Fluorescence of Beta-2-microglobulin in the Spent Dialysate

Beta 2-microglobulin (ß2-m) accumulation represents a possible complication of long term dialysis. It is therefore important to evaluate the capacity of removal of this molecule from the patient by different dialysis membranes. The present study is aimed at evaluating the mechanisms involved in ß2-m removal by three different synthetic membranes: a) highly asymmetric hydrophobic polysulfone (Biosulfane, NMC), b) moderately asymmetric and hydrophobic polysulfone (PS600, Fresenius), c) Polyacylonitrile (AN69HF, Hospal). The adsorption capacity and sieving coefficients of the three membranes for native and labeled ß2-m were studied in vitro utilizing human blood. The amount adsorbed by the membrane was measured by the elution of the molecule obtained with a detergent solution. Clearances, total removal and membrane adsorption were studied in six patients treated in a randomized sequence with the three membranes. For this purpose, plasma and dialysate measurements as well as total collection of spent dialysate and ß2-m elution from the used dialyzers were carried out. Ex novo generation of ß2-m did not take place during in vitro circulation. The molecule was removed by the studied membranes both by filtration and adsorption. The Biosulfane membrane removed ß2-m mostly by adsorption while the PS600 membrane removed ß2-m almost entirely by filtration. Intermediate behaviour was shown by AN69 membrane. Similar quantities of ß2-m were removed from the patients with the three membranes. Total removal could only be precisely measured by adding the quantity of ß2-m eluted from the membrane to the amount recovered in the spent dialysate. Out of total removal, adsorption was more than 90% with Biosulfane, while only 5% with the PS600. These findings contribute to the understanding of the discrepancy found between the clearance measured from the plasma side and that measured from the dialysate side. In conclusion, clearance and sieving measurements for ß2-m cannot be correctly performed unless the capacity of adsorption of the membrane is taken into account.

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Optical Estimation of Beta 2 Microglobulin during Hemodiafiltration - Does It Work?

Blood Purification ◽

10.1159/000381797 ◽

2015 ◽

Vol 40 (2) ◽

pp. 113-119 ◽

Cited By ~ 3

Author(s):

Fredrik Uhlin ◽

Jana Holmar ◽

Pia Yngman-Uhlin ◽

Anders Fernström ◽

Ivo Fridolin

Keyword(s):

Correlation Analysis ◽

Uv Radiation ◽

Relative Error ◽

The Other ◽

Uv Absorbance ◽

Dialysis Dose ◽

Spent Dialysate ◽

Beta 2 ◽

Beta 2 Microglobulin ◽

Surrogate Substances

Background: Currently, urea reduction seems to be the most widely used dialysis dose parameter. The aim of this study was to investigate the possibility to monitor beta 2-microglobulin (β2-M) elimination by utilizing the ultraviolet (UV) absorbance of spent dialysate. Methods: Blood and spent dialysate were collected during two week's sessions in 8 patients, one week in hemodialysis (HD) and one in hemodiafiltration (HDF). Correlation analysis between UV-wavelengths and concentrations of solutes in spent dialysate was performed. The reduction ratio (RR) of concentrations in blood, dialysate and UV-absorbance were compared. Results: Differences between HD and HDF were discovered in wavelength correlation maxima for the solutes. Relative error in RR (%) was larger (p < 0.05) for β2-M than for the other solutes. The most reasonable explanation is that β2-M does not absorb UV-radiation; instead, the absorbance of surrogate substances is measured. Conclusion: A high correlation between UV-absorbance and β2-M can be achieved for HDF but not for HD. Still, UV-absorbance could perhaps be used in solely HDF mode for estimation of β2-M removal.

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Beta-2 Microglobulin (B2 M) Genomic Alterations and Absent Protein Expression in Pediatric and Adolescent Classical Hodgkin Lymphoma

Klinische Pädiatrie ◽

10.1055/s-0034-1371104 ◽

2014 ◽

Vol 226 (02) ◽

Cited By ~ 1

Author(s):

L Giulino-Roth ◽

J Reichel ◽

J Teruya-Feldstein ◽

W Tam ◽

Y Tam ◽

...

