Kidney disease, chronic renal osteodystrophy

Renal osteodystrophy Altered bone turnover that results from sustained metabolic conditions that occur in chronic kidney disease, including secondary hyperparathyroidism, hyperphosphatemia, hypocalcemia, and vitamin D deficiency. 

FIGURE 76-7. Pathogenesis of secondary hyperparathyroidism and renal osteodystrophy in patients with chronic kidney disease. These adaptations are lost as renal failure progresses. (Ca, calcium, P04 phosphate PTH, parathyroid hormone.)... 

The major effects of hyperphosphatemia are related to the development of hypocalcemia (caused by phosphate inhibition of renal la-hydroxylase) and its related consequences, as well as vascular and organ damage resulting from the deposition of calcium-phosphate crystals. Extravascular calcification can result in band keratopathy, red eye, pruritus, and periarticular calcification, especially in renal failure patients (see Chap. 44). In addition, soft-tissue calcifications in the conjunctiva, skin, heart, cornea, lung, gastric mucosa, and kidney have been observed, primarily in chronic renal failure patients." Hyperphosphatemia associated with chronic renal disease may result in renal osteodystrophy because of overproduction of parathyroid hormone. This condition is discussed in detail in Chap. 44. 

Renal osteodystrophy (ROD)—The condition resulting from sustained metabolic changes that occur with chronic kidney disease including secondary hyperparathyroidism, hyperphosphatemia, hypocalcemia, and vitamin D deficiency. The skeletal complications associated with ROD include osteitis fibrosa cystica (high bone turnover disease), osteomalacia (low bone turnover disease), adynamic bone disease, and mixed bone disorders. 

Experimental Al administration to animals produces osteomalacia (Goodman 1986). Essentially all patients suffering from chronic renal failure exhibit some degree of renal osteodystrophy. In kidney disease there is a decreased... 

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