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1 imulating production of parathyroid hormone (secondary hyperparathyroidism).
2 omising therapy to improve the management of secondary hyperparathyroidism.
3 rathyroid hyperfunction, such as primary and secondary hyperparathyroidism.
4 hormone levels in patients with primary and secondary hyperparathyroidism.
5 parathyroidectomy in dialysis patients with secondary hyperparathyroidism.
6 associated with vitamin D insufficiency and secondary hyperparathyroidism.
7 lower in the TPN recipients, consistent with secondary hyperparathyroidism.
8 is a major independent determinant of uremic secondary hyperparathyroidism.
9 could be an ideal tool for the treatment of secondary hyperparathyroidism.
10 (PTH) and has been used in the treatment of secondary hyperparathyroidism.
11 ption explains, in part, low-protein-induced secondary hyperparathyroidism.
12 ing homes, which probably contributed to the secondary hyperparathyroidism.
13 l were similar in hemodialysis patients with secondary hyperparathyroidism.
14 hemodialysis patients with mild to moderate secondary hyperparathyroidism.
15 ression in diseases such as osteoporosis and secondary hyperparathyroidism.
16 senting recipients of renal transplants with secondary hyperparathyroidism.
17 mone levels and proteinuria in patients with secondary hyperparathyroidism.
18 ced eGFR in renal transplant recipients with secondary hyperparathyroidism.
19 ceiving hemodialysis with moderate to severe secondary hyperparathyroidism.
20 treatment, particularly in patients who had secondary hyperparathyroidism.
21 ociated hypocalcemia, hyperphosphatemia, and secondary hyperparathyroidism.
22 w ways by which to regulate PTH synthesis in secondary hyperparathyroidism.
23 the upregulation of parathyroid TGF-alpha in secondary hyperparathyroidism.
24 y parathyroid TGF-alpha self-upregulation in secondary hyperparathyroidism.
25 sttransplant hypercalcemia due to persistent secondary hyperparathyroidism.
26 to prevent deficiencies and the sequelae of secondary hyperparathyroidism.
27 he treatment of psoriasis, osteoporosis, and secondary hyperparathyroidism.
28 receiving hemodialysis who have uncontrolled secondary hyperparathyroidism.
31 act parathyroid hormone and the frequency of secondary hyperparathyroidism after kidney transplantati
32 of cinacalcet in the treatment of persistent secondary hyperparathyroidism after kidney transplantati
34 nary phosphorus and attenuate progression of secondary hyperparathyroidism among patients with CKD wh
36 ponse to GH may be affected by the degree of secondary hyperparathyroidism and concurrent treatment w
37 phosphorus diet (Nx-Phos) to induce advanced secondary hyperparathyroidism and divided into the follo
38 low calcium intake and is thought to lead to secondary hyperparathyroidism and increased risk for hip
39 rpS6 phosphorylation for the pathogenesis of secondary hyperparathyroidism and indicate that mTORC1 i
40 ed by an ABD characterized by the absence of secondary hyperparathyroidism and its successful treatme
42 calcium excretion and developed more severe secondary hyperparathyroidism and rachitic skeletal phen
43 has long been associated with progression of secondary hyperparathyroidism and renal osteodystrophy.
44 , vitamin D metabolism, and the treatment of secondary hyperparathyroidism and renal osteodystrophy.
45 increase was attended by the development of secondary hyperparathyroidism and severe osteomalacia.
46 , the DBP-/-, but not DBP+/+, mice developed secondary hyperparathyroidism and the accompanying bone
47 is an important factor in the development of secondary hyperparathyroidism and uremic bone disease.
