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1 ding severe cardiovascular disease and renal osteodystrophy.
2 d be used to improve the management of renal osteodystrophy.
3 ted the adynamic bone disorder form of renal osteodystrophy.
4 ous agent in treating animal models of renal osteodystrophy.
5 n of secondary hyperparathyroidism and renal osteodystrophy.
6 t of secondary hyperparathyroidism and renal osteodystrophy.
7 vating mutations lead to Albright hereditary osteodystrophy.
8 ack physical features of Albright hereditary osteodystrophy.
9  to ameliorate the skeletal lesions of renal osteodystrophy.
10  limited to PTH and lack Albright hereditary osteodystrophy.
11  somatic features termed Albright hereditary osteodystrophy.
12 the metabolic abnormalities that cause renal osteodystrophy.
13 tified in a patient with Albright hereditary osteodystrophy.
14 s in a syndrome called Albright's hereditary osteodystrophy.
15 ly predict the character of underlying renal osteodystrophy.
16 uld be evaluated in an animal model of renal osteodystrophy.
17 t had no effect on vascular calcification or osteodystrophy.
18 e implications for human Albright hereditary osteodystrophy, a condition caused by mutations in GNAS.
19 otopic ossification in Albright's hereditary osteodystrophy (AHO) and a recent report of two patients
20                       In Albright Hereditary Osteodystrophy (AHO) heterozygous loss of function mutat
21 tions lead to obesity in Albright hereditary osteodystrophy (AHO) patients, but only when the mutatio
22 h shares features of the Albright hereditary osteodystrophy (AHO) phenotype.
23                        Albright's Hereditary Osteodystrophy (AHO) was the first inherited disease ass
24                          Albright hereditary osteodystrophy (AHO), a disorder characterized by skelet
25                          Albright hereditary osteodystrophy (AHO), an autosomal dominant disorder cha
26 hing far beyond traditional notions of renal osteodystrophy and hyperparathyroidism.
27         Epilepsy, deafness, onychodystrophy, osteodystrophy and intellectual disability are associate
28 pilepsy, and DOOR (deafness, onychdystrophy, osteodystrophy, and mental retardation) syndrome, and id
29 idney disease, vascular calcification, renal osteodystrophy, and phosphate contribute substantially t
30 imulated bone formation rates, corrected the osteodystrophy, and prevented CKD-stimulated vascular ca
31 rrected the hyperphosphatemia, corrected the osteodystrophy, and prevented VC, compatible with skelet
32 only persists, and residual changes of renal osteodystrophy are slow to resolve.
33 an half of the patients presented with renal osteodystrophy at both biopsies, but histological findin
34 ith end-stage renal disease: a high-turnover osteodystrophy characterized by osteitis fibrosa, and a
35 ized by osteitis fibrosa, and a low-turnover osteodystrophy characterized initially by osteomalacia a
36 r DOORS syndrome (deafness, onychodystrophy, osteodystrophy, cognitive disability, and seizures).
37 a, secondary hyperparathyroidism, and a mild osteodystrophy developed in the CKD/chow-fed group, as e
38                     Five patients with renal osteodystrophy developed marked hyperostosis of the faci
39 oid bone disease, the major variety of renal osteodystrophy, from developing in patients with renal i
40 premenopausal group, and patients with renal osteodystrophy had higher BW (41.4% +/- 9.6) than the pr
41        These are related to underlying renal osteodystrophy, hypophosphatemia, and immunosuppressive
42      Our aim was to perform a pilot study on osteodystrophy in children undergoing LT and evaluate th
43 e DOORS syndrome: deafness, onychodystrophy, osteodystrophy, intellectual disability, and seizures.
44                                        Renal osteodystrophy is a state of impaired bone quality and s
45                                              Osteodystrophy is a well-described complication of chron
46                    The pathogenesis of renal osteodystrophy is related to phosphate retention, and it
47 mutated in patients with Albright hereditary osteodystrophy, is also imprinted.
48 latter analog, currently used to treat renal osteodystrophy, is more efficacious than 1,25(OH)2 D3 in
49                   Deafness, onychodystrophy, osteodystrophy, mental retardation, and seizures (DOORS)
50 f DOORS syndrome (deafness, onychodystrophy, osteodystrophy, mental retardation, and seizures), a con
51 d DOORS syndrome (deafness, onychodystrophy, osteodystrophy, mental retardation, seizures) to non-syn
52 o low- or high-turnover bone may treat renal osteodystrophy more effectively.
53  often acting on a background of preexisting osteodystrophy resulting from long-standing renal, hepat
54                                        Renal osteodystrophy (ROD) contributes substantially to morbid
55                                        Renal osteodystrophy (ROD) is a disorder of bone metabolism th
56  with extra-skeletal calcification and renal osteodystrophy (ROD).
57 Studies in patients with Albright hereditary osteodystrophy suggest a similar G(s)alpha imprinting pa
58 tissues, and the bone abnormalities of renal osteodystrophy that together result in an increased risk
59    Uremic mice exhibited high turnover renal osteodystrophy; treatment with sevelamer significantly d
60 n its inception, CKD-MBD is characterized by osteodystrophy, vascular calcification, and stimulation
61 Superimposing CKD resulted in a low turnover osteodystrophy, whereas VC worsened and hyperphosphatemi
62 but without evidence for Albright hereditary osteodystrophy who has paternal uniparental isodisomy of