الفهرس 
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Abstract
Idiopathic nephrotic syndrome (INS) is characterized by triad of heavy proteinuria, hypo-albuminemia, and oedema (1). Most of glomerular disorders in children present with nephrotic syndrome, the exact cause of this common childhood disease remains elusive despite substantial advances in our understanding of podocyte biology (1).
Idiopathic NS can be classified on the basis of response to steroid therapy, pattern of relapse, histopathology, or by genetic mutations. Most simply, INS is categorized on the basis of clinical response to steroid therapy, as steroid sensitive (SS) or steroid resistant (SR) (1). Although helpful for guiding therapy, this classification lends very little understanding to disease mechanism. Idiopathic NS is best defined as a podocytopathy due to loss or altered function of the podocytes, resulting in massive proteinuria.
This study aims of to evaluate the concentration of FGF-23 in children with nephrotic syndrome treated with Glucocorticosteroids in comparison to existing markers of bone metabolism.
This study was conducted on 80 children, 40 children taking steroids as therapy and were categorized intro three groups: steroid dependent, steroid resistant, and frequent relapse, and 40 children as control group. All patient groups were diagnosed with INS based on the criteria of the International Study of Kidney Disease in Children (ISKDC). Relapse group was recognized when urine-to-creatinine ratio (uPCR) was ≥2000 mg/g (≥200 mg/mmol).
All children were subjected to: detailed full history, clinical examinations, routine lab (CBC, serum creatinine, Urea, serum albumin), and specific lab investigations.
The results of the current study showed:
Serum calcium, phosphate, and parathyroid hormones were all significant in steroid groups compared to controls.
FGF-23 was higher in steroid groups compared to the control group.