49 ) diets can also ameliorate uremic symptoms, secondary hyperparathyroidism, and metabolic acidosis in
50 s disease, severe skeletal demineralization, secondary hyperparathyroidism, and muscle weakness can o
53 promoter completely avoided osteomalacia and secondary hyperparathyroidism, and simultaneously increa
55 olism (hyperphosphatemia, hypercalcemia, and secondary hyperparathyroidism) are potentially modifiabl
56 Disorders of mineral metabolism, including secondary hyperparathyroidism, are thought to contribute
57 testinal calcium absorption that resulted in secondary hyperparathyroidism as evidenced by increased
59 I, Nechama et al. demonstrate that in murine secondary hyperparathyroidism associated with CKD or Ca
60 hey are likely to become a major therapy for secondary hyperparathyroidism associated with renal fail
61 analog of 1,25-(OH)(2)D(3), is used to treat secondary hyperparathyroidism because it suppresses para
62 CKD not only to attenuate the progression of secondary hyperparathyroidism but also possibly to reduc
63 1 mug one time daily) significantly improved secondary hyperparathyroidism but did not alter measures
64 ffect of oral paricalcitol on posttransplant secondary hyperparathyroidism by conducting an open labe
66 with chronic renal failure show evidence of secondary hyperparathyroidism by the time maintenance he
73 mportant early factor in the pathogenesis of secondary hyperparathyroidism, could also play a role in
74 dialysis and who had inadequately controlled secondary hyperparathyroidism despite standard treatment
75 -one hemodialysis patients with uncontrolled secondary hyperparathyroidism, despite standard therapy
77 on, biochemical and histological evidence of secondary hyperparathyroidism develops in rats with mild
78 athyroid hormone (PTH) in many patients with secondary hyperparathyroidism due to end-stage renal dis
80 II calcimimetic agents for the treatment of secondary hyperparathyroidism focused on the development
81 es were more pronounced in participants with secondary hyperparathyroidism (group-by-time interaction
82 ated serum PTH concentrations in primary and secondary hyperparathyroidism have been associated with
83 d bone disorder (CKD-MBD) is associated with secondary hyperparathyroidism (HPT) and serum elevations
84 he usual management of hyperphosphatemia and secondary hyperparathyroidism (i.e., mineral salts).
87 that is being evaluated for the treatment of secondary hyperparathyroidism in chronic kidney disease
89 ential therapeutic tool for the treatment of secondary hyperparathyroidism in chronic renal failure.
94 073 when added to conventional treatment of secondary hyperparathyroidism in end-stage renal disease
95 ers a new therapeutic option for controlling secondary hyperparathyroidism in patients with chronic k
96 Thus, treatments used in the management of secondary hyperparathyroidism in renal failure have dive
97 horus (P) restriction is known to ameliorate secondary hyperparathyroidism in renal failure patients.
99 rnal calcium homeostasis promoted additional secondary hyperparathyroidism in the fetus, contributing
100 glands and the regulation of these miRNAs in secondary hyperparathyroidism indicates their importance
101 as activated in the parathyroid of rats with secondary hyperparathyroidism induced by either chronic
102 n D) in patients receiving hemodialysis with secondary hyperparathyroidism (intact parathyroid hormon
106 after therapy with injectable vitamin D for secondary hyperparathyroidism may accelerate vascular di
108 e, which results from nutritional and uremic secondary hyperparathyroidism, may provide a useful anim
109 signed 3883 patients with moderate-to-severe secondary hyperparathyroidism (median level of intact pa
111 paired, (b) that this is due to the state of secondary hyperparathyroidism of CRF since both acute an
112 ytes; (2) this defect is due to the state of secondary hyperparathyroidism of CRF; and (3) excess PTH
113 t of diseases such as psoriasis, cancer, and secondary hyperparathyroidism of renal failure, where a
117 Vitamin D deficiency is a common cause of secondary hyperparathyroidism, particularly in elderly p
118 osphate and in particular the development of secondary hyperparathyroidism play a central role in the
119 prevented parathyroid cell proliferation in secondary hyperparathyroidism rats and in vitro in uremi
121 ntly used in children with renal failure and secondary hyperparathyroidism require further studies to
122 D receptor (VDR) gene leads to hypocalcemia, secondary hyperparathyroidism, rickets, and osteomalacia
123 rbonate (CaCO(3)) in the control of serum P, secondary hyperparathyroidism (SH), and ectopic calcific
125 yperphosphatemia, calcitriol deficiency, and secondary hyperparathyroidism (SHPT) are common complica
127 s of recurrence of 2 surgical strategies for secondary hyperparathyroidism (SHPT) within 36 months of
128 maging (SPECT/CT) in a patient with advanced secondary hyperparathyroidism successfully treated with
129 urthermore, MRAs attenuate the appearance of secondary hyperparathyroidism that accompanies excretory
130 ceiving hemodialysis with moderate to severe secondary hyperparathyroidism, the use of etelcalcetide
131 t randomized 3883 hemodialysis patients with secondary hyperparathyroidism to receive cinacalcet or p
132 ceiving hemodialysis with moderate to severe secondary hyperparathyroidism, use of etelcalcetide comp
135 amin D analog developed for the treatment of secondary hyperparathyroidism, was evaluated in three do
137 women who are vitamin D insufficient develop secondary hyperparathyroidism, which is associated with
140 r events in patients with moderate-to-severe secondary hyperparathyroidism who were undergoing dialys
142 provides effective treatment for primary and secondary hyperparathyroidism with a predictable respons
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