Keyword(s):

Protein Expression ◽

Hodgkin Lymphoma ◽

Classical Hodgkin Lymphoma ◽

Genomic Alterations ◽

Beta 2 ◽

Beta 2 Microglobulin

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Faculty Opinions recommendation of Activation of nonclassical CD1d-restricted NK T cells induces airway hyperreactivity in beta 2-microglobulin-deficient mice.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.1122835.579924 ◽

2008 ◽

Author(s):

Santa Jeremy Ono

Keyword(s):

T Cells ◽

Airway Hyperreactivity ◽

Nk T Cells ◽

Beta 2 ◽

Beta 2 Microglobulin ◽

Deficient Mice

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Quantitative determination of the beta-2-microglobulin monomer by gel filtration chromatography

Chinese Journal of Chromatography ◽

10.3724/sp.j.1123.2018.11028 ◽

2019 ◽

Vol 37 (5) ◽

pp. 533

Author(s):

Xiaobo BAO ◽

Jun REN ◽

Yufeng WANG ◽

Lingyun JIA

Keyword(s):

Quantitative Determination ◽

Gel Filtration ◽

Gel Filtration Chromatography ◽

Beta 2 ◽

Beta 2 Microglobulin

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Serial Quantification of Urinary Protein Biomarkers to Predict Drug-induced Acute Kidney Injury

Current Drug Metabolism ◽

10.2174/1389200220666190711114504 ◽

2019 ◽

Vol 20 (8) ◽

pp. 656-664 ◽

Cited By ~ 4

Author(s):

Yi Da ◽

K. Akalya ◽

Tanusya Murali ◽

Anantharaman Vathsala ◽

Chuen-Seng Tan ◽

...

Keyword(s):

Acute Kidney Injury ◽

Cystatin C ◽

Calcineurin Inhibitors ◽

Kidney Injury ◽

Tubular Dysfunction ◽

Renal Tubular Dysfunction ◽

Protein Biomarkers ◽

Drug Induced ◽

Beta 2 ◽

Beta 2 Microglobulin

Background: : Drug-induced Acute Kidney Injury (AKI) develops in 10-15% of patients who receive nephrotoxic medications. Urinary biomarkers of renal tubular dysfunction may detect nephrotoxicity early and predict AKI. Methods:: We prospectively studied patients who received aminoglycosides, vancomycin, amphotericin, or calcineurin inhibitors, and collected their serial urine while on therapy. Patients who developed drug-induced AKI (fulfilling KDIGO criteria) were matched with non-AKI controls in a 1:2 ratio. Their urine samples were batch-analyzed at time-intervals leading up to AKI onset; the latter benchmarked against the final day of nephrotoxic therapy in non- AKI controls. Biomarkers examined include clusterin, beta-2-microglobulin, KIM1, MCP1, cystatin-C, trefoil-factor- 3, NGAL, interleukin-18, GST-Pi, calbindin, and osteopontin; biomarkers were normalized with corresponding urine creatinine. Results:: Nine of 84 (11%) patients developed drug-induced AKI. Biomarkers from 7 AKI cases with pre-AKI samples were compared with those from 14 non-AKI controls. Corresponding mean ages were 55(±17) and 52(±16) years; baseline eGFR were 99(±21) and 101(±24) mL/min/1.73m2 (all p=NS). Most biomarker levels peaked before the onset of AKI. Median levels of 5 biomarkers were significantly higher in AKI cases than controls at 1-3 days before AKI onset (all µg/mmol): clusterin [58(8-411) versus 7(3-17)], beta-2-microglobulin [1632(913-3823) versus 253(61-791)], KIM1 [0.16(0.13-0.76) versus 0.07(0.05-0.15)], MCP1 [0.40(0.16-1.90) versus 0.07(0.04-0.17)], and cystatin-C [33(27-2990) versus 11(7-19)], all p<0.05; their AUROC for AKI prediction were >0.80 (confidence intervals >0.50), with average accuracy highest for clusterin (86%), followed by beta-2-microglobulin, cystatin-C, MCP1, and KIM1 (57%) after cross-validation. Conclusion: : Serial surveillance of these biomarkers could improve the lead time for nephrotoxicity detection by days.

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