The biochemical alterations in renal osteodystrophy can be summarized as follows:

1. Azotemia, hyperphosphatemia, and changes in acid-base balance and electrolytes that reflect the chronic acidotic state

2. Low serum calcium level, in which case a larger percentage of the calcium is ionized because of the acidotic state but the total amount (including the nonionized calcium) is reduced not only as a result of the factors just described but because of a commonly observed decline in serum proteins.

3. Increased bone alkaline phosphatase activity due to the increased rate of new bone synthesis in hyperparathyroid and osteomalacic renal bone disease

4. Increased PTH level, which indicates the usually marked secondary hyperparathyroidism in hyperparathyroid renal bone disease. However, the serum PTH is often low for stage 4 and 5 CKD patients (<150 pg/mL) in adynamic renal bone disease.

5. Greatly diminished 1,25(OH)₂D levels, even with increased intake of vitamin D, and normal or high levels of 25(OH)D

6. Increased serum FGF-23 levels

Clinical Manifestations. In the growing child with renal osteodystrophy, rachitic changes in the epiphyseal plates are virtually identical to those seen in patients with other forms of rickets (see Plates 3-15 and 3-21). However, the growth rate of children with renal osteodystrophy is often greatly reduced, with the result that radiographic manifestations of the disease may appear somewhat less severe than the chemical aberrations suggest (see the paradox of rickets). However, increased axial height of the epiphyseal plates, cupping and flaring, and diminished density in the zone of provisional calcification are characteristic radiographic findings and are indistinguishable from the changes seen in the other forms of rachitic disease. For some unknown reason, slipped capital femoral epiphysis occurs much more frequently in patients with azotemic rickets than it does in patients with vitamin D deficiency or vitamin D–resistant disease.