[{"data":1,"prerenderedAt":-1},["ShallowReactive",2],{"health-study-detail:100653359":3},{"organization":4,"outcomesModule":7,"designInfo":18,"detailedDescription":21,"studyPopulation":22,"armGroups":23,"interventions":36,"overallOfficials":42,"centralContacts":46,"locations":56,"responsibleParty":67,"collaborators":17,"id":70,"slug":71,"hasResults":72,"nctId":73,"briefTitle":74,"officialTitle":74,"acronym":75,"eligibilityCriteria":76,"healthyVolunteers":77,"sex":78,"minAge":79,"maxAge":80,"enrollmentInfo":81,"targetDuration":84,"studyType":85,"phases":17,"briefSummary":86,"conditions":87,"keywords":17,"overallStatus":89,"whyStopped":17,"lastUpdateSubmitDate":90,"lastUpdatePostDateStruct":91,"startDateStruct":94,"completionDateStruct":96,"leadSponsor":98,"locationsCount":99},{"fullName":5,"class":6},"Assiut University","OTHER",{"primaryOutcomes":8,"secondaryOutcomes":13,"otherOutcomes":17},[9],{"measure":10,"description":11,"timeFrame":12},"To assess differences in kidney function and early renal injury between the study groups using urinary N-acetyl-β-D-glucosaminidase (NAG), Kidney Injury Molecule-1 (KIM-1), and to evaluate the diagnostic performance of these measures for the early detect","To assess differences in kidney function and early renal injury between the study groups using urinary N-acetyl-β-D-glucosaminidase (NAG), Kidney Injury Molecule-1 (KIM-1), and to evaluate the diagnostic performance of these measures for the early detection of sickle cell nephropathy and assessment of renal diffusion MRI parameters (DWI\u002FDTI), particularly fractional anisotropy (FA), in children with sickle cell disease.","1 year",[14],{"measure":15,"description":16,"timeFrame":12},"Evaluation of the diagnostic performance of urinary NAG and KIM-1 using ROC curve analysis and Correlation between renal DWI\u002FDTI findings and urinary NAG, KIM-1, ACR, and eGFR.","* Correlation of urinary NAG and KIM-1 levels with urinary albumin-to-creatinine ratio (ACR) and estimated glomerular filtration rate (eGFR).\n* Evaluation of the diagnostic performance of urinary NAG and KIM-1 using ROC curve analysis.\n* Determination of sensitivity, specificity, PPV, NPV, and diagnostic accuracy of the studied biomarkers.\n* Assessment of renal diffusion MRI parameters (DWI\u002FDTI), particularly fractional anisotropy (FA), in children with sickle cell disease.\n* Correlation between renal DWI\u002FDTI findings and urinary NAG, KIM-1, ACR, and eGFR.\n* Evaluation of the ability of DWI\u002FDTI to detect early renal microstructural changes before overt impairment of renal function.",null,{"allocation":17,"interventionModel":17,"interventionModelDescription":17,"primaryPurpose":17,"observationalModel":19,"timePerspective":20,"maskingInfo":17},"CASE_CONTROL","PROSPECTIVE","Sickle cell disease was the first condition to be understood as a molecular disease, as described by Pauling and colleagues in 1949, and later helped to elucidate principles of gene expression, haemoglobin switching, and globin gene regulation.\n\nSickle cell disease refers to a group of inherited red blood cell (RBC) disorders caused by pathogenic variants in the HBB gene, resulting in the production of sickle haemoglobin S (HbS). Individuals with one copy of the mutation have sickle cell trait a condition that confers partial protection against severe malaria while those with pathogenic variants on both alleles develop the clinical syndrome of sickle cell disease.\n\nThe defining pathophysiological mechanism of sickle cell disease is the polymerization of deoxygenated HbS, leading to red cell sickling, haemolysis, and vaso-occlusion accompanied by a cascade of complex pathophysiological events. This cascade drives the multisystem complications of the disease, including acute painful crisis, acute chest syndrome, stroke and cognitive impairment, and progressive organ damage.\n\nSickle nephropathy often begins in childhood with impaired urine concentrating ability and glomerular hyperfiltration, eventually progressing to albuminuria, reduced glomerular filtration rate, and end-stage renal disease.\n\nUp to one-third of adults with sickle cell disease develop overt proteinuria or decreased glomerular filtration rate, and kidney dysfunction is independently associated with early mortality. Hydroxyurea and angiotensin-converting enzyme inhibitors remain first-line therapies for reducing albuminuria and slowing progression.\n\nEarly onset SCN is a progressive kidney complication in SCD driven by chronic RBC sickling, vascular occlusion and hemolysis, typically begins in early childhood with hyperfiltration, hyposthenuria, and microalbuminuria.\n\nEnuresis is another frequent complication that affects quality of life. Genetic modifiers, such as high fetal hemoglobin (HbF) levels and α-thalassemia trait have a protective effect on nephropathy, possibly by reduced hemolysis and endothelial stress.\n\nRenal damage is common in children patients with SCD, which begins in childhood, progressing with age, a fact that makes nephropathy one of the possible complications. This can compromise patients' quality of life and decrease survival.