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1 bdominal pain, fever up to 40 degrees C, and polyuria.
2 ercise could mitigate salt-induced nocturnal polyuria.
3 olecular weight proteinuria, glycosuria, and polyuria.
4 hout signs of illness, except some degree of polyuria.
5 water, causing hypovolemia, hypokalemia, and polyuria.
6  thirst, fatigue, dry mouth, polydipsia, and polyuria.
7 e nephropathy is most likely a result of the polyuria.
8 incteric incontinence, polyuria or nocturnal polyuria.
9 QP3 null mice were grossly normal except for polyuria.
10 s, delayed arousal from sleep, and nocturnal polyuria.
11 rted to contribute to salt-induced nocturnal polyuria.
12 t principal cells, explaining the associated polyuria.
13 non-hyperglycaemic rats with sucrose-induced polyuria.
14 ed, although as adults they exhibited severe polyuria (10 ml/day), extreme hydronephrosis, low plasma
15 ta(-/-) but not LXRalpha(-/-) mice exhibited polyuria (abnormal daily excretion of highly diluted uri
16     The TAZ(f/f); HoxB7Cre mice demonstrated polyuria and a significant decrease in AQP2 abundance in
17 n humans, a syndrome characterized by severe polyuria and electrolyte imbalance.
18                    We propose that nocturnal polyuria and essential hypertension share some of the sa
19  atrophic and fluid-filled due to the severe polyuria and hydronephrosis.
20 mide treatment, ATP6v1b1-/- mice also showed polyuria and hyperchloremia versus Atp6v1b1+/+ .
21                The patient rapidly developed polyuria and hypernatremia with an inappropriate decreas
22  the water channel aquaporin 2, and improved polyuria and hypokalemia in mutant mice.
23 has been proposed as the underlying cause of polyuria and hypotension in patients with the Bartter's
24 in males was associated with albuminuria and polyuria and increased cAMP excretion in netrin-1 transg
25 lishment may be relevant to both UUO-induced polyuria and long-term development of fibrosis in UUO ki
26                          The mice had severe polyuria and nephrogenic diabetes insipidus, potentially
27 xpression in the proximal tubule, leading to polyuria and osmotic diuresis.
28 lycemia is usually slow and symptoms such as polyuria and polydipsia are often subtle and may go unre
29 truncates the AVP precursor (C67X) exhibited polyuria and polydipsia by 2 months of age and these fea
30 knockout of Ildr1 in the mouse kidney causes polyuria and polydipsia due to renal concentrating defec
31           Affected individuals with profound polyuria and polydipsia were homozygous for an autosomal
32 dividuals reported subjective improvement in polyuria and polydipsia with the use of dDAVP (1-desamin
33 insipidus (NDI), a disorder characterized by polyuria and polydipsia.
34 ty are decreased in FP KOs that exhibit mild polyuria and polydipsia.
35 1 diabetes usually involves symptoms such as polyuria and polydipsia.
36 littermates, HNF-1beta mutant mice exhibited polyuria and polydipsia.
37 s that disrupting both kinases causes severe polyuria and salt-wasting by generating SPAK/OSR1 double
38 hat disruption of both kinases would lead to polyuria and severe salt-wasting, and generated SPAK/OSR
39              OVE26 mice exhibited pronounced polyuria and significant albuminuria by 2 months of age
40 sis during childhood, hypercalciuria, and/or polyuria), and 26.0% had Gitelman-like syndrome (fortuit
41 e fertile but exhibit hypokalemia, hypotonic polyuria, and apparent mineralocorticoid activity of cor
42  such as indigestion, constipation, fatigue, polyuria, and depression, while LF significantly amelior
43 a decrease in urinary concentrating ability, polyuria, and hydronephrosis in mice.
44              Sglt2(-/-) mice had glucosuria, polyuria, and increased food and fluid intake without di
45 d urine concentrating ability of the kidney, polyuria, and polydipsia.
46 d Cl(-), reduced blood pressure, polydipsia, polyuria, and poor urinary concentrating ability.
47 a, storage or reduced bladder capacity, 24-h polyuria, and sleep-associated nocturia.
48  increase in blood glucose levels, developed polyuria, and succumbed to disease.
49 ncluding blood glucose, insulin, polydipsia, polyuria, and weight loss were measured.
50 logy; (6) attenuated diet-induced polydipsia/polyuria; and (7) reduced HbA1c.
51                   Elderly men with nocturnal polyuria are commonly referred for prostate surgery, whi
52 ive disorder that presents as polydipsia and polyuria as a consequence of a loss of secretion of the
53 ted disorder that presents as polydipsia and polyuria as a consequence of a loss of secretion of VP f
54 cturia causes were associated with nocturnal polyuria, bladder storage issues, metabolic syndrome, ab
55 ates had similar levels of hyperglycemia and polyuria, but EGFR(podKO) mice had significantly less al
56   Vitamin D receptor (VDR)-null mice develop polyuria, but the underlying mechanism remains unknown.
57                            VDR-null mice had polyuria, but the urine osmolarity was normal as a resul
58 emia, hyperglucagonemia, hyperketonemia, and polyuria caused by insulin deficiency in mice.
