A variety of metabolic bone disorders is associated with chronic renal disease, including secondary hyperparathyroidism and osteitis fibrosa, aluminum-induced osteomalacia, adynamic bone disease, and dialysis-related amyloidosis. Secondary hyperparathyroidism results from diminished renal production of 1,25-dihydroxyvitamin D3 coupled with phosphate binders. Calcium-containing phosphate binders such as calcium carbonate and calcium acetate are most effective an should be administered with meals. Administration of exogenous calcitriol also plays an important role in treating secondary hyperparathyroidism by elevating serum calcium and suppressing parathyroid hormone secretion. Patients treated with calcitriol must be followed closely for the development of hypercalcemia. Dialysis patients with severe secondary hyperparathyroidism refractory to medical therapy may require parathyroidectomy.
Aluminum bone disease results from aluminum ingestion, usually in the form of aluminum-containing phosphate binders. If present, this can be treated by chelation with deferoxamine.
Adynamic bone disease is a poorly understood form of osteomalacia seen in dialysis patients. It may be the result of aluminum intoxication or of long-standing suppression of parathyroid hormone secretion by calcitriol administration.
Bone disease resulting from dialysis-related amyloid is due to bone deposition of Beta2-microglobulin. Beta2-Microglobulin is a low-molecular-weight protein that is poorly cleared by dialysis and therefore accumulates to high levels in these patients. Carpal tunnel syndrome is a common complication of this disorder.
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