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Abstract Summary Disturbances in mineral and bone metabolism are prevalent in chronic kidney disease and are manifested by either one or a combination of the following, 1-Abnormalities of calcium, phosphorus, parathormone hormone, or vitamin D metabolism, 2- Abnormalities in bone turnover, mineralization, volume, linear growth, or strength, 3- Vascular or other soft tissue calcification disease . Children with CKD stage 2 usually have no signs or symptoms of bone abnormalities. However, these children may have evidence of abnormalities on laboratory testing eg, decreased serum level of 1, 25(OH) 2D and elevated serum parathyroid hormone. The kidney is the primary source of 25(OH)D-1α hydroxylase ,the enzyme needed to convert 25(OH)D to its active metabolite(1-25(OH)2D) so decreased 25(OH)D-1α-hydoxylase activity in kidney failure has traditionally been attributed to two main factors:1-Diminished renal mass, leading to progressive loss of the enzyme in proximal tubule cells, 2- Phosphate retention, which is thought to directly inhibit the enzyme via increasing intracellular phosphate. However, although these factors likely play an important role in contributing to decreased 1,25(OH)2D synthesis in moderate-to-severe kidney disease, on their own, they have proved inadequate to explain the initial decline in 1,25(OH)2D synthesis in early kidney disease for two reasons: First, 1, 25(OH) 2D levels begin to decline very early in the course of kidney failure (ranging from a creatinine clearance of 60 to 80 ml/min) |