scholarly journals Levels of Beta-2 Microglobulin and Cystatin C in Beta Thalassemia Major Patients

2015 ◽  
Vol 6 (3) ◽  
Author(s):  
Ayse Gonca Kacar
Keyword(s):  
Cystatin C ◽  
Thalassemia Major ◽  
Beta Thalassemia ◽  
Beta Thalassemia Major ◽  
Beta 2 ◽  
Beta 2 Microglobulin

scholarly journals Role of serum cystatin-C and beta-2 microglobulin as early markers of renal dysfunction in children with beta thalassemia major

2017 ◽  
Vol Volume 10 ◽  
pp. 261-268 ◽  
Author(s):  
Ola Galal Behairy ◽  
Eman Abd Almonaem ◽  
Neveen Abed ◽  
Omima Abdel Haiea ◽  
Rasha Zakaria ◽  
...  
Keyword(s):  
Renal Dysfunction ◽  
Cystatin C ◽  
Thalassemia Major ◽  
Beta Thalassemia ◽  
Serum Cystatin C ◽  
Serum Cystatin ◽  
Early Markers ◽  
Beta 2 ◽  
Beta 2 Microglobulin

scholarly journals Assessment of Subclinical Renal Glomerular and Tubular Dysfunction in Children with Beta Thalassemia Major

Children ◽  
2021 ◽  
Vol 8 (2) ◽  
pp. 100
Author(s):  
Asmaa A. Mahmoud ◽  
Doaa M. Elian ◽  
Nahla MS. Abd El Hady ◽  
Heba M. Abdallah ◽  
Shimaa Abdelsattar ◽  
...  
Keyword(s):  
Cystatin C ◽  
Kidney Injury ◽  
Thalassemia Major ◽  
Beta Thalassemia ◽  
Good Survival ◽  
Control Group ◽  
Healthy Children ◽  
Serum Cystatin C ◽  
Serum Cystatin ◽  
Beta Thalassemia Major

Background: A good survival rate among patients with beta thalassemia major (beta-TM) has led to the appearance of an unrecognized renal disease. Therefore, we aimed to assess the role of serum cystatin-C as a promising marker for the detection of renal glomerular dysfunction and N-acetyl beta-D-glucosaminidase (NAG) and kidney injury molecule 1 (KIM-1) as potential markers for the detection of renal tubular injury in beta-TM children. Methods: This case-control study was implemented on 100 beta-TM children receiving regular blood transfusions and undergoing iron chelation therapy and 100 healthy children as a control group. Detailed histories of complete physical and clinical examinations were recorded. All subjected children underwent blood and urinary investigations. Results: There was a significant increase in serum cystatin-C (p < 0.001) and a significant decrease in eGFR in patients with beta-TM compared with controls (p = 0.01). There was a significant increase in urinary NAG, KIM-1, UNAG/Cr, and UKIM-1/Cr (p < 0.001) among thalassemic children, with a significant positive correlation between serum cystatin-C, NAG and KIM-1 as regards serum ferritin, creatinine, and urea among thalassemic patients. A negative correlation between serum cystatin-C and urinary markers with eGFR was noted. Conclusion: Serum cystatin-C is a good marker for detection of glomerular dysfunction. NAG and KIM-1 may have a predictive role in the detection of kidney injury in beta-TM children.

scholarly journals SERUM NEUTROPHIL GELATINASE-ASSOCIATED LIPOCALIN (NGAL) AND URINARY NGAL EXCRETION AS A BIOMARKER OF RENAL INJURY IN CHILDREN WITH BETA THALASSEMIA MAJOR

2021 ◽  
pp. 1-3
Author(s):  
Ruchi Bhatt ◽  
Alok Hemal ◽  
Meetu Singh ◽  
Zeeshan Ahmed
Keyword(s):  
Cystatin C ◽  
Renal Injury ◽  
Linear Regression Analysis ◽  
Thalassemia Major ◽  
Beta Thalassemia ◽  
P Value ◽  
Urinary Ngal ◽  
Urine Ngal ◽  
Beta Thalassemia Major ◽  
Serum And Urine

Background Frequent blood transfusions among patients with beta thalassemia major leads to iron overload state and leads to damage of various organs including kidney. Very few studies have explored on Serum and urinary NGAL as a biomarkers of renal injury in thalassemia major children. Therefore, this study is planned to investigate the renal injury in beta thalassemic children by measuring serum and urinary NGAL levels and correlating it with cystatin c and creatinine clearance. Methods: The study was a cross-sectional conducted among 25 patients with β thalassemia major, aged 1-18 years, having undergone regular blood transfusion and chelation therapy. Levels of plasma and urinary NGAL were measured and compared to the standard values of the normal range. Linear regression analysis was done. Results: Mean(SD) serum NGAL value in 1- 5 years of age was 1.6(0.26) , in 5-10 years was 2.15(0.23), in 10- 15 years was 2.6 (0.11) and > 15 years it was 18.11(33.76). ( p value <0.005).Mean (SD) urine NGAL value in 1- 5 years of age was 0.66 (0.11) , in 5-10 years was 1.13(0.13), in 10- 15 years was 1.38 (0.18) and > 15 years it was 1.94(0.25). ( p value <0.005).The mean values of plasma N-GAL, and Urinary N-GAL were significantly higher in our patients as compared to that of standard population values(p<0.05). Conclusions: Serum and urine NGAL values are found to be much higher in those with longer duration of transfusion and chelation. Positive correlation was found between urine NGAL levels and cystatin C. Serum and urine NGAL values are fair markers of renal injury in thalassemia major patients on multiple transfusions.

Detection of Renal Insufficiency in a Cohort of Patients With Beta-thalassemia Major Using Cystatin-C

2021 ◽  
Vol Publish Ahead of Print ◽  
Author(s):  
Mona Hamdy ◽  
Iman Shaheen ◽  
Zinab M. El-Gammal ◽  
Yasmin M. Ramadan
Keyword(s):  
Renal Insufficiency ◽  
Cystatin C ◽  
Thalassemia Major ◽  
Beta Thalassemia ◽  
Beta Thalassemia Major

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

2019 ◽  
Vol 20 (8) ◽  
pp. 656-664 ◽  
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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