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1 ression of secondary hyperparathyroidism and renal osteodystrophy.
2 eatment of secondary hyperparathyroidism and renal osteodystrophy.
3  shown to ameliorate the skeletal lesions of renal osteodystrophy.
4 st of the metabolic abnormalities that cause renal osteodystrophy.
5 curately predict the character of underlying renal osteodystrophy.
6 nt should be evaluated in an animal model of renal osteodystrophy.
7  including severe cardiovascular disease and renal osteodystrophy.
8 s could be used to improve the management of renal osteodystrophy.
9 ssociated the adynamic bone disorder form of renal osteodystrophy.
10 ficacious agent in treating animal models of renal osteodystrophy.
11 t reaching far beyond traditional notions of renal osteodystrophy and hyperparathyroidism.
12 onic kidney disease, vascular calcification, renal osteodystrophy, and phosphate contribute substanti
13 m commonly persists, and residual changes of renal osteodystrophy are slow to resolve.
14 ore than half of the patients presented with renal osteodystrophy at both biopsies, but histological
15                           Five patients with renal osteodystrophy developed marked hyperostosis of th
16 rathyroid bone disease, the major variety of renal osteodystrophy, from developing in patients with r
17 n the premenopausal group, and patients with renal osteodystrophy had higher BW (41.4% +/- 9.6) than
18              These are related to underlying renal osteodystrophy, hypophosphatemia, and immunosuppre
19                                              Renal osteodystrophy is a state of impaired bone quality
20                          The pathogenesis of renal osteodystrophy is related to phosphate retention,
21  that latter analog, currently used to treat renal osteodystrophy, is more efficacious than 1,25(OH)2
22 ally to low- or high-turnover bone may treat renal osteodystrophy more effectively.
23                                              Renal osteodystrophy (ROD) contributes substantially to
24                                              Renal osteodystrophy (ROD) is a disorder of bone metabol
25 esents with extra-skeletal calcification and renal osteodystrophy (ROD).
26  soft tissues, and the bone abnormalities of renal osteodystrophy that together result in an increase
27          Uremic mice exhibited high turnover renal osteodystrophy; treatment with sevelamer significa