Kidney failure osteodystrophy

Renal osteodystrophy [due to decreased synthesis of 1,25-(0H)2D secondary to kidney failure] is treatable with synthetic l,25-(OH)2D or la-(OH)D. These compounds are also useful in other renal disorders such as hypoparathyroidism and vitamin D-dependent rickets. 

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.)... 

Because the kidney is the only significant source of la-OHase, inadequate formation of l,25-(OH)2D3 occurs in renal failure [168], Not only is the mass of kidney tissue and therefore of enzyme decreased, but also with renal failure, phosphate excretion is reduced and serum phosphate rises. Increased phosphate inhibits la-OHase so that little l,25-(OH)2D3 is formed. Acidosis, a frequent result of renal failure, also impairs la-OHase activity [169, 170]. Deficiency of the active form of vitamin D causes osteomalacia, a prominent feature of renal osteodystrophy. Therapy is directed toward use of l,25-(OH)2D3, reduction of serum phosphate, and correction of acidosis, so that residual la-OHase can be expressed. 

Renal osteodystrophy is a disease resulting from renal failure. The hallmarks of this disease are low plasma l,25-(OH)2D3, hyperparathyroidism, and hy-perphosphataemia. The loss of kidney function results in phosphate retention, and in addition, renal la-OHase is dysfunctional, causing low serum... 

Renal failure is associated with an osteomalacia-like syndrome, renal osteodystrophy, as a result of the loss of calcidiol 1-hydroxylase activity. The condition may be complicated by defective reabsorption of calcium and phosphate from the urine. Furthermore, the half-life of parathyroid hormone is increased, because the principal site of its catabolism is the kidney, so there is increased parathyroid hormone-stimulated osteoclastic action without the compensatory action of calcitriol (Mawer etal., 1973). 

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. 

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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