colitis. Crohn’s can affect any part of the digestive tract and involves all layers of the intestinal wall, while ulcerative colitis primarily affects the colon and rectum’s inner lining. Symptoms often include abdominal pain, diarrhea, weight loss, and fatigue. The exact cause is unknown, but it involves an abnormal immune response, genetics, and environmental factors. IBD is a long-term condition that requires ongoing management to reduce inflammation and control symptoms (1-3).

Reliable biomarkers for monitoring inflammatory bowel disease (IBD) continue to be an unmet clinical need, especially in patients undergoing biologic therapies where C-reactive protein (CRP) responses may be diminished. Leucine-rich alpha-2 glycoprotein (LRG) is a new acute-phase reactant regulated by various cytokines, potentially less reliant on interleukin-6 compared to CRP (4).

Monitoring Inflammatory Bowel Disease with Serum Marker LRG

A systematic review and meta-analysis indicated that LRG may be a valuable marker for assessing IBD activity. It appears to be particularly effective in detecting disease activity in patients with normal CRP levels. Additionally, LRG demonstrated greater accuracy in monitoring disease activity in patients with Crohn’s disease (CD) compared to those with other forms of IBD (5).

Discover BIOMEDICA´s Leucine-rich alpha-2-glycoprotein (LRG1) ELISA | cat. no. BI-LRG

• RELIABLE – full validation package 
• CONVENIENT – comes with 7 calibrators, 2 controls, and ample buffers included (protocol booklet)
• REFERENCE values for normal and pathological samples
• OPTIMIZED assay range – no additional dilution and testing required
• EASY – results in 3 h, all reagents included

Example of a typcial Biomedica ELISA assay kit

Monitoring Inflammatory Bowel Disease with Serum Marker LRG

 

 

Therapeutic potential of Lactobacillus plantarum HBUAS68394 in mitigating DSS-induced colitis. Yousef  F, Hussein M, Taha R, Mwaheb M.  EJBO. 2025. DOI: 10.21608/ejbo.2025.363646.3211.

The study explored how the probiotic strain Lactobacillus plantarum HBUAS68394 can help reduce inflammation and promote healing in models of colitis, a common form of inflammatory bowel disease. The findings suggest that Lactobacillus plantarum HBUAS68394 may offer a promising, natural approach to managing colitis symptoms and restoring gut health. The study also successfully utilized our LRG ELISA to monitor inflammatory responses.

 

Literature

1. Medical management of inflammatory bowel diseases. Hashash JG, Limdi JK, Shapiro JM, Shah SA. BMJ. 2025 Dec 19;391:e079050. doi: 10.1136/bmj-2025-079050. PMID: 41419296.
2. Inflammatory Bowel Disease. Bruner LP, White AM, Proksell S. Prim Care. 2023 Sep;50(3):411-427. doi: 10.1016/j.pop.2023.03.009. Epub 2023 May 10. PMID: 37516511.
3. Monitoring Inflammatory Bowel Disease Activity: When, How, and Why. Gaidos JKJ, Hashash JG. Am J Gastroenterol. 2025 Jun 9;120(8):1732-1741. doi: 10.14309/ajg.0000000000003582. PMID: 40488637.           
4. A Role for Leucine-Rich α2-Glycoprotein in Leukocyte Trafficking and Mucosal Inflammation in Inflammatory Bowel Disease. Mishima T, Fujimoto M, Urushima H, Funajima E, Suzuki Y, Ohkawara T, Murata O, Serada S, Naka T. Inflamm Bowel Dis. 2025 Jun 13;31(6):1637-1648. doi: 10.1093/ibd/izaf022. Erratum in: Inflamm Bowel Dis. 2025 Oct 1;31(10):2952. doi: 10.1093/ibd/izaf198. PMID: 39918378.
5. The usefulness of serum leucine-rich alpha-2 glycoprotein as a novel biomarker in monitoring inflammatory bowel disease: a systematic review and meta-analysis. Ojaghi Shirmard F, Pourfaraji SM, Saeedian B, Bagheri T, Ismaiel A, Matsumoto S, Babajani N. Eur J Gastroenterol Hepatol. 2025 Aug 1;37(8):891-904. doi: 10.1097/MEG.0000000000002952. Epub 2025 Feb 18. PMID: 39976047.
6. Microbiota in inflammatory bowel disease: mechanisms of disease and therapeutic opportunities. Iliev ID, Ananthakrishnan AN, Guo CJ. Nat Rev Microbiol. 2025 Aug;23(8):509-524. doi: 10.1038/s41579-025-01163-0. Epub 2025 Mar 10. Erratum in: Nat Rev Microbiol. 2025 Aug;23(8):541. doi: 10.1038/s41579-025-01175-w. PMID: 40065181; PMCID: PMC12289240

Understanding how immunosuppressants in transplant therapy cause blood vessel damage – C4d staining in liver tissue

The study titled “Modeling antithymocyte globulin-induced microvasculopathy using human iPSC-derived vascularized liver organoids” aims to better understand the vascular side effects caused by antithymocyte globulin (ATG), a drug used in transplant medicine. Researchers created vascularized liver organoids from human induced pluripotent stem cells (iPSCs) to simulate human liver blood vessels. Using this model, they investigated how ATG induces microvasculopathy, or small blood vessel damage. This platform offers new insights into the mechanisms of ATG-related vascular injury and could help develop safer treatments to reduce side effects in transplant patients.

C4d staining in Paraffin-Embedded (FFPE) liver tissue was performed with the BIOMEDICA anti-C4d antibody.

Anti-C4d Antibody | BI-RC4D 

for the identification of human complement split product C4d in paraffin and frozen sections as well as by flow cytometry.

 Product Highlights:

 Anti-C4d Antibody  cat. no. BI-RC4D

• TRUSTED – widely cited in over 100 citations
• MULTI-USE – for immunohistochemistry on paraffin embedded tissue and frozen sections
• The C4d antibody has been utilized in kidney, heart, liver and other transplants
• working protocol

 

Anti-C4d Antibody (FITC) | BI-RC4D-FITC

• Protocol for cell- or solid-phase bound C4 and C4d split product by flow cytometry
• working protocol

-Discover our anti-C4d antibodies for IHC and FITC.

 

How Immunosuppressants in Transplant Therapy cause Blood Vessel Damage

Publication: Modeling antithymocyte globulin-induced microvasculopathy using human iPSC-derived vascularized liver organoids. Kawamura S, Yoneyama Y, Saiki N, Wu Y, Moriya C, Ohmura R, Maezawa M, Shimada Y, Wang Y, Mori K, Okada N, Onishi Y, Sanada Y, Hirata Y, Sakuma Y, Takebe T. Cell Rep Med. 2025 Nov 18;6(11):102433. doi: 10.1016/j.xcrm.2025.102433. Epub 2025 Nov 6. PMID: 41202806; PMCID: PMC12711670.

Abstract

Antithymocyte globulin (ATG) is a widely used immunosuppressive agent, yet its off-target vascular effects remain a clinical challenge in part due to a lack of relevant human models. Here, we uncover a biphasic mechanism of ATG-induced microvasculopathy using a humanized liver organoid platform derived from induced pluripotent stem cells (iPSCs). We show that ATG triggers a rapid, complement-dependent phase of injury restricted to human iPSC-derived liver sinusoidal endothelial cells (iLSECs), leading to C3 deposition and acute thrombosis specifically in human but not in mouse vessels. Transcriptomics reveals a delayed transforming growth factor β (TGF-β) pathway-driven proinflammatory program that coincides with neutrophil recruitment and degranulation, while pharmacological TGF-β blockade attenuates thrombosis and flow disturbance. Our findings reveal a pathogenic sequence of complement and TGF-β pathway activation and establish a translational platform for dissecting human liver-specific microvasculopathy in vivo.

Related literature

Anti-thymocyte globulin-induced hyperbilirubinemia in patients with myelofibrosis undergoing allogeneic hematopoietic cell transplantation. Ecsedi M, Schmohl J, Zeiser R, Drexler B, Halter J, Medinger M, Duyster J, Kanz L, Passweg J, Finke J, Bethge W, Lengerke C. Ann Hematol. 2016 Oct;95(10):1627-36. doi: 10.1007/s00277-016-2758-z. Epub 2016 Aug 2. PMID: 27480090.

Complement component 4d immunostaining in liver allografts of patients with de novo immune hepatitis. Aguilera I, Sousa JM, Gavilan F, Gomez L, Alvarez-Márquez A, Núñez-Roldán A. Liver Transpl. 2011 Jul;17(7):779-88. doi: 10.1002/lt.22302. PMID: 21425430.

Influence of preformed donor-specific antibodies and C4d on early liver allograft function. Perera MT, Silva MA, Murphy N, Briggs D, Mirza DF, Neil DA. Scand J Gastroenterol. 2013 Dec;48(12):1444-51. doi: 10.3109/00365521.2013.845795. Epub 2013 Oct 16. PMID: 24131305.

