الفهرس 
Chronic kidney disease
Complications of CKD:Only 14 pages are availabe for public view
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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)