59     Epac1(-/-) and Epac2(-/-) mice developed polyuria despite elevated arginine vasopressin levels.
60   This exercise also alleviated salt-induced polyuria during inactive periods (diurnal polyuria index
61 xercise-induced improvements in salt-induced polyuria during inactive periods are caused by increases
62 angiotensin system activity and salt-induced polyuria during inactive periods in 80-week-old mice.
63    Biallelic SLC34A1 variant carriers showed polyuria, failure to thrive, vomiting, constipation, hyp
64 h back pain, general discomfort, polydipsia, polyuria, fatigue and recent weight loss of 10 kg.
65 kiuria: 12 [3%] for both doses vs one [<1%]; polyuria: four [<1%] for both doses vs two [<1%]).
66 pared with controls, patients with nocturnal polyuria have higher nocturnal sodium excretion but not
67                                          The polyuria, hypercalciuria, and proteinuria of the -/- adu
68 , a human genetic condition characterized by polyuria, hypokalemia, and alkalosis.
69        Water deprivation revealed persisting polyuria, impaired urinary concentration ability, and au
70 so significantly ameliorated lithium-induced polyuria, improved urine concentrating ability and AQP2
71 the downregulation of AQP2 and the resulting polyuria in NHE3 null mice.
72  treatment method for salt-induced nocturnal polyuria in older adults.
73  Associated symptoms include weight loss and polyuria in the absence of eating or drinking deficits.
74                                    Nocturnal polyuria in the elderly is associated with hypertension:
75 ally, studying the pathogenesis of nocturnal polyuria in the elderly may advance our understanding of
76 ded by maximal voided volume), the nocturnal polyuria index (nocturnal urine volume divided by 24-hou
77 2 vs 2 or higher (1.39 vs 3.60), a nocturnal polyuria index of less than 33% vs 33% or higher (1.83 v
78 x of less than 2 vs 2 or higher, a nocturnal polyuria index of less than 33% vs 33% or higher, and no
79 ed polyuria during inactive periods (diurnal polyuria index: Sed vs. Mod-Ex, 0.292 +/- 0.027 vs. 0.19
80 habits, obesity, Parkinson's disease, global polyuria, insomnia, sleep disturbances, heart failure, a
81                                    Nocturnal polyuria is a major cause of nocturia, which affects qua
82                                    Nocturnal polyuria is common in the elderly.
83 retention in elderly patients with nocturnal polyuria is illogical and potentially hazardous; nocturi
84                          DI was diagnosed by polyuria, low urine specific gravity, and increasing ser
85       Together, these data indicate that the polyuria observed in VDR-null mice is not caused by impa
86 adult patients with polydipsia and hypotonic polyuria or a known diagnosis of AVP deficiency to under
87 , sensory urgency, sphincteric incontinence, polyuria or nocturnal polyuria.
88 ated a significant polydipsia (P < 0.03) and polyuria (P < 0.04), with a lower urine osmolality (P <
89                    Among adult patients with polyuria polydipsia syndrome, AVP deficiency was more ac
90 ability to concentrate urine, which leads to polyuria, polydipsia and the risk of hypertonic dehydrat
91 eversal of clinical diabetes markers such as polyuria, polydipsia, and polyphagia.
92 l characteristic symptoms of XNDI, including polyuria, polydipsia, and resistance to the antidiuretic
93 tation is acute, with a few days to weeks of polyuria, polydipsia, and weight loss and lack of a prec
94 ease in mice included lethargy, dehydration, polyuria, polydypsia, and death.
95 r two had transient massive salt-wasting and polyuria reminiscent of antenatal Bartter's syndrome.
96 te the presence of persistent hyperglycemia, polyuria, renal hypertrophy, and hyperfiltration.
97 In addition, these mice suffered from marked polyuria resistant to desmopressin administration.
98 ffect of diabetes insipidus - polydipsia and polyuria seen in Hom rats due to loss of AVP facilitatio
99 ategorized into organized subsets: nocturnal polyuria, storage or reduced bladder capacity, 24-h poly
100 letions of both Pax2 and Pax8 exhibit severe polyuria that can be attributed to significant changes i
101    Thus absence of NKCC2 in the mouse causes polyuria that is not compensated elsewhere in the nephro
102 in-2 (AQP2) in the renal collecting duct and polyuria upon reversal.
103  malaise or fatigue, joint pain or myalgias, polyuria, weakness, abdominal pain, and headache at 3 ye
104 nt pain or myalgias, constipation, insomnia, polyuria, weakness, abdominal pain, headache, nausea, am
105  HbA1c, parent with diabetes, and absence of polyuria were significant independent predictors of MODY
106 specific conditional KO (cKO) of Wnk1 caused polyuria with decreased urine osmolality that persisted
107  of Osr1 and Spak in the OVLT in mice caused polyuria with relative hypotonic urine that persisted in

 
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