 

 

Chronic kidney disease (CKD) is a progressive condition affecting over 800 million individuals, accounting for roughly 13% of the global population (1). Over the past two decades, CKD has remained one of the leading causes of mortality. Due to its asymptomatic early stages, CKD is frequently diagnosed at advanced stages when severe complications have already developed. Recent research has identified new biomarkers linked to the underlying mechanisms of CKD, including chronic inflammation, tubular injury, and outcomes such as bone and mineral metabolism disorders, cardiovascular events, and overall mortality (2). The discovery and application of these emerging biomarkers, such as FGF23, Endostatin ,  Vanin-1 , and Periostin are  promising avenues for the early detection of e.g.  microvascular tissue injuries and renal tubular damage in drug-induced acute kidney injury and for the detection and improved management of CKD

Biomarker ELISA assay kits in Clinical Nephrology – FGF23 ∙ Endostatin ∙ Periostin ∙ Vanin-1

ELISA kits developed and produced by BIOMEDICA

Click here to view our brochure: Biomarkers for Clinical Nephrology 

BIOMEDICA´s ELISA Assay Highlights
• EASY – ready to use calibrators & controls included
• RELIABLE – full validation according to international quality guidelines
• TRUSTED – widely cited in over 1600 publications

 

 

Emerging Biomarkers in Kidney Disease

FGF23 ∙ Endostatin ∙ Periostin ∙ Vanin-1

 

Fibroblast Growth Factor 23 (FGF23) is a hormone primarily produced by osteocytes and osteoblasts in the bone. It plays a crucial role in regulating phosphate and vitamin D metabolism (3). FGF23 helps maintain phosphate balance by reducing phosphate reabsorption in the kidneys and decreasing the production of active vitamin D (calcitriol). Elevated levels of circulating FGF23 are associated with a higher risk of adverse outcomes, notably cardiovascular disease, in individuals with CKD as well as in the general population (4).

Vanin-1 is an enzyme belonging to the pantetheinase family, involved in the metabolism of pantothenic acid (vitamin B5). In recent years, Vanin-1 has emerged as a crucial factor in the development and progression of certain diseases, owing to its enzymatic activity. Additionally, Vanin-1 has been suggested to function as an oxidative stress sensor, as its expression increases in response to oxidative injury and it plays a role in maintaining redox homeostasis (5, 6). Vanin-1’s enzymatic activity influences oxidative stress regulation through cysteamine production, which can impact inflammation and tissue repair processes in the renal system.

Vanin-1 plays a significant role in kidney disease, particularly as a biomarker for the early detection of drug-induced acute kidney injury (7): elevated Vanin-1 levels in urine reflect ongoing oxidative stress and tissue damage in the kidneys. Due to its rapid release during kidney injury, Vanin-1 is viewed as a promising early biomarker for detecting renal damage, which could allow for earlier intervention and improved disease management. Continued research is actively investigating its complete diagnostic and therapeutic potential in kidney-related conditions.

Endostatin is an endogenous protein that functions as an inhibitor of angiogenesis, the formation of new blood vessels. It originates from collagen XVIII, a constituent of the extracellular matrix. Endostatin is crucial in controlling blood vessel growth, which is vital in processes such as cancer development, wound repair, and vascular disorders (8). Additionally, it is being studied as a biomarker for several diseases characterized by abnormal blood vessel formation (9).

In kidney disease, Endostatin was strongly associated with kidney outcomes in patients with type 2 diabetes: participants in the highest quartile of plasma Endostatin, had approximately four times the risk of the kidney outcome compared to those in the lowest quartile (10). In addition, elevated levels of plasma Endostatin have been shown to be linked to chronic kidney disease: the findings suggest that higher plasma Endostatin levels are significantly and independently linked to CKD (11).

Periostin is a matricellular protein that plays a crucial role in tissue repair, remodeling, and cell adhesion. Analysis of kidney biopsies from healthy donors revealed a consistent presence of Periostin at the vascular pole of the glomerulus and surrounding Bowman’s capsule, while it was absent in the tubules. Interestingly, some other studies found no periostin expression in kidney samples from individuals without renal pathology (12). However, recent studies have shown that Periostin is abnormally expressed in various types of chronic kidney disease (CKD), with its levels correlating to the extent of interstitial fibrosis and the deterioration of kidney function (13).

Literature

1. New and Emerging Biomarkers in Chronic Kidney Disease. Dopierała M, Nitz N, Król O, Wasicka-Przewoźna K, Schwermer K, Pawlaczyk K. Biomedicines. 2025; 13(6):1423. https://doi.org/10.3390/biomedicines13061423
2. Biomarkers of Acute and Chronic Kidney Disease. Zhang WR, Parikh CR. Annu Rev Physiol. 2019 Feb 10;81:309-333. doi: 10.1146/annurev-physiol-020518-114605. PMID: 30742783; PMCID: PMC7879424.
3. Regulation of FGF23 production and phosphate metabolism by bone-kidney interactions. Agoro R, White KE.Nat Rev Nephrol. 2023 Mar;19(3):185-193. doi: 10.1038/s41581-022-00665-x. Epub 2023 Jan 9. PMID: 36624273.
4. FGF23 and Klotho in chronic kidney disease. Olauson H, Larsson TE.Curr Opin Nephrol Hypertens. 2013 Jul;22(4):397-404. doi: 10.1097/MNH.0b013e32836213ee. PMID: 23666415.
5. Role of the Vnn1 pantetheinase in tissue tolerance to stress. Biochem Soc Trans. Naquet P, Pitari G, Duprè S, Galland F. 2014 Aug;42(4):1094-100. doi: 10.1042/BST20140092. PMID: 25110008.
6. Oxidative Stress in the Pathophysiology of Kidney Disease: Implications for Noninvasive Monitoring and Identification of Biomarkers. Gyurászová M, Gurecká R, Bábíčková J, Tóthová Ľ.Oxid Med Cell Longev. 2020 Jan 23;2020:5478708. doi: 10.1155/2020/5478708. PMID: 32082479; PMCID: PMC7007944.
7. Urinary vanin-1 associated with chronic kidney disease in hypertensive patients: A pilot study. Hosohata K et al.,  J Clin Hypertens (Greenwich). 2020 Aug;22(8):1458-1465
8. Endostatin in Renal and Cardiovascular Diseases. Li M, Popovic Z, Chu C, Krämer BK, Hocher B.Kidney Dis (Basel). 2021 Sep 9;7(6):468-481. doi: 10.1159/000518221. PMID: 34901193; PMCID: PMC8613550.
9. Endostatin in fibrosis and as a potential candidate of anti-fibrotic therapy. Zhang Z, Liu X, Shen Z, Quan J, Lin C, Li X, Hu G. Drug Deliv. 2021 Dec;28(1):2051-2061. doi: 10.1080/10717544.2021.1983071. PMID: 34595978; PMCID: PMC8491667.
10. Plasma endostatin predicts kidney outcomes in patients with type 2 diabetes. Chauhan K, Verghese DA, Rao V, Chan L, Parikh CR, Coca SG, Nadkarni GN. Kidney Int. 2019 Feb;95(2):439-446. doi: 10.1016/j.kint.2018.09.019. Epub 2018 Dec 24. PMID: 30591223; PMCID: PMC6342645.
11. Elevated plasma levels of endostatin are associated with chronic kidney disease. Chen J, Hamm LL, Kleinpeter MA, Husserl F, Khan IE, Chen CS, Liu Y, Mills KT, He C, Rifai N, Simon EE, He J.Am J Nephrol. 2012;35(4):335-40. doi: 10.1159/000336109. Epub 2012 Mar 27. PMID: 22456114; PMCID: PMC3362190.
12. The role of periostin in kidney diseases. Turczyn A, Pańczyk-Tomaszewska M. Cent Eur J Immunol. 2021;46(4):494-501. doi: 10.5114/ceji.2021.110317. Epub 2021 Nov 1. PMID: 35125949; PMCID: PMC8808300.
13. Periostin in the Kidney. Wallace DP. Adv Exp Med Biol. 2019;1132:99-112. doi: 10.1007/978-981-13-6657-4_11. PMID: 31037629.

 

Approximately 1 in 10 people are affected by chronic kidney disease (CKD), impacting over 800 million individuals globally (1-3). CKD is a progressive condition where the kidneys gradually lose their ability to function properly.

Early intervention is essential to preserving kidney health, slowing the progression of kidney disease and its complications, decreasing the risk of risk of cardiovascular disease, and preventing early death related to kidney and cardiovascular conditions (4).

World Kidney Day – March 12, 2026

What are the contributing factors to CKD?

Age over 60, diabetes, high blood pressure, heart disease, obesity, and certain medications are some of the known risk factors for kidney disease. 

 How can we maintain healthy kidneys?

Good nutrition, regular exercise, and adequate fluid intake are some of the ways to support kidney health.

