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1 ible with a diagnosis of partial nephrogenic diabetes insipidus.
2 ndling of water in health and in nephrogenic diabetes insipidus.
3 might be necessary in patients with central diabetes insipidus.
4 in AVP-expressing neurons, developed central diabetes insipidus.
5 treatment of mice and a patient with central diabetes insipidus.
6 a (increased water intake), both features of diabetes insipidus.
7 autoreactive CD8 T cells can trigger central diabetes insipidus.
8 ing, the absence of which causes nephrogenic diabetes insipidus.
9 s a potential therapeutic use in nephrogenic diabetes insipidus.
10 main of the human vasopressin gene can cause diabetes insipidus.
11 defect and hypernatremic dehydration due to diabetes insipidus.
12 essin analog), characteristic of nephrogenic diabetes insipidus.
13 alleles responsible for X-linked nephrogenic diabetes insipidus.
14 ing from congenital cataracts to nephrogenic diabetes insipidus.
15 mice produces distinct forms of nephrogenic diabetes insipidus.
16 he pathogenesis of familial neurohypophyseal diabetes insipidus.
17 t tissue and nodal involvement, and four had diabetes insipidus.
18 another three patients due to development of diabetes insipidus.
19 ions or downregulation can cause nephrogenic diabetes insipidus.
20 a, twins or triplets, or subclinical central diabetes insipidus, a transient diabetes insipidus may e
21 Autosomal dominant familial neurohypophyseal diabetes insipidus (adFNDI) is a progressive, inherited
22 autosomal dominant familial neurohypophyseal diabetes insipidus (adFNDI), a rare inherited disorder t
23 effect of donor hyperosmolarity secondary to diabetes insipidus, an almost universal occurrence among
24 e an autosomal recessive form of nephrogenic diabetes insipidus and absence of the Colton blood group
27 ts identify a novel mechanism of nephrogenic diabetes insipidus and uncover a role of SOCE in renal w
28 icant risk factor for lower scores, but sex, diabetes insipidus, and cranial radiotherapy were not.
30 enerative origin of optic atrophy, deafness, diabetes insipidus, and incontinence, (2) other previous
31 dentified growth hormone deficiency, central diabetes insipidus, and male hypogonadism as new feature
33 function, including hypochloremic alkalosis, diabetes insipidus, and salt-sensitive hypotension, with
34 attleboro rats, with hereditary hypothalamic diabetes insipidus, and Sprague-Dawley rats, with normal
40 eatures subsequently emerged, and "DIDMOAD" (diabetes insipidus, diabetes mellitus, optic atrophy, an
41 ble organ donors without clinically apparent diabetes insipidus display a defect in the baroreflex-me
42 tis pigmentosa, color blindness, nephrogenic diabetes insipidus, familial ACTH resistance, and famili
47 veloped as the disease progressed, including diabetes insipidus, growth hormone deficiency, primary h
48 nt inhibitor of GSK3beta, causes nephrogenic diabetes insipidus, GSK3beta may play a crucial role in
49 2 receptor and aquaporin 2 cause nephrogenic diabetes insipidus; however, expression of these genes i
50 ascular complications, visual complications, diabetes insipidus, hypopituitarism and cranial nerve in
51 etal defects in 42%, dental problems in 30%, diabetes insipidus in 25%, growth failure in 20%, sex ho
54 hich is associated with familial nephrogenic diabetes insipidus, induces constitutive arrestin-mediat
55 most common cause of hereditary nephrogenic diabetes insipidus is a nonfunctional vasopressin (VP) r
57 Autosomal dominant familial neurohypophyseal diabetes insipidus is caused by mutations in the arginin
60 ver, proAVP misfolding in hereditary central diabetes insipidus likely shares common physiopathologic
62 erimental iron overload leads to nephrogenic diabetes insipidus marked by AVP-resistant urinary conce
63 ical central diabetes insipidus, a transient diabetes insipidus may ensue from this vasopressinase-me
64 Mechanisms underlying the pathogenicity of diabetes insipidus mutations were probed by studying the
65 (AQP2) point mutants that cause nephrogenic diabetes insipidus (NDI) are retained in the endoplasmic
69 n family with partial congenital nephrogenic diabetes insipidus (NDI) that resulted from a mutation i
70 utations that cause non-X-linked nephrogenic diabetes insipidus (NDI) were characterized to establish
71 nts treated with lithium develop nephrogenic diabetes insipidus (NDI), a disorder characterized by po
72 ary concentrating ability, i.e., nephrogenic diabetes insipidus (NDI), but the molecular mechanism is
73 ting a transgenic mouse model of nephrogenic diabetes insipidus (NDI), we have analyzed the mouse aqu
76 re of the possibility of sevoflurane-induced diabetes insipidus not only during general anesthesia bu
77 lex, followed by a hyperdynamic response and diabetes insipidus, occurred in every animal following b
79 Our findings establish a form of nephrogenic diabetes insipidus produced by impaired water permeabili
80 with these effects, Grhl2-deficient mice had diabetes insipidus, produced dilute urine, and failed to
81 associated with Charcot-Marie-Tooth disease, diabetes insipidus, retinitis pigmentosa, cystic fibrosi
83 hree children affected with neurohypophyseal diabetes insipidus, suggesting autosomal recessive inher
85 (AdAVP) in an AVP-deficient animal model of diabetes insipidus (the Brattleboro rat), which allowed
86 that a molecular determinant for nephrogenic diabetes insipidus, the vasopressin receptor with a subs
87 id organ donors without clinical evidence of diabetes insipidus; we also investigated the vasopressor
88 shing phenomenon, hyperdynamic response, and diabetes insipidus were observed in each animal after BD
90 hormone arginine vasopressin (AVP) underlies diabetes insipidus, which is characterized by the excret
91 -) mice represent a new model of nephrogenic diabetes insipidus with unique molecular etiology, and w
92 mutation known to cause X-linked nephrogenic diabetes insipidus (XNDI) in humans (Glu242stop) into th
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