\n\nSickle cell nephropathy (SCN) is a severe complication of SCA, characterized by early, often asymptomatic onset in childhood and a potential progression to chronic kidney disease (CKD) . SCN presents a significant challenge in the clinical management of patients with sickle cell anemia, contributing to a reduction in life expectancy by approximately 20 to 30 years. The clinical progression of SCN is age-dependent, with renal dysfunction typically emerging during childhood and gradually advancing to chronic kidney disease and, ultimately, kidney failure by the third or fourth decade of life.\n\nClassical biomarkers such as creatinine, are not able to detect early renal lesions, which makes kidney injury molecule-1 (Kim-1) and N-acetyl-b-D-glucosaminidase (NAG) possible biomarker candidates in the prediction of renal disease in sickle cell anemia patients.\n\nDespite advancements in treatment of sickle cell disease (SCD), hydroxyurea, a ribonucleotide reductase inhibitor, remains the cornerstone of therapy. While its primary effect is the elevation of fetal hemoglobin (HbF), hydroxyurea's mechanisms of action are multifaceted. Hydroxyurea (HU) reduces leukocyte and platelet counts, decreases the expression of endothelial adhesion molecules CD36 and CD49d, and increases nitric oxide and cyclic nucleotide levels, which may facilitate vascular dilation and further HbF induction.","The study population will include children with confirmed sickle cell disease attending the Hematology Unit, Assiut University Children's Hospital, during the study period.",[24,29,33],{"label":25,"type":17,"description":26,"interventionNames":27},"Group I (SCD patients on regular hydroxyurea therapy)","Children with confirmed sickle cell disease receive hydroxyurea regularly, regardless of the presence or absence of early renal involvement.",[28],"Drug: Hydroxy Urea",{"label":30,"type":17,"description":31,"interventionNames":32},"Group II (SCD patients on irregular hydroxyurea therapy)","Children with confirmed sickle cell disease receiving hydroxyurea irregularly or demonstrating poor adherence to treatment, regardless of the presence or absence of early renal involvement.",[28],{"label":34,"type":17,"description":35,"interventionNames":17},"Apparently healthy age- and sex-matched children with no history of sickle cell disease","Apparently healthy age- and sex-matched children with no history of sickle cell disease, renal disease, hypertension, or diabetes mellitus.",[37],{"type":38,"name":39,"description":40,"armGroupLabels":41,"otherNames":17},"DRUG","Hydroxy Urea","* Assessment of the diagnostic performance of urinary N-acetyl-β-D-glucosaminidase (NAG) and Kidney Injury Molecule-1 (KIM-1) for early detection of early onset of sickle cell nephropathy in children with sickle cell disease on regular hydroxyurea\n* Assessment of renal diffusion MRI parameters (DWI\u002FDTI), particularly fractional anisotropy (FA), in children with sickle cell disease.",[25,30],[43],{"name":44,"affiliation":5,"role":45},"Endy MR Mahmoud, assistant lecturer","PRINCIPAL_INVESTIGATOR",[47,52],{"name":48,"role":49,"phone":50,"phoneExt":17,"email":51},"Endy MR Endy Mohammed Rashad, assistant lecturer","CONTACT","01064463176","endyrashad@aun.edu.eg",{"name":53,"role":49,"phone":54,"phoneExt":17,"email":55},"Mohamed MHG Mohamed Mahmoud Hamdy Ghazaly, Professor","01001296603","ghazally@aun.edu.eg",[57],{"facility":5,"status":17,"city":58,"state":17,"zip":17,"country":59,"countryCode":60,"cosmosGeoPoint":61,"geoPoint":66,"contacts":17},"Asyut","Egypt","EG",{"type":62,"coordinates":63},"Point",[64,65],31.18368,27.18096,{"lat":65,"lon":64},{"type":45,"investigatorFullName":68,"investigatorTitle":69,"investigatorAffiliation":5,"oldNameTitle":17,"oldOrganization":17},"Endy Mohammed Rashad Mahmoud","assistant lecturer of pediatric","100653359","clinical-utility-of-urinary-n-acetyl--d-glucosaminidase-nag-kidney-injury-molecule-1-kim-1-and-diffusion-weighted-renal-mri-for-the-early-detection-of-sickle-cell-nephropathy-in-children-100653359",false,"NCT07785752","Clinical Utility of Urinary N-Acetyl-β-D-Glucosaminidase (NAG), Kidney Injury Molecule-1 (KIM-1), and Diffusion-Weighted Renal MRI for the Early Detection of Sickle Cell Nephropathy in Children","sickle nephro","Inclusion Criteria:\n\n* • Children and adolescents aged less than 18 years.\n\n  * Confirmed diagnosis of sickle cell disease by hemoglobin electrophoresis and\u002For high-performance liquid chromatography (HPLC).\n  * Clinically stable patients at the time of enrollment, with no acute vaso-occlusive crisis or acute illness.\n\nExclusion Criteria:\n\n* • Age ≥18 years.\n\n  * Acute sickle cell crisis at least 3 week prior to sample collection\n  * Acute infection or fever.\n  * Known chronic kidney disease due to causes other than sickle cell disease.\n  * Congenital renal anomalies.\n  * Diabetes mellitus.\n  * Hypertension.\n  * Current use of nephrotoxic medications.",true,"ALL","4 Years","18 Years",{"count":82,"type":83},90,"ESTIMATED","1 Year","OBSERVATIONAL","To evaluate the diagnostic performance of urinary N-acetyl-β-D-glucosaminidase (NAG) and kidney injury molecule-1 (KIM-1) Biomarkers for detection of early onset of Sickle Cell Nephropathy in children under HU therapy",[88],"Sickle Cell Nephropathy","NOT_YET_RECRUITING","2026-08-22",{"date":92,"type":93},"2026-08-25","ACTUAL",{"date":95,"type":83},"2026-10-01",{"date":97,"type":83},"2027-12-01",{"name":5,"class":6},1]