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1 erlying lithium-induced nephrogenic diabetes insipidus.
2 its perturbation is associated with diabetes insipidus.
3 hree patients due to development of diabetes insipidus.
4 ownregulation can cause nephrogenic diabetes insipidus.
5 duced, ameliorating the symptoms of diabetes insipidus.
6 pressing neurons, developed central diabetes insipidus.
7 a diagnosis of partial nephrogenic diabetes insipidus.
8 water in health and in nephrogenic diabetes insipidus.
9 necessary in patients with central diabetes insipidus.
10 of mice and a patient with central diabetes insipidus.
11 sed water intake), both features of diabetes insipidus.
12 ive CD8 T cells can trigger central diabetes insipidus.
13 absence of which causes nephrogenic diabetes insipidus.
14 tial therapeutic use in nephrogenic diabetes insipidus.
15 he human vasopressin gene can cause diabetes insipidus.
16 nd hypernatremic dehydration due to diabetes insipidus.
17 log), characteristic of nephrogenic diabetes insipidus.
18 esponsible for X-linked nephrogenic diabetes insipidus.
19 congenital cataracts to nephrogenic diabetes insipidus.
20 duces distinct forms of nephrogenic diabetes insipidus.
21 enesis of familial neurohypophyseal diabetes insipidus.
22 and nodal involvement, and four had diabetes insipidus.
23 or triplets, or subclinical central diabetes insipidus, a transient diabetes insipidus may ensue from
24 diabetes, diabetic ketoacidosis, or diabetes insipidus; a need for renal replacement therapy; severe
25 dominant familial neurohypophyseal diabetes insipidus (adFNDI) is a progressive, inherited neurodege
26 dominant familial neurohypophyseal diabetes insipidus (adFNDI), a rare inherited disorder that prese
27 ite a paucity of published reports, diabetes insipidus after discontinuation of vasopressin infusion
29 investigate the occurrence rate of diabetes insipidus after discontinuation of vasopressin infusion
33 dings demonstrate the occurrence of diabetes insipidus after discontinuation of vasopressin infusion
34 donor hyperosmolarity secondary to diabetes insipidus, an almost universal occurrence among brain-de
35 somal recessive form of nephrogenic diabetes insipidus and absence of the Colton blood group antigens
36 nistration (FDA) in 1978 for use in diabetes insipidus and bleeding disorders, but it is also prescri
38 ipolar disorder, causes nephrogenic diabetes insipidus and hypercalcemia in about 20% and 10% of pati
41 fy a novel mechanism of nephrogenic diabetes insipidus and uncover a role of SOCE in renal water hand
42 sis, diagnosis of low-grade glioma, diabetes insipidus, and central precocious puberty were associate
45 origin of optic atrophy, deafness, diabetes insipidus, and incontinence, (2) other previously report
46 growth hormone deficiency, central diabetes insipidus, and male hypogonadism as new features of PCSK
47 Improvement in bone lesions, pain, diabetes insipidus, and other manifestations was gradual over man
48 including hypochloremic alkalosis, diabetes insipidus, and salt-sensitive hypotension, with depletio
49 rats, with hereditary hypothalamic diabetes insipidus, and Sprague-Dawley rats, with normal pituitar
50 rteen months post-OLT she developed diabetes insipidus, bilateral ear discharge, and new osteolytic l
52 ocellular cells or a side effect of diabetes insipidus, but favors the hypothesis that central, parvo
53 tal tubular acidosis or nephrogenic diabetes insipidus can be caused by autoantibodies targeting the
55 rophy which is often accompanied by diabetes insipidus, deafness, urological and neurological complic
56 thermore, in a patient with central diabetes insipidus, desmopressin reduced the excretion of ECVs de
60 icated for the treatment of central diabetes insipidus (DI), bedwetting, haemophilia A and von Willeb
63 ubsequently emerged, and "DIDMOAD" (diabetes insipidus, diabetes mellitus, optic atrophy, and deafnes
64 donors without clinically apparent diabetes insipidus display a defect in the baroreflex-mediated se
65 t have utility in treating forms of diabetes insipidus (e.g., X-linked nephrogenic diabetes insipidus
66 ntosa, color blindness, nephrogenic diabetes insipidus, familial ACTH resistance, and familial hypoca
71 s the disease progressed, including diabetes insipidus, growth hormone deficiency, primary hypogonadi
72 tor of GSK3beta, causes nephrogenic diabetes insipidus, GSK3beta may play a crucial role in regulatin
73 r and aquaporin 2 cause nephrogenic diabetes insipidus; however, expression of these genes is maintai
74 omplications, visual complications, diabetes insipidus, hypopituitarism and cranial nerve injury.