Are your kidneys healthy? Take the quiz

 

 BIOMEDICA´s Biomarker ELISA Kits in Clinical Nephrology

• FGF23 (C-terminal) |BI-20700 and FGF23 intact ELISA |BI-20700
• Vanin-1 (urine) ELISA | BI-VAN1U  
• Endostatin ELISA | BI-20742
• Periostin ELISA | BI-20422
• Sclerostin ELISA |BI-20492 and Bioactive Sclerostin ELISA |BI-20472

 

 

Related Products:

Osteoprotegerin ELISA, NT-proBNP ELISA, Anti-C4d Antibody

Why laboratories choose BIOMEDICA ELISA kits

• ROBUST & RELIABLE ASSAYS
• Widely cited in over 1700 peer-reviewed publications
• Validated according to international guidelines
• High specificity, enabling reliable biomarker measurement in healthy individuals

 

Are you planning a clinical study ELISA kits for clinical research in kidney disease

Biomarkers in Clinical Nephrology – check out our broshure

 More information on kidney health can be found on the following websites:

1. ISN, World Kidney Day 2026 – International Society of Nephrology
2. Are your kidneys healthy- Quiz – 20 years World Kidney Day
3. Detect early, protect kidney health: World Kidney Day 2025. Waith FM, Bresolin NL, Antwi S. Pediatr Nephrol. 2025 May;40(5):1511-1514. doi: 10.1007/s00467-025-06714-4. Epub 2025 Feb 17. PMID: 39960639. For full publication- click here 
4. Are your kidneys ok? Detect early to protect kidney health. Vassalotti JA, Francis A, Soares Dos Santos AC Jr, Correa-Rotter R, Abdellatif D, Hsiao LL, Roumeliotis S, Haris A, Kumaraswami LA, Lui SF, Balducci A, Liakopoulos V; World Kidney Day Joint Steering Committee. Ren Fail. 2025 Dec;47(1):2503514. PMID: 40394853

 

Abstract

Early identification of kidney disease can protect kidney health, prevent kidney disease progression and related complications, reduce cardiovascular disease risk and decrease mortality. We must ask “Are your kidneys ok?” using serum creatinine to estimate kidney function and urine albumin to assess for kidney and endothelial damage. Evaluation for causes and risk factors for chronic kidney disease (CKD) includes testing for diabetes and measurement of blood pressure and body mass index. This World Kidney Day we assert that case-finding in high-risk populations, or even population level screening, can decrease the burden of kidney disease globally. Early-stage CKD is asymptomatic, simple to test for and recent paradigm shifting CKD treatments such as sodium glucose co-transporter-2 inhibitors dramatically improve outcomes and favor the cost-benefit analysis for screening or case-finding programs. Despite this, numerous barriers exist, including resource allocation, healthcare funding, healthcare infrastructure and healthcare-professional and population awareness of kidney disease. Coordinated efforts by major kidney non-governmental organizations to prioritize the kidney health agenda for governments and aligning early detection efforts with other current programs will maximize efficiencies.

Additonal publications:

IPNA’s commitment to world kidney day 2026: caring for little kidneys and protecting the planet. Shroff R, Sivaram P, Tarter A, Phiri EM, Antwi S, Ocheke I, Penido MG, Mccarthy F, Lou-Meda R, Adalat S, He G, Kermond R, Bayazit AK, Raina R; IPNA Green Nephrology Taskforce, IPNA Special Projects Committee. Pediatr Nephrol. 2026 Feb 24. PMID: 41733668.

Exciting research in glycobiology using our EZ4U cell viability assay!

Scientists developed innovative sugar compounds that combine features of natural molecules through advanced synthesis methods. These novel molecules have shown promising biological effects on human skin cells (dermal fibroblasts).

The First Simplified Heparan Sulphate-Alginate Hybrid Trisaccharides: Synthesis and Biological Effects on Human Dermal Fibroblasts.

Key highlights:

• At tested doses, the compounds did not impact cell viability or collagen production.
• Some molecules exhibited anti-inflammatory properties.
• These findings suggest potential applications in reducing inflammation and promoting skin healing.

 

Evaluating Cell Viability with EZ4U

“Cell viability was evaluated in dermal fibroblasts using the EZ4U assay (Biomedica, Wien, Austria), following the manufacturer’s instructions. In this method, mitochondrial dehydrogenases catalyze the conversion of a non-toxic tetrazolium compound into a soluble formazan dye. In brief, cells were seeded in 96-well plates, cultured for 24 hours, and then treated with various compounds for 24, 48, and 72 hours. After treatment, 20 µL of the tetrazolium substrate solution was added to 200 µL of phenol red-free culture medium in each well, followed by a two-hour incubation. The resulting formazan dye’s absorbance was then measured at 450 nm (with a reference at 620 nm)”

EZ4U (Easy for You!)  Cell Viability & Cytotoxicity Assay (cat.no. BI-5000)

– Method: Cell proliferation and cytotoxicity assay , 10 x 96 tests, method based on the reduction of tetrazolium salt to colored formazan

-Sample type: Cell culture

-Assay time: 2-5 hours depending on the metabolic capacity of the living cells

Reliable & Sensitive

• One step incubation  – for use on living cells
• Widely used – referenced in +290 publications

 

Download the BROCHURE – EZ4U cell proliferation and cytotoxicity assay and the PROTOCOL BOOKLET

Literature

The First Simplified Heparan Sulphate-Alginate Hybrid Trisaccharides: Synthesis and Biological Effects on Human Dermal Fibroblasts. Kútvölgyi K, Peleskei Z, Demeter F, Barta RA, Mándi A, Homoki E, Oláh A, Hajkó J, Herczeg M, Lisztes E. Int J Mol Sci. 2025 Aug 27;26(17):8305. doi: 10.3390/ijms26178305. PMID: 40943230; PMCID: PMC12428572.

Abstract

Glycosaminoglycans (GAGs) are linear, high molecular weight polydisperse heteropolysaccharides consisting of repeating disaccharide units, which always contain a uronic acid building block (e.g., d-glucuronic acid or l-iduronic acid). Their analogues containing d-mannuronic acid were not known until now. Another important class of the linear negatively charged polisaccharides are alginates, which are also present in the cell surface in the cell wall. They are composed of blocks of 1,4-linked β-d-mannuronic acid and its C-5 epimer α-l-guluronic acid in alternating or random order. Both groups of molecules have significant biological activity (e.g., cell growth inhibitory activity, anti-inflammatory effect, etc.). In the course of our research, we combined the structural characteristics of these two groups of molecules and produced a series of heparan sulphate analogue trisaccharides containing d-mannuronic acid, with a simplified structure, in which α- and β-mannosidic bonds are also found. Since trisaccharides may exert diverse biological effects and alginate derivatives can influence wound healing processes, we investigated the effects of the synthesized compounds on primary human dermal fibroblasts. We found that, when applied at 10 μM, none of the compounds influenced viability or spontaneous collagen production; however, some derivatives exhibited anti-inflammatory activity and suppressed the poly(I:C)-induced release of interleukin 6.

 

INTERNATIONAL SALES AND DISTRIBUTION MANAGER FOR BIOMEDICA
IMMUNOASSAYS (M/F/D)

Are you ready to take the next step in international Life Science sales? We are looking for an “International Sales and Distribution Manager” to join the Biomedica Immunoassays team in Bratislava, Slovakia, starting March 2026.

About Biomedica

Biomedica Slovakia is part of the Biomedica Group headquartered in Vienna, Austria. We have been on the forefront as a distributor of medical devices, in vitro diagnostics, products for Life Sciences, and Clinical IT for more than 40 years.

About Biomedica Immunoassays

Biomedica Immunoassays develops and produces internationally recognized high-quality ELISA kits used by leading scientific institutions, CROs, and pharmaceutical laboratories worldwide.

We started our own R&D programme in 1988 and now produce a range of innovative and high-quality immunoassays for clinical research in the field of cardiorenal diseases as well as mineral and bone disorders.

We are setting the standard for clinical research using serum-based calibrators and controls, thus enabling researchers to collect biologically reliable data. The supplied immunoassays are validated following international quality guidelines.

For specific markers, Biomedica has become a market leader with a continuously growing portfolio. A worldwide distribution network has been established for these products as well as an analytical testing service, which offers customers in-house analysis of their samples.

Are you ready to take the next step in international Life Science?

We are looking to strengthen our team with an

INTERNATIONAL SALES AND DISTRIBUTION MANAGER FOR BIOMEDICA IMMUNOASSAYS (M/F/D)

located in Bratislava, Slovakia. Full-time, starting March 2026

 

Your responsibilities

 

• Manage an international distribution network
• Provide technical support of distributors and end-users with product specific information
• Build and maintain relationships with key international customers
• Provide end-clients with customized quotations, negotiating contracts and oversee logistics and export documentation
• Drive market expansion by identifying new opportunities, emerging markets and new segments
• Monitor competitors and market prices
• Collect and analyse customer feedback
• Participation in international congresses, symposia and exhibitions
• Budget and sales planning in a cooperation with responsible manager
• Support production in creating production plans
• Handle complaints and troubleshoot in cooperation with the laboratory team

 

Your profile

 

• Bachelor’s degree, Master’s degree or Postgraduate in biology, chemistry, biotechnology or a related field
• Experience in international sales or distribution management
• Language skills: English – fluency in spoken and written
• Strong self-organization and ability to work independently
• Strong negotiation and cross- cultural communication and presentation skills
• Friendly and polite behaviour
• High social competence and team spirit
• Willingness to learn
• Flexibility and willingness to travel (travel activity up to approx. 20%, driving license B required)
• Microsoft Office skills

 

We offer

 

• Long-term employment in a well-known and growing international company
• Full time job
• Good company atmosphere
• Independent working
• Established product line of high quality
• Intensive training opportunities
• Company notebook and mobile phone
• Competitive salary based on individual agreement
• Attractive bonus system

 

The gross monthly salary for this position starts at EUR 2,000 (full-time) and will be discussed and agreed on an individual basis, depending on qualifications and professional experience.

