Asmaa A Mahmoud1, Doaa M Elian1,2, Nahla Ms Abd El Hady1, Heba M Abdallah3, Shimaa Abdelsattar4, Fatma O Khalil5, Sameh A Abd El Naby1. 1. Department of Pediatrics, Faculty of Medicine, Menoufia University, Shebin Elkom 32511, Egypt. 2. Department of Pediatrics, College of Medicine, King Faisal University, Al-Ahsa 31982, Saudi Arabia. 3. Department of Clinical Pathology, National Liver Institute, Menoufia University, Shebin Elkom 32511, Egypt. 4. Department of Clinical Biochemistry and Molecular Diagnostics, National Liver Institute, Menoufia University, Shebin Elkom 32511, Egypt. 5. Department of Clinical and Molecular Microbiology and Immunology, National Liver Institute, Menoufia University, Shebin Elkom 32511, Egypt.
Abstract
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.
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-TMchildren. METHODS: This case-control study was implemented on 100 beta-TMchildren 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 thalassemicchildren, with a significant positive correlation between serum cystatin-C, NAG and KIM-1 as regards serum ferritin, creatinine, and urea among thalassemicpatients. 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-TMchildren.
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