Michael P. D'Alessandro, M.D.
Peer Review Status: Internally Peer Reviewed
Due to chronic renal dysfunction.
Renal tubular defects result in a loss of calcium and phosphate in the urine leading to children with deficient mineralization of growing bone and rickets.
Renal glomerular defects inhibit phosphate excretion and Vitamin D activity in resorbing calcium which leads to high serum phosphate and low serum calcium which leads to secondary hyperparathyroidism. Glomerular defects can complicate end stage tubular defects. Skeletal changes occur after a few of months in infants but may require a few years to show up in older children.
The radiographic changes of rickets include uncalcified osteoid which leads to widening of the growth plate, loss of the zone of provisional calcification, metaphyseal cupping, flaring, and irregularity.
Radiographic changes of secondary hyperparathyroidism include subperiosteal bone resportion and demineralization. The resorption is most commonly seen in the phalanges / distal radius and clavicles / ribs / symphysis pubis / SI joints /femoral necks. Osteosclerosis is related to secondary hyperparathyroidism and results in generalized increased bony density. It may also be seen in a localized form is the spine where "rugger jersey" spine can be seen due to sclerosis of the vertebral body endplates.
See References Chapter.
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