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ISSN 2063-5346
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Assessment of Sclerostin as a Bone Metabolism Marker in Egyptian Children with Nephrotic Syndrome

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Mona Hamed Gehad, Hossam Mostafa Kamal, Aya Mohamed Fouad Ibrahim, Weam Ibrahim Ismail
ยป doi: 10.53555/ecb/2023.12.Si12.331

Abstract

Background: Nephrotic syndrome (NS) is one of the common chronic diseases observed in the childhood. Idiopathic nephrotic syndrome (INS)is the most common type , it constitutes about 90% of NS in the childhood. In children, nephrotic syndrome (NS) is defined as protein excretion of more than 40 mg/m2/h or a first-morning urine protein/creatinine of 2-3 mg/mg creatinine or greater. it is composed of NS and primary glomerular disease without an identifiable causative disease or infection, up to 85%โ€“90% of children with INS are steroid sensitive, but follow a relapsing and remitting course in the majority of cases. Sclerostin (SOST) is a glycoprotein and a product of the SOST gene located on chromosome 17q12-q21 , It is not only secreted from osteocytes, but also by other cells such as chondrocytes, cementocytes as well as from the kidney and liver. Sclerostin negative regulator of bone formation, has been originally known as an osteocyte product. Recently, it has been also detected in hypertrophic chondrocytes, distinctive cells of avascular cartilage which is invaded by capillaries and then replaced by vascularized bone. In the treatment of idiopathic nephrotic syndrome (INS) in children, glucocorticosteroids (GCSs) remain the main medication. Recurrent nature of the disease and steroid dependence imply a long-term therapy and probably increa sed risk of bone metabolism disorders. To this time, pediatrics population has not been analyzed in the context of changes in bone parameters during steroid therapy.

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