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1 imulating production of parathyroid hormone (secondary hyperparathyroidism).
2 ceiving hemodialysis with moderate to severe secondary hyperparathyroidism.
3 omising therapy to improve the management of secondary hyperparathyroidism.
4 rathyroid hyperfunction, such as primary and secondary hyperparathyroidism.
5  hormone levels in patients with primary and secondary hyperparathyroidism.
6  parathyroidectomy in dialysis patients with secondary hyperparathyroidism.
7  associated with vitamin D insufficiency and secondary hyperparathyroidism.
8 lower in the TPN recipients, consistent with secondary hyperparathyroidism.
9 is a major independent determinant of uremic secondary hyperparathyroidism.
10  could be an ideal tool for the treatment of secondary hyperparathyroidism.
11  (PTH) and has been used in the treatment of secondary hyperparathyroidism.
12 ption explains, in part, low-protein-induced secondary hyperparathyroidism.
13 ing homes, which probably contributed to the secondary hyperparathyroidism.
14 l were similar in hemodialysis patients with secondary hyperparathyroidism.
15  hemodialysis patients with mild to moderate secondary hyperparathyroidism.
16 arathyroid glands and reinstated CKD-induced secondary hyperparathyroidism.
17 roughout life, with relevance to CKD-induced secondary hyperparathyroidism.
18 life and for the pathogenesis of CKD-induced secondary hyperparathyroidism.
19  is a safe and effective method for treating secondary hyperparathyroidism.
20 senting recipients of renal transplants with secondary hyperparathyroidism.
21 mone levels and proteinuria in patients with secondary hyperparathyroidism.
22 ced eGFR in renal transplant recipients with secondary hyperparathyroidism.
23  treatment, particularly in patients who had secondary hyperparathyroidism.
24 ociated hypocalcemia, hyperphosphatemia, and secondary hyperparathyroidism.
25 w ways by which to regulate PTH synthesis in secondary hyperparathyroidism.
26 the upregulation of parathyroid TGF-alpha in secondary hyperparathyroidism.
27 y parathyroid TGF-alpha self-upregulation in secondary hyperparathyroidism.
28 sttransplant hypercalcemia due to persistent secondary hyperparathyroidism.
29  to prevent deficiencies and the sequelae of secondary hyperparathyroidism.
30 he treatment of psoriasis, osteoporosis, and secondary hyperparathyroidism.
31 ression in diseases such as osteoporosis and secondary hyperparathyroidism.
32 receiving hemodialysis who have uncontrolled secondary hyperparathyroidism.
33 phosphate binders on the skeletal lesions of secondary hyperparathyroidism (2 degrees HPT).
34       Patients with ESRD commonly experience secondary hyperparathyroidism, a condition primarily man
35 act parathyroid hormone and the frequency of secondary hyperparathyroidism after kidney transplantati
36 of cinacalcet in the treatment of persistent secondary hyperparathyroidism after kidney transplantati
37 while calcium and vitamin D deficiencies and secondary hyperparathyroidism also contribute.
38 nary phosphorus and attenuate progression of secondary hyperparathyroidism among patients with CKD wh
39 ineffective and should not be used to manage secondary hyperparathyroidism among those undergoing dia
40 s lead to a fall in [Ca2+]o and [Mg2+]o with secondary hyperparathyroidism and bone resorption.
41 ponse to GH may be affected by the degree of secondary hyperparathyroidism and concurrent treatment w
42 phosphorus diet (Nx-Phos) to induce advanced secondary hyperparathyroidism and divided into the follo
43 ctivity in 5/6 nephrectomized (Nx) rats with secondary hyperparathyroidism and in Nx rats with clampe
44 low calcium intake and is thought to lead to secondary hyperparathyroidism and increased risk for hip
45 rpS6 phosphorylation for the pathogenesis of secondary hyperparathyroidism and indicate that mTORC1 i
46 ed by an ABD characterized by the absence of secondary hyperparathyroidism and its successful treatme
47                                              Secondary hyperparathyroidism and loose stools were more
48  calcium excretion and developed more severe secondary hyperparathyroidism and rachitic skeletal phen
49 has long been associated with progression of secondary hyperparathyroidism and renal osteodystrophy.
50 , vitamin D metabolism, and the treatment of secondary hyperparathyroidism and renal osteodystrophy.
51  increase was attended by the development of secondary hyperparathyroidism and severe osteomalacia.
52 , the DBP-/-, but not DBP+/+, mice developed secondary hyperparathyroidism and the accompanying bone
53 is an important factor in the development of secondary hyperparathyroidism and uremic bone disease.
54 evels in individuals on hemodialysis who had secondary hyperparathyroidism and varying degrees of hyp
55                           Hyperphosphatemia, secondary hyperparathyroidism, and a mild osteodystrophy
56 is, hyperphosphatemia, vitamin D deficiency, secondary hyperparathyroidism, and anemia.