 

Informationt about the selection process

 

This is a unique opportunity to join an innovative international company in a growing industry that can provide career security and genuine advancement opportunities for those who show potential.

We are seeking candidates with initial experience in international sales and distribution management within the life science industry. In managing relationships with our distributors and end-clients, you should demonstrate excellent communication and presentation skills, along with the ability to interact effectively with diverse cultures and personalities.

We look forward to receiving your written application (your CV and letter of motivation).

Please send your application by email to petra.bafrncova@bmgrp.sk

Join us and make a difference!

Worldwide, cardiovascular diseases (CVDs) are the primary cause of mortality (1). They involve a variety of underlying mechanisms, with increased oxidative stress being one of the key contributing factors.

Behavioral risk factors like poor diet, lack of physical activity, and tobacco use are connected to CVDs. Conditions that heighten the risk include obesity, high blood sugar, hypertension, increased low-density lipoprotein (LDL) cholesterol, and oxidative stress (1).

Understanding oxidative stress

 

Oxidative stress occurs when there is an imbalance between the production of free radicals (reactive oxygen species – ROS) and the body’s antioxidant defenses (endogenous antioxidant capacity) (2). ROS are by-products of cellular metabolism and can be triggered by various factors such as pollutants, heavy metals, tobacco, drugs, and others. It is believed that oxidative stress plays a role in the development and progression of numerous diseases, including cancer (3), diabetes (4), metabolic syndrome (5), Alzheimer´s disease (6), atherosclerosis (7), and cardiovascular conditions (8).

Biomarkers of Oxidative Stress in Cardiovascular Diseases

Oxidized LDL (oxLDL) and Autoantibodies Against Oxidized LDL

Atherosclerosis is a disease characterized by the accumulation of lipids, fibrous tissue, and calcification in large arteries. The process starts with endothelial activation, followed by a series of events that result in vessel narrowing and the activation of inflammatory pathways, leading to the formation of atheromatous plaques. These mechanisms collectively contribute to cardiovascular complications (9).

Oxidized LDL (OxLDL) and anti-OxLDL antibodies are closely linked and play crucial roles in the development of atherosclerosis, contributing to plaque formation, inflammation, and rupture. While OxLDL encourages foam cell development, anti-OxLDL antibodies, may provide a protective effect against coronary artery disease (CAD). Both are promising candidates as diagnostic biomarkers and targets for imaging in assessing cardiovascular risk (10).

Autoantibodies targeting oxidatively modified LDL (anti-oxLDL Ab) have been identified in both patients with atherosclerosis and healthy individuals. It is proposed that these antibodies reflect ongoing oxidation processes occurring within the body.

Anti-oxLDL Ab levels can be quantified in human blood samples using a standard ELISA assay . Several studies suggest that autoantibodies to oxLDL may enhance cardiovascular risk assessment and stratification (11).

 

Methods for Measuring Oxidative Status and Oxidative Stress

    1. MEASUREMENT OF ANTI-OXIDIZED LDL AUTOANTIBODIES (anti-oxLDL antibodies)

ELISA for the detection of Anti-oxidized LDL Autoantibodies (oLAB ) | BI-20032

• Sample type – serum
• Sample volume –  50µl/well
• Incubation time –  1.5 h / 30 min / 15 min
• Detection range – 0 – 1200 mU / ml
• Sensitivity – 48 mU / ml
• Precision-  In-between-run (n=5): ≤ 8 % CV, Within-run (n=8): ≤ 4 % CV
• Use – Research use only
• Widely cited in over 70 publications

Protocol booklet and MSDS

 

2. MEASUREMENT OF BIOLOGICAL PEROXIDES 

Oxidative Stress Test – OXYSTAT Assay | BI-5007

Quick and easy assay to measure total peroxides in biological fluids.

• Method – colorimetric assay, 96 wells
• Sample type – serum, plasma, biological fluids
• Sample volume – 10µl/well
• Assay time – 15 min
• Detection range – 0 – 660 µmol/l
• Sensitivity – 7 µmol/l
• Use – Research use only
• Widely cited in over 60 publications

 Protocol booklet and MSDS

Results indicate a direct relationship between free radicals and circulating biological peroxides, enabling the assessment of oxidative status in biological samples.

 

Literature

1. Cardiovascular diseases (CVDs). World Health Organization; 2025.
2. Free radicals and oxidative stress: Mechanisms and therapeutic targets. Hassan HA, Ahmed HS, Hassan DF. Hum Antibodies. 2024;32(4):151-167. doi: 10.3233/HAB-240011. PMID: 39031349.
3. Interplay of oxidative stress, cellular communication and signaling pathways in cancer. Iqbal MJ, Kabeer A, Abbas Z, Siddiqui HA, Calina D, Sharifi-Rad J, Cho WC. Cell Commun Signal. 2024 Jan 2;22(1):7. doi: 10.1186/s12964-023-01398-5. PMID: 38167159; PMCID: PMC10763046.
4. Oxidative Stress: Pathogenetic Role in Diabetes Mellitus and Its Complications and Therapeutic Approaches to Correction. Darenskaya MA, Kolesnikova LI, Kolesnikov SI. Bull Exp Biol Med. 2021 May;171(2):179-189. doi: 10.1007/s10517-021-05191-7. Epub 2021 Jun 26. PMID: 34173093; PMCID: PMC8233182.
5. Mechanisms of Oxidative Stress in Metabolic Syndrome. Masenga SK, Kabwe LS, Chakulya M, Kirabo A. Int J Mol Sci. 2023 Apr 26;24(9):7898. doi: 10.3390/ijms24097898. PMID: 37175603; PMCID: PMC10178199.
6. Oxidative stress: The core pathogenesis and mechanism of Alzheimer’s disease. Bai R, Guo J, Ye XY, Xie Y, Xie T. Ageing Res Rev. 2022 May;77:101619. doi: 10.1016/j.arr.2022.101619. Epub 2022 Apr 5. PMID: 35395415.
7. The Role of Oxidative Stress in Atherosclerosis. Batty M, Bennett MR, Yu E. Cells. 2022 Nov 30;11(23):3843. doi: 10.3390/cells11233843. PMID: 36497101; PMCID: PMC9735601.
8. Oxidative Stress in Cardiovascular Diseases. Dubois-Deruy E, Peugnet V, Turkieh A, Pinet F. Antioxidants (Basel). 2020 Sep 14;9(9):864. doi: 10.3390/antiox9090864. PMID: 32937950; PMCID: PMC7554855.
9. Pathophysiology of Atherosclerosis. Jebari-Benslaiman S, Galicia-García U, Larrea-Sebal A, Olaetxea JR, Alloza I, Vandenbroeck K, Benito-Vicente A, Martín C. Int J Mol Sci. 2022 Mar 20;23(6):3346. doi: 10.3390/ijms23063346. PMID: 35328769; PMCID: PMC8954705.
10. Oxidized LDL and anti-oxidized LDL antibodies in atherosclerosis – Novel insights and future directions in diagnosis and therapy. Hartley A, Haskard D, Khamis R. Trends Cardiovasc Med. 2019 Jan;29(1):22-26. doi: 10.1016/j.tcm.2018.05.010. Epub 2018 Jun 4. PMID: 29934015.

11. Overview of Clinical Relevance of Antibodies Against Oxidized Low-Density Lipoprotein (oLAb) Within Three Decades by ELISA Technology. Antioxidants (Basel). Wonisch W, Tatzber F, Lindschinger M, Falk A, Resch U, Mörkl S, Zarkovic N, Cvirn G 2024 Dec 19;13(12):1560. doi: 10.3390/antiox13121560. PMID: 39765889; PMCID: PMC11672888.

 

NT-proBNP at Dialysis Initiation-Predictor of Heart Disease Hospitalization: Patients with end-stage kidney disease (ESKD) face a cardiovascular (CV) death risk approximately 10 to 20 times higher than that of the general population. Cardiac biomarkers serve as a valuable tool to predict CV morbidity and mortality in asymptomatic individuals.

About NT-proBNP

N-terminal pro-BNP (NT-proBNP) is a biomarker released by the heart in response to ventricular stretch and stress. It is commonly used to diagnose and manage heart failure, as elevated levels indicate cardiac dysfunction. NT-proBNP levels can also provide prognostic information regarding cardiovascular risk and outcomes in various conditions, including coronary artery disease, sepsis, and in patients with end-stage kidney disease (1).

