BackgroundGlucose-6-phosphate dehydrogenase (G6PD) deficiency anemia is associated with intravascular hemolysis. The freely filtered hemoglobin can damage the kidney. We aimed to assess any subclinical renal injury in G6PD children.MethodsSixty children were included. Thirty G6PD deficiency anemia children were enrolled during the acute hemolytic crisis and after the hemolytic episode had elapsed. Another thirty healthy children were included as controls. Serum cystatin C, creatinine levels, and urinary albumin/creatinine (A/C) ratio were measured, and the glomerular filtration rate (GFR) was calculated.ResultsSignificantly higher urinary A/C ratio (p=0.001,0.002 respectively) and lower GFR (p=0.001 for both) were found during hemolysis and after the hemolytic episode compared to the controls. Also, significant higher serum cystatin C (p=0.001), creatinine (p=0.05) and A/C (p= 0.001) ratio and insignificant lower GFR (p=0.3) during acute hemolytic crisis compared to the same children after the hemolytic episode subsided.ConclusionsG6PD deficiency anemia is associated with a variable degree of acute renal injury during acute hemolytic episodes which may persist after elapsing of the hemolytic crises.
Beta Thalassemia represents a major public health problem in Egypt. The carrier rate varies between 5.5% to > 9%. It is estimated that there are 1000/1.5 million per year live births born with beta thalassemia. (1) β thalassemia occurs when there is a quantitative reduction of β globin chains that are usually structurally normal. (2) They are caused by mutations that nearly all affect the β globin locus and are extremely heterogeneous. Almost every possible defect affecting gene expression at transcription or post-transcriptional level, including translation, have been identified in β thalassemia. (3) These genetic defects lead to a variable reduction in β globin output ranging from a minimal deficit (mild β+ thalassemia alleles) to complete absence (β° thalassemia). Aim of the work:We aimed in this study to assess the molecular changes in transfusion dependent Beta thalassemia patients and the correlation of these molecular changes with their clinical outcomes. Patients & methods: This study will include 40 transfusion dependent β thalassemia patients with age range of 2 -18 years, recruiting the Pediatric Hematology unit in Minia University children hospital. Study procedure: β-Thalassemia mutation identification of samples will be performed by the reverse dot blot hybridization technique (RDB). For RDB, a panel of primers and probes using the beta globin strip assay well be used (β-Globin Strip Assay MED kit, VIENNA lab
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