|
Year |
2007 |
|---|---|
|
Question Number |
22 |
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Category |
Orthopaedic Science |
Question
Which of the following pathophysiologic mechanisms is responsible for renal osteodystrophy
1- Insufficient synthesis of 25(OH) vitamin D
2- Phosphate retention secondary to uremia
3- Hypercalcemia
4- Metabolic alkalosis
5- Decreased parathyroid hormone in serum
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Answer (click for answer)
Preferred response: 2 – Phosphate retention secondary to uremia
Retention of phosphate by abnormal kidneys results in hyperphosphatemia, which causes hypocalcemia and results in secondary hyperparathyroidism. Although dysfunction in any one of the metabolic steps in the biosynthesis of Vitamin D may result in rickets and osteomalacia in the growing child, as well as osteomalacia and secondary hyperPTH in the adult, the primary cause of hyperPTH in renal osteodystrophy lies in phosphate retention. Likewise, although metabolic alkalosis may aid in the deposition of high calcium-phosphate into soft tissues, it is not by itself Hyperphosphatemia itself decreases the efficacy of 1-hydroxylase, which decreases the levels of 1-25 dihydroxyvitamin D and, thus, the ability of the gut to absorb calcium.
HyperPTH in renal osteodystrophy increases bone resorption, which may normalize serum calcium levels by releasing the osseous storage of calcium. The various sites of bone resorption include the subperiosteal region of the phalanges, the phalangeal tufts, proximal femur, proximal tibia, proximal humerus, distal clavicle, and calvarial trabeculae.
Of note, aluminum-induced bone disease is an additional cause of osteomalacia. Aluminum negatively affects bone formation through inhibition of osteoblastic activity, as well as by hydroxyapatite crystal formation. Aluminum may be introduced from dialysate solutions, antacids, or aluminum-containing phosphate-binding agents used to combat the hyperphosphatemia of renal failure.
Reference: Buckwalter JA, Einhorn TA, Simon SR (eds): Orthopaedic Basic Science: Biology and Biomechanics of the Musculoskeletal System, ed 2. Rosemont, IL, AAOS, 2000, pp 319-369.