NT-proBNP at Dialysis Initiation-Predictor of Heart Disease Hospitalization

A study by Shimohata H. et al, investigated if NT-proBNP measurement at the initiation of dialysis therapy is useful to predict later hospitalization for ischemic heart disease (IHD). The results demonstrated that NT-proBNP measurement at the initiation of dialysis therapy is useful to predict later hospitalization for IHD .

NT-pro BNP level at dialysis initiation is a useful biomarker for predicting hospitalization for ischemic heart disease.

NT-proBNP was measured with the ELISA assay from BIOMEDICA

NT-proBNP ELISA assay kit (cat. no. SK-1204)

EASY – simple 2 step protocol, can be run in every lab
CONVENIENT – high and low kit controls included 
RELIABLE – validated according to international quality guidelines (see validation data )
TRUSTED – widely cited in 140 publications

 

Related Products:

Rat NT-proBNP ELISA (cat. no. BI-1204R)

BNP Fragment EIA (cat. no. 20852W)

 

Literature

1. NT-pro BNP level at dialysis initiation is a useful biomarker for predicting hospitalization for ischemic heart disease. Shimohata H, Usui J, Tawara-Iida T, Ebihara I, Ishizu T, Maeda Y, Kobayashi H, Numajiri D, Kaneshige A, Sega M, Yamashita M, Ohgi K, Maruyama H, Takayasu M, Hirayama K, Kobayashi M, Yamagata K; Study Group of the Ibaraki Dialysis Initiation Cohort Study. Clin Exp Nephrol. 2024 May;28(5):457-464. doi: 10.1007/s10157-023-02442-x.
2. Association of NT-proBNP and BNP With Future Clinical Outcomes in Patients With ESKD: A Systematic Review and Meta-analysis. Harrison TG, Shukalek CB, Hemmelgarn BR, Zarnke KB, Ronksley PE, Iragorri N, Graham MM, James MT. Am J Kidney Dis. 2020 Aug;76(2):233-247. doi: 10.1053/j.ajkd.2019.12.017. Epub 2020 May 6. PMID: 32387090.

 

Abstract

Background: Patients with end-stage kidney disease (ESKD) are at high risk of cardiovascular disease including stroke, heart failure, and ischemic heart disease (IHD). To prevent the occurrence and progression of CVD, a reliable prognostic cardiac biomarker is essential. We investigated the prognostic value of NT-proBNP for each incident type of CVD.

Methods: Male patients from the Ibaraki Dialysis Initiation Cohort (iDIC) study with preserved serum samples from dialysis initiation day (n = 212) were analyzed. Patients were classified into four groups according to quartiles of baseline NT-pro BNP levels. The relationship between NT-proBNP levels at the initiation of dialysis and the subsequent incidence of hospitalization events due to IHD, heart failure, and stroke was analyzed.

Results: The incidence rate for hospitalization due to IHD was significantly higher in the highest NT-proBNP category (Log rank p = 0.008); those of stroke and heart failure showed no significant differences among quartiles. Cox proportional hazards regression analysis revealed that serum NT-proBNT was the only prognostic factor for hospitalization for IHD after adjustment by major known IHD risk factors. (HR, 1.008; 95% confidence interval, 1.002-1.014; p = 0.01) The ROC curve analysis for the incidence of hospitalization due to IHD showed that NT-proBNP had an area under the curve (AUC) of 0.759 (95% CI 0.622-0.897; p = 0.004) at a cut-off value of 956.6 pg/mL.

Conclusion: NT-proBNP measurement at the initiation of dialysis therapy is useful to predict later hospitalization for IHD.

 

 

Big Endothelin-1 (Big ET-1) is the precursor to the most potent vasoconstrictor peptide Endothelin-1 (ET-1), which is mainly produced by endothelial cells (1). Interestingly, there is evidence of stimulated ET-1 release from various immune cells, including macrophages and dendritic cells, indicating that these cells can also synthesize ET-1 (2).

While ET-1 is essential in regulating vascular tone and blood pressure, Big ET-1 itself is biologically inactive and mainly functions as a reservoir for ET-1. Big ET-1 has a longer half-life compared to ET-1 and circulates in equal molar amounts, making it a more stable and reliable biomarker (3). Elevated levels of Big ET-1 can signal vascular dysfunction and are linked to cardiovascular conditions such as hypertension and heart failure (4).

Prognostic value of Big Endothelin-1 in heart failure

A study recently explored the prognostic value of Big ET-1 in 4,368 patients hospitalized with heart failure with a median follow-up of 875 days (5).

Key findings:

• Elevated Big ET-1 was independently associated with cardiovascular death in patients with HF.
• Big ET-1 is a promising indicator of HF prognosis.

 

Big Endothelin-1 and NT-proBNP were measured with the following ELISA assay kits:

Big Endothelin-1 ELISA | BI-20082H

• Direct measurement – 50µl serum/plasma per well.
• High Quality – fully validated according to international quality guidelines
• Trusted – cited in over 90 publications
• Protocol booklet click here

 

NT-proBNP ELISA | SK-1204

• Convenient – ready -to-use reagents
• Flexible – can be run in every lab
• Two controls included
• High quality – fully validated according to international quality guidelines
• Trusted- cited in over 140 publications
• Protocol booklet click here

 

 

Literature

1. Endothelin-1 in Health and Disease. Banecki KMRM, Dora KA. Int J Mol Sci. 2023 Jul 10;24(14):11295. doi: 10.3390/ijms241411295. PMID: 37511055; PMCID: PMC10379484.
2. Endothelin-1 in Health and Disease. Banecki KMRM, Dora KA. Int J Mol Sci. 2023 Jul 10;24(14):11295. doi: 10.3390/ijms241411295. PMID: 37511055; PMCID: PMC10379484.
3. Biomarkers in aortic dissection. Wen D, Zhou XL, Li JJ, Hui RT. Clin Chim Acta. 2011 Apr 11;412(9-10):688-95. doi: 10.1016/j.cca.2010.12.039. Epub 2011 Jan 13. PMID: 21237193.
4. Plasma concentration of big endothelin-1 and its relation with plasma NT-proBNP and ventricular function in heart failure patients. Rivera M, Cortés R, Portolés M, Valero R, Sancho-Tello MJ, Martínez-Dolz L, Sevilla B, Taléns-Visconti R, Jordán A, Miró V, Pérez-Boscá JL, Marín F, Climent V, García de Burgos F, Payá R, Sogorb F, Bertomeu V, Salvador A. Rev Esp Cardiol. 2005 Mar;58(3):278-84. Spanish. PMID: 15766450.
5. Prognostic Value of Plasma Big Endothelin-1 in Patients Hospitalized for Heart Failure. Wang J, Feng J, Tse G, Zhai M, Huang Y, Zhou Q, Zhuang X, Liu H, Zhang Y, Zhang J. Korean Circ J. 2025 Aug;55(8):705-717. doi: 10.4070/kcj.2024.0354. Epub 2025 Apr 11. PMID: 40345830; PMCID: PMC12314060.  

 

 

Prognostic Value of Plasma Big Endothelin-1 in Patients Hospitalized for Heart Failure.

Abstract:

Background and objectives: Endothelin-1 (ET-1) is a potent vasoconstrictor and multifunctional neuroendocrine hormone that is closely associated with the pathophysiology of heart failure (HF). Currently, the evidence about the predictive value of big ET-1 in HF remains insufficient. This study aims to investigate the prognostic importance of big ET-1 in HF.

Methods: We examined the incidence of cardiovascular death in a single-center retrospective cohort of HF (de novo, worsening, or chronic included).

Results: The 4,368 hospitalized HF patients were enrolled. During the median follow-up of 875 (365-1,400) days, 851 (19.5%) patients had primary outcome events. Big ET-1 was independently associated with cardiovascular death as a continuous variable (hazard ratio [HR], 1.13; 95% confidence interval [CI], 1.06-1.21; p<0.001) and by tertiles (HR, 1.35; 95% CI, 1.06-1.72; p=0.017 for tertile 2 and HR, 1.70; 95% CI, 1.32-2.19; p<0.001 for tertile 3). This pattern of risk was maintained after further adjustment for NT-proBNP (HR, 1.11; 95% CI, 1.03-1.19; p=0.006 for continuous variable, HR, 1.30; 95% CI, 1.02-1.67; p=0.035 for tertile 2, and HR, 1.69; 95% CI, 1.23-2.05; p=0.034 for tertile 3). Net reclassification index (NRI) and integrated discrimination improvement (IDI) analysis showed that big ET-1 provided additional predictive power in combination with NT-proBNP (NRI, 0.11; 95% CI, 0.04-0.17; p=0.012 and IDI, 0.012; 95% CI, 0.003-0.017; p<0.001).

Conclusions: Elevated big ET-1 was independently associated with cardiovascular death in patients with HF. Big ET-1 may be a promising indicator of HF prognosis. In combination with NT-proBNP, big ET-1 may provide incremental predictive information.

 

 

 

 

 

 

 

 

 

 

February is designated as “Heart Month,” a time to raise awareness about cardiovascular health, promoting healthy lifestyles, and encouraging prevention of heart disease. It aims to educate the public on the risk factors, symptoms, and treatments associated with heart-related conditions, highlighting the importance of maintaining a healthy heart through proper nutrition, regular exercise, avoiding smoking, managing stress, and monitoring blood pressure and cholesterol levels (1-3).

