Download biomedica product listResearchers have identified the c-terminal fragment of the phosphate regulating hormone FGF23 (cFGF23) to better predict the risk of graft loss in kidney transplant recipients (KTRs) than its biologically active form (intact FGF23). The prospective observational cohort study included 562 maintenance KTRs with a median follow-up of 4 years.
C-terminal and intact FGF23 in kidney transplant recipients and their associations with overall graft survival. Chu C et al.,BMC Nephrology (2021) 22:125.
FGF23 (intact) and FGF23 (C-terminal) can reliably be measured by ELISA
√ CE-marked – for IVD use in the EU
√ CORRELATE with existing ELISA methods
√ Excellent stability in all matrices
√ For plasma & serum
√ HIGH QUALITY – fully validated according to international guidelines (ICH/FDA/EMEA)
Researchers have identified the soluble WNT pathway inhibitor SCLEROSTIN as an independent risk factor for all-cause #mortality in patients after kidney transplantation.
600 stable renal transplant recipients were followed for all-cause mortality for 3 years.
Sclerostin is an independent risk factor for all-cause mortality in kidney transplant recipients.
Zeng S et al., Clin Exp Nephrology (2020). Click link for full text.
Biomedica Sclerostin ELISA: https://www.bmgrp.com/product/cardiovascular/sclerostin-elisa-human-sost-biomedica/
√ HIGH QUALITY – fully validated assay according to ICH/FDA/EMEA guidelines
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√ MOST REFERENCED Sclerostin ELISA
Also available: Bioactive Sclerostin ELISA https://www.bmgrp.com/product/cardiovascular/biomedica-bioactive-sclerostin-elisa-human-sost/
√ specific antibodies targeting the receptor binging region
The expression level of klotho decreases in patients with #CKD (chronic kidney disease) and is accompanied by renal disorders.
In rodent models with CKD, #KLOTHO deficiency causes high circulating levels of phosphate and vascular calcification. Conversely, overexpression of klotho can enhance phosphaturia, improve renal function, and reduce calcification.
In CKD, KLOTHO levels start declining due to altered activin and ActRIIA signalling. This in turn limits KLOTHO’s regulation of FGF23 production and leaves #hyperphosphataemia as the principal regulator of FGF23 secretion in CKD.
Since KLOTHO levels change at an early stage of CKD, KLOTHO is a sensitive biomarker for the decline in kidney function.
To learn more about the mechanism of KLOTHO signalling check out https://bmcnephrol.biomedcentral.com/articles/10.1186/s12882-018-1094-z.
Learn more about our KLOTHO assay
- CE-certified
- convenient (direct measurement, 10µl sample/well only)
- highly specific
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C4d has been regarded as an indirect footprint of an antibody-mediated response against an allograft. While C4d has emerged as a potential marker for antibody-mediated-rejection (AMR) after transplantation over the last decade, its use as a prognostic tool is still under debate.
A recent study has shown a positive association of C4d with cardiac allograft vasculopathy and death in heart transplant recipients. Late C4d positivity (> 1-year post-transplant) demonstrated an even higher risk for developing cardiac allograft vasculopathy and poor prognosis than early C4d positivity (within 1 year). The authors of the study suggest a prognostic role for C4d in heart transplantation warranting routine long-term detection of this marker in the pathologic evaluation of cardiac AMR.
Biomedica’s Anti C4d Antibodies allow the identification of human complement split product C4d in paraffin and frozen sections, and by flow cytometry.
Husain et al. Routine C4d immunohistochemistry in cardiac allografts: Long-term outcomes. J Heart Lung Transplant 2017: 36(12):1329-1335
Check out the Biomedica anti-C4d antibodies for ICH and FITC.