75 cts in 42%, dental problems in 30%, diabetes insipidus in 25%, growth failure in 20%, sex hormone def
79 ation (which could explain acquired diabetes insipidus in patients receiving lithium) is unclear.
80 sipidus (e.g., X-linked nephrogenic diabetes insipidus) in which the kidney responds inappropriately
81 ssociated with familial nephrogenic diabetes insipidus, induces constitutive arrestin-mediated desens
82 mon cause of hereditary nephrogenic diabetes insipidus is a nonfunctional vasopressin (VP) receptor t
85 dominant familial neurohypophyseal diabetes insipidus is caused by mutations in the arginine vasopre
89 VP misfolding in hereditary central diabetes insipidus likely shares common physiopathological mechan
90 reduce lithium-induced nephrogenic diabetes insipidus (lithium-NDI), patients with bipolar disorder
91 iron overload leads to nephrogenic diabetes insipidus marked by AVP-resistant urinary concentrating
92 ral diabetes insipidus, a transient diabetes insipidus may ensue from this vasopressinase-mediated de
93 sms underlying the pathogenicity of diabetes insipidus mutations were probed by studying their effect
94 oint mutants that cause nephrogenic diabetes insipidus (NDI) are retained in the endoplasmic reticulu
95 f a variety of acquired nephrogenic diabetes insipidus (NDI) disorders have identified a common featu
98 Hereditary non-X-linked nephrogenic diabetes insipidus (NDI) is caused by mutations in the aquaporin-
99 imal models of acquired nephrogenic diabetes insipidus (NDI) that loss of the aquaporin-2 (AQP2) prot
100 with partial congenital nephrogenic diabetes insipidus (NDI) that resulted from a mutation in the aqu
101 that cause non-X-linked nephrogenic diabetes insipidus (NDI) were characterized to establish the cell
102 ed with lithium develop nephrogenic diabetes insipidus (NDI), a disorder characterized by polyuria an
103 ntrating ability, i.e., nephrogenic diabetes insipidus (NDI), but the molecular mechanism is unknown.
104 ansgenic mouse model of nephrogenic diabetes insipidus (NDI), we have analyzed the mouse aquaporin-2
109 possibility of sevoflurane-induced diabetes insipidus not only during general anesthesia but also in
111 owed by a hyperdynamic response and diabetes insipidus, occurred in every animal following brain deat
113 poarousal could be a side effect of diabetes insipidus - polydipsia and polyuria seen in Hom rats due
115 had severe polyuria and nephrogenic diabetes insipidus, potentially due to greatly reduced AQP2 and A
116 many countries for the treatment of diabetes insipidus, primary nocturnal enuresis, nocturia, and coa
117 ngs establish a form of nephrogenic diabetes insipidus produced by impaired water permeability in col
118 e effects, Grhl2-deficient mice had diabetes insipidus, produced dilute urine, and failed to adequate
119 d with Charcot-Marie-Tooth disease, diabetes insipidus, retinitis pigmentosa, cystic fibrosis, and se
121 dren affected with neurohypophyseal diabetes insipidus, suggesting autosomal recessive inheritance.
123 in an AVP-deficient animal model of diabetes insipidus (the Brattleboro rat), which allowed us to mon
124 lecular determinant for nephrogenic diabetes insipidus, the vasopressin receptor with a substitution
126 donors without clinical evidence of diabetes insipidus; we also investigated the vasopressor effect o
128 or treatment of shock, criteria for diabetes insipidus were observed in two of 1,320 subjects (0.15%)
130 rginine vasopressin (AVP) underlies diabetes insipidus, which is characterized by the excretion of ab
131 epresent a new model of nephrogenic diabetes insipidus with unique molecular etiology, and we have id
132 known to cause X-linked nephrogenic diabetes insipidus (XNDI) in humans (Glu242stop) into the mouse g