57 deficiency, altered calcium homeostasis, and secondary hyperparathyroidism, and may contribute to car
58 ) diets can also ameliorate uremic symptoms, secondary hyperparathyroidism, and metabolic acidosis in
59 s disease, severe skeletal demineralization, secondary hyperparathyroidism, and muscle weakness can o
60 in D deficiency, with mineral abnormalities, secondary hyperparathyroidism, and osteomalacia.
61  growth retarded and developed hypocalcemia, secondary hyperparathyroidism, and rickets.
62 promoter completely avoided osteomalacia and secondary hyperparathyroidism, and simultaneously increa
63                        Hyperphosphatemia and secondary hyperparathyroidism are common complications o
64 olism (hyperphosphatemia, hypercalcemia, and secondary hyperparathyroidism) are potentially modifiabl
65 abolic acidosis, hyperkalemia, or persistent secondary hyperparathyroidism, are highly prevalent afte
66   Disorders of mineral metabolism, including secondary hyperparathyroidism, are thought to contribute
67 testinal calcium absorption that resulted in secondary hyperparathyroidism as evidenced by increased
68                                              Secondary hyperparathyroidism as the result of chronic k
69 I, Nechama et al. demonstrate that in murine secondary hyperparathyroidism associated with CKD or Ca
70 hey are likely to become a major therapy for secondary hyperparathyroidism associated with renal fail
71 analog of 1,25-(OH)(2)D(3), is used to treat secondary hyperparathyroidism because it suppresses para
72 CKD not only to attenuate the progression of secondary hyperparathyroidism but also possibly to reduc
73 1 mug one time daily) significantly improved secondary hyperparathyroidism but did not alter measures
74 ffect of oral paricalcitol on posttransplant secondary hyperparathyroidism by conducting an open labe
75                             The treatment of secondary hyperparathyroidism by correction of serum cal
76  with chronic renal failure show evidence of secondary hyperparathyroidism by the time maintenance he
77             At dosages sufficient to correct secondary hyperparathyroidism, calcitriol and paricalcit
78                                              Secondary hyperparathyroidism classically appears during
79                                              Secondary hyperparathyroidism commonly complicates CKD a
80 ypertension, anaemia, metabolic acidosis and secondary hyperparathyroidism contribute to cardiovascul
81                                              Secondary hyperparathyroidism contributes to extraskelet
82                                              Secondary hyperparathyroidism contributes to extraskelet
83                                              Secondary hyperparathyroidism contributes to post-transp
84 mportant early factor in the pathogenesis of secondary hyperparathyroidism, could also play a role in
85 dialysis and who had inadequately controlled secondary hyperparathyroidism despite standard treatment
86 -one hemodialysis patients with uncontrolled secondary hyperparathyroidism, despite standard therapy
87                                              Secondary hyperparathyroidism develops in most patients
88 on, biochemical and histological evidence of secondary hyperparathyroidism develops in rats with mild
89 athyroid hormone (PTH) in many patients with secondary hyperparathyroidism due to end-stage renal dis
90                                           In secondary hyperparathyroidism, enhanced expression of TG
91  II calcimimetic agents for the treatment of secondary hyperparathyroidism focused on the development
92 es were more pronounced in participants with secondary hyperparathyroidism (group-by-time interaction
93 ated serum PTH concentrations in primary and secondary hyperparathyroidism have been associated with
94 d bone disorder (CKD-MBD) is associated with secondary hyperparathyroidism (HPT) and serum elevations
95 he usual management of hyperphosphatemia and secondary hyperparathyroidism (i.e., mineral salts).
96                                   Persistent secondary hyperparathyroidism (i.e., TH) requiring surgi
97          VDR 4-1 also effectively suppressed secondary hyperparathyroidism in 1alpha-hydroxylase knoc
98 that is being evaluated for the treatment of secondary hyperparathyroidism in chronic kidney disease
99 ucidation for understanding the aetiology of secondary hyperparathyroidism in chronic kidney disease
100                         Current treatment of secondary hyperparathyroidism in chronic kidney failure
101 ential therapeutic tool for the treatment of secondary hyperparathyroidism in chronic renal failure.
102 ntestinal CYP24A1 could be targeted to treat secondary hyperparathyroidism in CKD.
103 nce of parathyroid hormone may contribute to secondary hyperparathyroidism in CKD.
104 secretion and is involved in the etiology of secondary hyperparathyroidism in CKD.
105 present a previously unreported mechanism of secondary hyperparathyroidism in CKD.
106                          The pathogenesis of secondary hyperparathyroidism in early renal failure is
107  073 when added to conventional treatment of secondary hyperparathyroidism in end-stage renal disease
108 ers a new therapeutic option for controlling secondary hyperparathyroidism in patients with chronic k
109   Thus, treatments used in the management of secondary hyperparathyroidism in renal failure have dive
110 horus (P) restriction is known to ameliorate secondary hyperparathyroidism in renal failure patients.
111          There is a significant incidence of secondary hyperparathyroidism in short-limb GBP patients
112 rnal calcium homeostasis promoted additional secondary hyperparathyroidism in the fetus, contributing
113 glands and the regulation of these miRNAs in secondary hyperparathyroidism indicates their importance
114 roid hormone (PTH) levels but do not develop secondary hyperparathyroidism induced by CKD.