HEART MONTH – focusing on heart health and prevention

Biomarkers in cardiovascular disease

Biomarkers can serve as biochemical indicators that offer crucial insights into disease prognosis and progression, and in predicting the response to treatments. Biomarkers are also utilized in clinical trials or applied in toxicology, including preclinical drug safety evaluations. Advances in biomarker research have transformed how heart conditions are diagnosed and managed (4).

Biomedica offers a wide range of ELISA kits for the accurate measurement of biomarkers related to heart and cardiovascular diseases including NT-proBNP, Big Endothelin-1, FGF23, and markers related to oxidative stress.

• NT-proBNP – human (cat. no. SK-1204)
• NT-proBNP- rat  (cat. no. BI-1204R)
• NT-proANP – human, rodent (cat. no. BI-20892 )
• Big Endothelin-1 (cat. no. BI-20082H)
• FGF23 intact (cat. no. BI-20700)
• FGF23 c-terminal (cat. no. BI-20702)
• Endostatin
• Oxidized LDL (low density lipoprotein) antibodies, oLAB – (BI-20032)
• IL-6 (cat. no. BI-IL6)

 

NT-proBNP ∙ NT-proANP ∙ BigET-1 ∙ FGF23 ∙ Endostatin ∙ LRG1 ∙ oxLDL Antibodies ∙ IL-6

 

NT-proBNP (N-terminal pro b-type natriuretic peptide) is the inactive amino-terminal fragment cleaved from proBNP, a prohormone produced predominantly by ventricular myocytes in response to increased myocardial wall stress and volume overload. Due to its stability and longer half-life compared to active BNP, NT-proBNP serves as a sensitive and specific biomarker for the diagnosis of heart failure.  NT-proBNP is commonly used in the diagnosis and management of heart failure, reflecting increased intracardiac pressures and ventricular dilation (5-7). It aids in differentiating cardiac from non-cardiac causes of dyspnea, stratifying disease severity, guiding therapeutic decisions, and predicting morbidity and mortality outcomes in heart failure patients (8).

NT-proANP (N-terminal pro-atrial natriuretic peptide) is a biomarker released by the heart in response to atrial stretching and elevated blood volume. It is utilized to evaluate heart failure and detect cardiac stress, helping in the diagnosis and management of various cardiovascular conditions (9).

Big Endothelin-1 (Big ET-1) is a vasoconstrictive peptide and the precursor to Endothelin-1 (ET-1), which is the biologically active form. Elevated levels of Big ET-1 serve as an independent marker of heart failure in cases of congestive heart disease (10). Due to its longer half-life compared to ET-1 and its presence in circulation in equimolar amounts with ET-1, Big ET-1 is considered a more reliable biomarker.

Fibroblast Growth Factor-23 (FGF23) is a hormone involved in regulating phosphate metabolism. It has emerged as a potential biomarker for cardiovascular risk, with elevated circulating FGF23 levels being linked to adverse outcomes such as heart failure and arrhythmias (11, 12).

Endostatin, a fragment derived from collagen XVIII, is an extracellular matrix protein that plays a crucial role in the development of chronic kidney and heart diseases. In this study by Yaghoubi A et al, Endostatin levels were found to be elevated in patients hospitalized with acute dyspnea who had a history of chronic heart failure (CHF), and these elevated levels were associated with increased mortality at 3 months. Additionally, endostatin was linked to both 1-month and 3-month mortality in patients presenting with acute dyspnea who had no previous history of CHF (13, 14).

Leucine-rich alpha-2-glycoprotein (LRG) is a secreted protein that plays a significant role in pathological ocular neovascularization. It is also implicated in various conditions such as cardiovascular disease, diabetes, inflammatory disorders, and cancer. Recent research has identified LRG as an independent predictor of diastolic dysfunction (DD), due to myocardial fibrosis (15).

Oxidized LDL (low density lipoprotein) antibodies, oLAB 

Oxidized LDL (oxLDL) antibodies are directed against epitopes on oxidized low-density lipoprotein particles. OxLDL results from the oxidative modification of native LDL particles, involving lipid peroxidation and protein oxidation, which generate neoantigens recognized as foreign by the immune system (12). The production of anti-oxLDL antibodies, predominantly IgG and IgM subclasses, reflects ongoing oxidative stress and lipid peroxidation processes within atherosclerotic lesions. These antibodies can participate in immune complex formation, potentially influencing atherogenesis through pro-inflammatory or anti-inflammatory mechanisms. Elevated levels of anti-oxLDL antibodies have been correlated with the presence and progression of atherosclerotic plaques, making them valuable biomarkers for cardiovascular disease risk assessment. Their precise role in atherosclerosis pathophysiology remains complex, involving both protective clearance of modified lipoproteins and pro-inflammatory immune responses that may exacerbate vascular injury (16-18).

Interleukin-6 (IL-6)

IL-6 signaling plays a critical role in the inflammatory processes underlying cardiovascular disease (CVD). IL-6 is a cytokine that promotes inflammation, endothelial dysfunction, and plaque formation in atherosclerosis (15). It signals through its receptor complex, activating pathways such as JAK/STAT, which contribute to vascular inflammation and instability. Anti-IL-6 therapeutics, including monoclonal antibodies like tocilizumab, target this cytokine or its receptor to reduce inflammation. These agents have shown potential in lowering cardiovascular risk by modulating inflammatory responses, making IL-6 inhibition a promising strategy for managing CVD associated with chronic inflammation (19, 20).

 

