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CLINICAL REVIEW 20 Recent Advances in the Pathogenesis and Therapy of Uremic Secondary Hyperparathyroidism

Chromalloy American Kidney Center and the Renal Division, Department of Medicine, Washington University School of Medicine St. Louis, Missouri 63110

Address requests for reprints to: James A. Delmez, M.D., Chromalloy American Kidney Center, One Barnes Hospital Plaza, St. Louis, Missouri 63110.

THE association of renal failure with metabolic bone disease has been recognized since the time of Albright. The term "renal osteodystrophy" is not specific. It encompasses the lesions of osteitis fibrosa, osteomalacia, mixed lesions, osteoporosis, and growth retardation. The histological features of osteitis fibrosa include osteoclastosis, increased bone resorption, and marrow fibrosis. In addition, osteoblastic activity is increased with an abnormally large percent of bone surface involved in bone formation. This state of high bone turnover is also characterized by increased quantities of woven osteoid. It differs from normal lamellar osteoid in that there is a haphazard arrangement of collagen fibers. Although woven osteoid can be mineralized, the calcium is deposited as amorphous calcium-phosphate instead of hydroxyapatite. It is clear that osteitis fibrosa (and probably other uremic derangements) is the result of excessive secretion of PTH. With the advent of effective dialysis therapy, it is now common for patients to live for 10–20 yr without renal function, yet develop progressive uremic hyperparathyroidism.

Received August 20, 1990.

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