115 as activated in the parathyroid of rats with secondary hyperparathyroidism induced by either chronic
116 n D) in patients receiving hemodialysis with secondary hyperparathyroidism (intact parathyroid hormon
117                                              Secondary hyperparathyroidism is a frequent complication
118                                Management of secondary hyperparathyroidism is challenging with tradit
119                                              Secondary hyperparathyroidism is characterized by increa
120  after therapy with injectable vitamin D for secondary hyperparathyroidism may accelerate vascular di
121                     Surgical amelioration of secondary hyperparathyroidism may outweigh the risk of p
122 e, which results from nutritional and uremic secondary hyperparathyroidism, may provide a useful anim
123 signed 3883 patients with moderate-to-severe secondary hyperparathyroidism (median level of intact pa
124                                              Secondary hyperparathyroidism occurred in 6.3% of the co
125                                              Secondary hyperparathyroidism of CKD contributes signifi
126 paired, (b) that this is due to the state of secondary hyperparathyroidism of CRF since both acute an
127 ytes; (2) this defect is due to the state of secondary hyperparathyroidism of CRF; and (3) excess PTH
128 t of diseases such as psoriasis, cancer, and secondary hyperparathyroidism of renal failure, where a
129                                              Secondary hyperparathyroidism often occurs in chronic ki
130         Subjects developed hypocalciuria and secondary hyperparathyroidism on day 4 of the low-protei
131 increase the availability of Mg(2+), such as secondary hyperparathyroidism or ischemia, respectively.
132                             In rat and human secondary hyperparathyroidism, parathyroid AP2 expressio
133    Vitamin D deficiency is a common cause of secondary hyperparathyroidism, particularly in elderly p
134 osphate and in particular the development of secondary hyperparathyroidism play a central role in the
135  prevented parathyroid cell proliferation in secondary hyperparathyroidism rats and in vitro in uremi
136                    Twenty-nine subjects with secondary hyperparathyroidism received oral paricalcitol
137    The underlining mechanisms of CKD-induced secondary hyperparathyroidism remain elusive.
138  lowering plasma PTH levels among those with secondary hyperparathyroidism remains robust despite sub
139 ntly used in children with renal failure and secondary hyperparathyroidism require further studies to
140 D receptor (VDR) gene leads to hypocalcemia, secondary hyperparathyroidism, rickets, and osteomalacia
141 rbonate (CaCO(3)) in the control of serum P, secondary hyperparathyroidism (SH), and ectopic calcific
142                                           In secondary hyperparathyroidism (SH), VDR content is reduc
143                                              Secondary hyperparathyroidism (SHP) is a common complica
144                                              Secondary hyperparathyroidism (SHPT) affects nearly all
145 of parathyroid hyperplasia for patients with secondary hyperparathyroidism (SHPT) and to compare the
146 yperphosphatemia, calcitriol deficiency, and secondary hyperparathyroidism (SHPT) are common complica
147                                              Secondary hyperparathyroidism (SHPT) is an important com
148 s of recurrence of 2 surgical strategies for secondary hyperparathyroidism (SHPT) within 36 months of
149 maging (SPECT/CT) in a patient with advanced secondary hyperparathyroidism successfully treated with
150 urthermore, MRAs attenuate the appearance of secondary hyperparathyroidism that accompanies excretory
151 ceiving hemodialysis with moderate to severe secondary hyperparathyroidism, the use of etelcalcetide
152 t randomized 3883 hemodialysis patients with secondary hyperparathyroidism to receive cinacalcet or p
153                                Patients with secondary hyperparathyroidism underwent ultrasound guide
154 ceiving hemodialysis with moderate to severe secondary hyperparathyroidism, use of etelcalcetide comp
155                                              Secondary hyperparathyroidism was manifested in 28% of p
156            Serum iPTH increased with age and secondary hyperparathyroidism was observed in 17% of the
157 amin D analog developed for the treatment of secondary hyperparathyroidism, was evaluated in three do
158                                Patients with secondary hyperparathyroidism were excluded.
159         Fifty-two hemodialysis patients with secondary hyperparathyroidism were given single orally a
160 women who are vitamin D insufficient develop secondary hyperparathyroidism, which is associated with
161                                              Secondary hyperparathyroidism, which is defined by a hig
162          Vitamin D deficiency contributes to secondary hyperparathyroidism, which occurs early in chr
163 r events in patients with moderate-to-severe secondary hyperparathyroidism who were undergoing dialys
164                 Study in primary and uraemic secondary hyperparathyroidism will indicate whether the
165 provides effective treatment for primary and secondary hyperparathyroidism with a predictable respons
166               We examined the association of secondary hyperparathyroidism with risk of preeclampsia.
167                                 Treatment of secondary hyperparathyroidism with vitamin D and calcium
168 rythropoietin, and controlling the degree of secondary hyperparathyroidism with vitamin D.

 
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