Literature

1. 2021 Dietary Guidance to Improve Cardiovascular Health: A Scientific Statement From the American Heart Association. Lichtenstein AH, Appel LJ, Vadiveloo M, Hu FB, Kris-Etherton PM, Rebholz CM, Sacks FM, Thorndike AN, Van Horn L, Wylie-Rosett J. Circulation. 2021 Dec 7;144(23):e472-e487. doi: 10.1161/CIR.0000000000001031. Epub 2021 Nov 2. PMID: 34724806.
2. A Heart-Healthy Diet for Cardiovascular Disease Prevention: Where Are We Now? Diab A, Dastmalchi LN, Gulati M, Michos ED. Vasc Health Risk Manag. 2023 Apr 21;19:237-253. doi: 10.2147/VHRM.S379874. PMID: 37113563; PMCID: PMC10128075.
3. Physical Activity Over the Lifecourse and Cardiovascular Disease. Perry AS, Dooley EE, Master H, Spartano NL, Brittain EL, Pettee Gabriel K. Circ Res. 2023 Jun 9;132(12):1725-1740. doi: 10.1161/CIRCRESAHA.123.322121. Epub 2023 Jun 8. PMID: 37289900; PMCID: PMC10254078.
4. Advancements in Biomarkers for Early Detection and Risk Stratification of Cardiovascular Diseases-A Literature Review. Nazir A, Nazir A, Afzaal U, Aman S, Sadiq SUR, Akah OZ, Jamal MSW, Hassan SZ. Health Sci Rep. 2025 May 26;8(5):e70878. doi: 10.1002/hsr2.70878. PMID: 40432692; PMCID: PMC12106349.
5. Natriuretic Peptides: Role in the Diagnosis and Management of Heart Failure: A Scientific Statement From the Heart Failure Association of the European Society of Cardiology, Heart Failure Society of America and Japanese Heart Failure Society. Tsutsui H, Albert NM, Coats AJS, Anker SD, Bayes-Genis A, Butler J, Chioncel O, Defilippi CR, Drazner MH, Felker GM, Filippatos G, Fiuzat M, Ide T, Januzzi JL Jr, Kinugawa K, Kuwahara K, Matsue Y, Mentz RJ, Metra M, Pandey A, Rosano G, Saito Y, Sakata Y, Sato N, Seferovic PM, Teerlink J, Yamamoto K, Yoshimura MJ Card Fail. 2023 May;29(5):787-804. doi: 10.1016/j.cardfail.2023.02.009. Epub 2023 Apr 17. PMID: 37117140.
6. Practical algorithms for early diagnosis of heart failure and heart stress using NT-proBNP: A clinical consensus statement from the Heart Failure Association of the ESC. Bayes-Genis A, Docherty KF, Petrie MC, Januzzi JL, Mueller C, Anderson L, Bozkurt B, Butler J, Chioncel O, Cleland JGF, Christodorescu R, Del Prato S, Gustafsson F, Lam CSP, Moura B, Pop-Busui R, Seferovic P, Volterrani M, Vaduganathan M, Metra M, Rosano G. Eur J Heart Fail. 2023 Nov;25(11):1891-1898. doi: 10.1002/ejhf.3036. Epub 2023 Sep 26. PMID: 37712339.
7. Essential biochemistry and physiology of (NT-pro)BNP. Hall C.Eur J Heart Fail. 2004;6:257–260. doi:10.1016/j.ejheart.2003.12.015.
8. Comprehensive Review of Cardiovascular Disease Management: Cardiac Biomarkers, Imaging Modalities, Pharmacotherapy, Surgical Interventions, and Herbal Remedies. Netala VR, Teertam SK, Li H, Zhang Z. A Cells. 2024 Sep 1;13(17):1471. doi: 10.3390/cells13171471. PMID: 39273041; PMCID: PMC11394358.
9. Prognostic value of NT-proANP levels on major cardiovascular outcomes in a 31-year follow-up study depends on baseline morbidity. Sakko S, Perkiömäki J, Ylitalo A, Huikuri H, Ukkola O, Koivunen P, Tapio J. Sci Rep. 2025 May 28;15(1):18660. doi: 10.1038/s41598-025-03819-6. PMID: 40436983; PMCID: PMC12119872.
10. Elevated Plasma Big Endothelin-1 at Admission Is Associated With Poor Short-Term Outcomes in Patients With Acute Decompensated Heart Failure. Mo R, Yang YM, Yu LT, Tan HQ, Zhu J. Front Cardiovasc Med. 2021 Mar 11;8:629268. doi: 10.3389/fcvm.2021.629268. PMID: 33778022; PMCID: PMC7990871.
11. An Overview of FGF-23 as a Novel Candidate Biomarker of Cardiovascular Risk. Vázquez-Sánchez S, Poveda J, Navarro-García JA, González-Lafuente L, Rodríguez-Sánchez E, Ruilope LM, Ruiz-Hurtado G. Front Physiol. 2021 Mar 9;12:632260. doi: 10.3389/fphys.2021.632260. PMID: 33767635; PMCID: PMC7985069.
12. Discharge FGF23 level predicts one year outcome in patients admitted with acute heart failure. Vergaro G, Aimo A, Taurino E, Del Franco A, Fabiani I, Prontera C, Masotti S, Musetti V, Emdin M, Passino C. Int J Cardiol. 2021 Aug 1;336:98-104. doi: 10.1016/j.ijcard.2021.05.028. Epub 2021 May 19. PMID: 34019969.
13. Endostatin in Renal and Cardiovascular Diseases. Li M, Popovic Z, Chu C, Krämer BK, Hocher B. Kidney Dis (Basel). 2021 Sep 9;7(6):468-481. doi: 10.1159/000518221. PMID: 34901193; PMCID: PMC8613550.
14. Association between endostatin and mortality in patients with acute dyspnoea, with or without congestive heart failure: a single-centre, prospective, observational study. Yaghoubi A, Heijl C, Khoshnood AM, Wändell PE, Carlsson AC, Wessman T. BMJ Open. 2025 Jan 11;15(1):e085238. doi: 10.1136/bmjopen-2024-085238. PMID: 39800400; PMCID: PMC11752042.
15. Leucine-Rich Alpha-2-Glycoprotein: A Novel Predictor of Diastolic Dysfunction. Loch A, Tan KL, Danaee M, Idris I, Ng ML. Biomedicines. 2023 Mar 20;11(3):944. doi: 10.3390/biomedicines11030944. PMID: 36979923; PMCID: PMC10045934.
16. Immune response to lipoproteins in atherosclerosis. Samson S, Mundkur L, Kakkar VV. 2012;2012:571846. doi: 10.1155/2012/571846. Epub 2012 Aug 23. PMID: 22957222; PMCID: PMC3432325.
17. Antibodies against human oxidized low-density lipoprotein (LDL) as markers for human plasma modified lipoproteins. Radulescu L, Stancu C, Antohe F. Med Sci Monit. 2004 Jul;10(7):BR207-14. Epub 2004 Jun 29. PMID: 15232494.
18. Oxidized LDL and anti-oxidized LDL antibodies in atherosclerosis – Novel insights and future directions in diagnosis and therapy .Hartley A, Haskard D, Khamis R. Trends Cardiovasc Med. 2019 Jan;29(1):22-26. doi: 10.1016/j.tcm.2018.05.010. Epub 2018 Jun 4. PMID: 29934015.
19. IL-6 and Cardiovascular Risk: A Narrative Review. Mehta NN, deGoma E, Shapiro MD. Curr Atheroscler Rep. 2024 Nov 26;27(1):12. doi: 10.1007/s11883-024-01259-7. PMID: 39589436; PMCID: PMC11599326.
20. Interleukin-6 Signaling and Anti-Interleukin-6 Therapeutics in Cardiovascular Disease. Ridker PM, Rane M. Circ Res. 2021 May 28;128(11):1728-1746. doi: 10.1161/CIRCRESAHA.121.319077. Epub 2021 May 17. PMID: 33998272.

 

 

 

Effect of left atrial appendage closure on heart failure biomarker NT-proANP.

Atrial fibrillation (AF) is the most prevalent cardiac arrhythmia, affecting about 1-2% of the general population. The incidence of AF increases with age and AF carries a five-fold increased risk of cardioembolic events, accounting for roughly 20% of all strokes. Strokes related to AF tend to be more severe, often resulting in worse neurological outcomes (1).  

The left atrial appendage (LAA) is a finger-shaped extension originating from the main body of the left atrium. In AF, thrombus formation often occurs within the LAA due to decreased contractile function and blood flow stasis. 90% of thrombi in nonvalvular AF patients and 57% in valvular AF patients are located in the left atrial appendage (LAA). Though oral anticoagulants serve as the primary treatment for preventing strokes in patients with atrial fibrillation, they are not suitable for all patients due to certain contraindications. Targeting the LAA has emerged as an alternative treatment approach to decrease the risk of stroke or systemic embolism in patients with atrial fibrillation (2-5).

In a study published in 2024, researchers investigated the impact of left atrial appendage (LAA) closure on systemic homeostasis in patients with atrial fibrillation. The study aimed to understand how occluding the LAA influences systemic biomarkers related to coagulation, inflammation, and endothelial function. Results suggest that LAA closure not only reduces stroke risk but may also favorably modulate systemic physiological processes, potentially contributing to improved overall cardiovascular health in these patients (5).

Effect of left atrial appendage closure on heart failure biomarker NT-proANP

In the subanalysis of this trial, researchers also examined the effects of left atrial appendage (LAA) closure on heart failure biomarkers, including NT-proBNP, NT-proANP, Galectin-3, and GDF-15 in patients with atrial fibrillation. The results demonstrated that LAA closure did not significantly influence the levels of HF biomarkers 6 months after the procedure. (6).

In a recent study researchers investigated the hemodynamic and echocardiography changes during and after LAA closure (7). Biomarkers for heart failure were measured including, N-terminal pro-B-type natriuretic peptide (NT-proBNP), N-terminal-pro-atrial natriuretic peptide (NT-proANP) and growth-differentiation factor-15 (GDF-15). The results show that LAA Closure was associated with an acute increase in both rest and postexercise LA pressure. The acute changes during LAAC were explained mostly by the saline and contrast dye given during LAAC and not by the worsening of the reservoir function associated with the procedure. In addition, no increase in NT-proANP and other HF biomarkers or changes in echocardiography parameters after 3 or 6 months after the procedure were observed (7).

About NT-proANP

NT-proANP (N-terminal pro-atrial natriuretic peptide) is a biomarker derived from the precursor of atrial natriuretic peptide (ANP), a hormone produced primarily by the atria of the heart. It plays a key role in regulating blood pressure, blood volume, and electrolyte balance by promoting natriuresis (excretion of sodium) and vasodilation.

Elevated levels of NT-proANP are often associated with conditions involving increased atrial pressure and volume overload, such as heart failure, atrial fibrillation, and other cardiac dysfunctions. Because it is relatively stable and easier to measure than active ANP, NT-proANP is frequently used in clinical settings to assess and monitor cardiac function.

About NT-proBNP

NT-proBNP (N-terminal pro-B-type natriuretic peptide) is a biomarker released from the heart in response to increased wall stress, typically due to conditions like heart failure. It is a non-active fragment of the prohormone BNP (B-type natriuretic peptide), which is produced mainly by the ventricles of the heart when they are under strain.

Elevated levels of NT-proBNP are indicative of cardiac stress and are commonly used in clinical practice to diagnose, assess the severity, and monitor the progression of heart failure. It also helps differentiate cardiac from non-cardiac causes of symptoms such as shortness of breath. Because NT-proBNP is stable in blood samples and has a longer half-life than BNP, it is a reliable biomarker for evaluating cardiac function across various clinical settings.

 

NT proANP ELISA (cat. No. BI-20892) Assay Kit

• CONVENIENT – small sample volume – 10 µl / well
• HIGH QUALITY kit – full validation package
• TRUSTED – cited in over 175 publications
• EASY – color coded and ready to use reagents
• FLEXIBLE- assay is suitable for human and non-human samples (rodents and others)

 

NT-proBNP (cat. no. SK-1204) ELISA Assay Kit

• TRUSTED – widely cited in over 140 publications 
• HIGH QUALITY kit – fully validated assays following international quality guidelines
• CONVENIENT – kits include pre-diluted calibrators and 2 controls

 

RAT NT-proBNP ELISA (BI-1204R) Assay Kit

• CONVENIENT – 10µl sample/well, kit control included
• TRUSTED – sample values provided

 

 

 Literature 

1. Left Atrial Appendage Closure and Systemic Homeostasis: The LAA HOMEOSTASIS Study. Lakkireddy D, Turagam M, Afzal MR, Rajasingh J, Atkins D, Dawn B, Di Biase L, Bartus K, Kar S, Natale A, Holmes DJ Jr.J Am Coll Cardiol. 2018 Jan 16;71(2):135-144. doi: 10.1016/j.jacc.2017.10.092. Erratum in: J Am Coll Cardiol. 2018 Feb 6;71(5):590. doi: 10.1016/j.jacc.2018.01.005. PMID: 29325636.
2. The Left Atrial Appendage: Target for Stroke Reduction in Atrial Fibrillation. Ramlawi B, Abu Saleh WK, Edgerton J. Methodist Debakey Cardiovasc J. 2015 Apr-Jun;11(2):100-3. doi: 10.14797/mdcj-11-2-100. PMID: 26306127; PMCID: PMC4547664.
3. The left atrial appendage: anatomy, function, and noninvasive evaluation. Beigel R, Wunderlich NC, Ho SY, Arsanjani R, Siegel RJ. JACC Cardiovasc Imaging. 2014 Dec;7(12):1251-65. doi: 10.1016/j.jcmg.2014.08.009. PMID: 25496544.
4. Left atrial appendage exclusion in atrial fibrillation. Rozen G, Margolis G, Marai I, Roguin A, Rahamim E, Planer D, Heist EK, Amir O, Tahiroglu I, Ruskin J, Mansour M, Elbaz-Greener G. Front Cardiovasc Med. 2022 Sep 13;9:949732. doi: 10.3389/fcvm.2022.949732. PMID: 36176999; PMCID: PMC9513198.
5. Left atrial appendage closure for stroke prevention in atrial fibrillation: current status and perspectives. Landmesser U, Skurk C, Tzikas A, Falk V, Reddy VY, Windecker S. Eur Heart J. 2024 Aug 21;45(32):2914-2932. doi: 10.1093/eurheartj/ehae398. PMID: 39027946; PMCID: PMC11335376.
6. The effect of left atrial appendage closure on heart failure biomarkers: A PRAGUE-17 trial subanalysis. Herman D, Osmancik P, Neuzil P, Hala P, Lekesova V, Benesova K, Hozman M, Jarkovsky J, Novackova M, Widimsky P, Reddy VY; PRAGUE-17 Trial Investigators. J Cardiovasc Electrophysiol. 2021 Oct;32(10):2645-2654. doi: 10.1111/jce.15206. Epub 2021 Aug 26. PMID: 34402135.
7. Acute and Short‐Term Hemodynamic and Echocardiography Changes During and After Left Atrial Appendage Closure. Dalibor Herman, Petr Peichl, Marek Hozman, Bronislav Janek, Tomas Knize, Teodora Vichova, Hana Linkova, Jana Vesela, Jakub Karch, Naďa Valosková, Eva Borisincova, Pavel Osmancik, J Interventional Cardiology, Dec. 2025. https://doi.org/10.1155/joic/5515180Digital Object Identifier (DOI)

Children and adolescents with type 1 diabetes (T1D) frequently encounter issues related to bone health. Research consistently shows that young individuals with T1D have lower bone mineral density (BMD) than their healthy counterparts. Moreover, children with T1D exhibit compromised bone microarchitecture and decreased bone turnover. Together, these factors heighten the risk of fractures throughout their lifetime (1). In addition, advanced imaging techniques have revealed that the negative impact of T1D on the growing skeleton goes beyond reduced bone density, affecting bone size, shape, and strength (2).

Type 1 diabetes in adolescents linked to low bone mass and altered bone biomarkers

In a recent study, researchers investigated whether adolescents with well-controlled, long-duration type 1 diabetes (T1D) have differences in bone mass and bone biomarkers in comparison with healthy individuals (3). The researchers measured various biomarkers including receptor activator nuclear factor κB ligand (RANKL*), Osteoprotegerin (OPG*), Sclerostin (SOST*), and C-terminal telopeptide of type I collagen (CTX).

Highlights

• Type 1 diabetes (T1D) is linked to a higher risk of fractures.
• Prolonged T1D leads to low bone mass and impaired microarchitecture.
• The T1D group showed decreased levels of RANKL and CTX.

 

In summary: young people with long-term T1D show decreased gain in bone mass, impaired microarchitecture, and suppressed RANKL-driven osteoclast formation, leading to decreased bone resorption. Monitoring bone health is recommended for adolescents with T1D.

*Biomedica ELISA kits were used in this study.

BIOMEDICA´s ELISA kit highlights:
• Widely cited in clinical studies
• Reliable – validated according to international guidelines
• High sensitivity – measurable concentrations in healthy subjects
• HIGH quality guaranteed 

FREE soluble RANKL HS ELISA | BI-20462

•  High sensitivity – measurable concentrations in healthy subjects
• Only ELISA that measures free, uncomplexed soluble RANKL

 

 

Literature

1. Bone Health in Children and Adolescents with Type 1 Diabetes: Optimizing Bone Accrual and Preventing Fractures. Levran N, Shalev-Goldman E, Levy-Shraga Y. Nutrients. 2025 Jul 23;17(15):2400. doi: 10.3390/nu17152400. PMID: 40805986; PMCID: PMC12348532.
2. Bone accrual in children and adolescents with type 1 diabetes: current knowledge and future directions. Weber DR Curr Opin Endocrinol Diabetes Obes. 2021 Aug 1;28(4):340-347. doi: 10.1097/MED.0000000000000638. PMID: 33965967.
3. Adolescents with long-duration type 1 diabetes have low bone mass and reduced levels of bone indices reflecting altered bone resorption. Swolin-Eide D, Pundziute Lyckå A, Novak D, Andersson B, Forsander G, Magnusson P.Bone. 2025 Oct;199:117560. doi: 10.1016/j.bone.2025.117560. Epub 2025 Jun 4. PMID: 40480641.

Intense exercise and load carriage can lead to high mechanical and metabolic stress on the skeleton, disrupting calcium metabolism (1). Studies have shown that load carriage exercise increases calcium absorption and retention in healthy young women (2). Integrating women into military service necessitates research on gender-specific effects of military training and operational activities (3). In a randomized controlled crossover trial researchers investigated the effect of calcium supplementation on calcium and bone metabolism in women during load carriage (1).  

The effect of calcium supplementation on bone calcium balance and calcium and bone metabolism during load carriage in women: a randomized controlled crossover trial. Coombs CV et al., 2025.

Study details:

• a total of 48 women volunteered for the study, including 38 military personnel and 10 civilians.
• each participant completed two load carriage exercise sessions in a randomized order:

•  One session after taking a 1000 mg calcium supplement, 60 minutes prior to load carriage
•  One session without any supplement (control)

• during each session, participants walked 12.8 km on a treadmill at a speed of 6.4 km/h for 120 minutes while carrying a 20 kg rucksack.

Calcium supplementation and bone health in woman during load carriage

Key findings:

• Intense exercise stresses the skeleton and disrupts calcium metabolism.
• Calcium supplementation leads to increased serum ionized calcium, reduced PTH levels, and decreased bone resorption.
• Calcium supplementation had no effect on markers of bone formation, including Sclerostin.
• Taking 1000 mg of calcium 60 minutes before load carriage helps protect bone health and calcium balance.

 

SCLEROSTIN was measured with the BIOMEDICA Sclerostin assay:

Sclerostin (SOST) ELISA  (cat. no. BI-20492)

• Most referenced Sclerostin ELISA in over 330 citations
• Low sample volume – 20µl / well
• Full validation package – download here

 

 

Related products:

Bioactive Sclerostin ELISA (cat. no. BI-20472)

OPG – Osteoprotegerin ELISA (cat. no. BI-20403)

FREE soluble RANKL HS ELISA (cat. no BI-20462)

 

Literature:

1. The effect of calcium supplementation on bone calcium balance and calcium and bone metabolism during load carriage in women: a randomized controlled crossover trial. Coombs CV, Greeves JP, Young CD, Irving AS, Eisenhauer A, Kolevica A, Heuser A, Tang JCY, Fraser WD, O’Leary TJ. J Bone Miner Res. 2025 Jun 3;40(6):753-765. doi: 10.1093/jbmr/zjaf004. PMID: 39804018.
2. Load carriage exercise increases calcium absorption and retention in healthy young women. Gaffney-Stomberg E, Nakayama AT, Lutz LJ, McClung JP, O’Brien KO, Staab JS. J Bone Miner Res. 2024 Mar 4;39(1):39-49. doi: 10.1093/jbmr/zjad003. PMID: 38630876.
3. Load carriage changes tibiofemoral arthrokinematics during ambulatory tasks in recruit-aged women. Johnson CC, Dzewaltowski AC, Dever DE, Krajewski KT, Rai A, Ahamed NU, Allison KF, Flanagan SD, Graham SM, Lovalekar M, Anderst WJ, Connaboy C. Sci Rep. 2024 Apr 25;14(1):9542. doi: 10.1038/s41598-024-60187-3. PMID: 38664550; PMCID: PMC11045865.