ライフサイエンスコーパス: polyuria

1 hout signs of illness, except some degree of polyuria.

2 water, causing hypovolemia, hypokalemia, and polyuria.

3 thirst, fatigue, dry mouth, polydipsia, and polyuria.

4 e nephropathy is most likely a result of the polyuria.

5 incteric incontinence, polyuria or nocturnal polyuria.

6 QP3 null mice were grossly normal except for polyuria.

7 s, delayed arousal from sleep, and nocturnal polyuria.

8 ed, although as adults they exhibited severe polyuria (10 ml/day), extreme hydronephrosis, low plasma

9 ta(-/-) but not LXRalpha(-/-) mice exhibited polyuria (abnormal daily excretion of highly diluted uri

10 n humans, a syndrome characterized by severe polyuria and electrolyte imbalance.

11 We propose that nocturnal polyuria and essential hypertension share some of the sa

12 atrophic and fluid-filled due to the severe polyuria and hydronephrosis.

13 The patient rapidly developed polyuria and hypernatremia with an inappropriate decreas

14 the water channel aquaporin 2, and improved polyuria and hypokalemia in mutant mice.

15 lycemia is usually slow and symptoms such as polyuria and polydipsia are often subtle and may go unre

16 truncates the AVP precursor (C67X) exhibited polyuria and polydipsia by 2 months of age and these fea

17 knockout of Ildr1 in the mouse kidney causes polyuria and polydipsia due to renal concentrating defec

18 Affected individuals with profound polyuria and polydipsia were homozygous for an autosomal

19 dividuals reported subjective improvement in polyuria and polydipsia with the use of dDAVP (1-desamin

20 insipidus (NDI), a disorder characterized by polyuria and polydipsia.

21 littermates, HNF-1beta mutant mice exhibited polyuria and polydipsia.

22 ty are decreased in FP KOs that exhibit mild polyuria and polydipsia.

23 1 diabetes usually involves symptoms such as polyuria and polydipsia.

24 s that disrupting both kinases causes severe polyuria and salt-wasting by generating SPAK/OSR1 double

25 hat disruption of both kinases would lead to polyuria and severe salt-wasting, and generated SPAK/OSR

26 OVE26 mice exhibited pronounced polyuria and significant albuminuria by 2 months of age

27 sis during childhood, hypercalciuria, and/or polyuria), and 26.0% had Gitelman-like syndrome (fortuit

28 e fertile but exhibit hypokalemia, hypotonic polyuria, and apparent mineralocorticoid activity of cor

29 a decrease in urinary concentrating ability, polyuria, and hydronephrosis in mice.

30 Sglt2(-/-) mice had glucosuria, polyuria, and increased food and fluid intake without di

31 d urine concentrating ability of the kidney, polyuria, and polydipsia.

32 d Cl(-), reduced blood pressure, polydipsia, polyuria, and poor urinary concentrating ability.

33 a, storage or reduced bladder capacity, 24-h polyuria, and sleep-associated nocturia.

34 increase in blood glucose levels, developed polyuria, and succumbed to disease.

35 ncluding blood glucose, insulin, polydipsia, polyuria, and weight loss were measured.

36 Elderly men with nocturnal polyuria are commonly referred for prostate surgery, whi

37 ive disorder that presents as polydipsia and polyuria as a consequence of a loss of secretion of the

38 ted disorder that presents as polydipsia and polyuria as a consequence of a loss of secretion of VP f

39 cturia causes were associated with nocturnal polyuria, bladder storage issues, metabolic syndrome, ab

40 ates had similar levels of hyperglycemia and polyuria, but EGFR(podKO) mice had significantly less al

41 Vitamin D receptor (VDR)-null mice develop polyuria, but the underlying mechanism remains unknown.

42 VDR-null mice had polyuria, but the urine osmolarity was normal as a resul

43 emia, hyperglucagonemia, hyperketonemia, and polyuria caused by insulin deficiency in mice.

44 kiuria: 12 [3%] for both doses vs one [<1%]; polyuria: four [<1%] for both doses vs two [<1%]).

45 pared with controls, patients with nocturnal polyuria have higher nocturnal sodium excretion but not

46 The polyuria, hypercalciuria, and proteinuria of the -/- adu

47 , a human genetic condition characterized by polyuria, hypokalemia, and alkalosis.

48 so significantly ameliorated lithium-induced polyuria, improved urine concentrating ability and AQP2

49 the downregulation of AQP2 and the resulting polyuria in NHE3 null mice.

50 Associated symptoms include weight loss and polyuria in the absence of eating or drinking deficits.

51 Nocturnal polyuria in the elderly is associated with hypertension:

52 ally, studying the pathogenesis of nocturnal polyuria in the elderly may advance our understanding of

53 ded by maximal voided volume), the nocturnal polyuria index (nocturnal urine volume divided by 24-hou

54 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

55 x of less than 2 vs 2 or higher, a nocturnal polyuria index of less than 33% vs 33% or higher, and no

56 habits, obesity, Parkinson's disease, global polyuria, insomnia, sleep disturbances, heart failure, a

57 Nocturnal polyuria is common in the elderly.

58 retention in elderly patients with nocturnal polyuria is illogical and potentially hazardous; nocturi

59 Together, these data indicate that the polyuria observed in VDR-null mice is not caused by impa

60 , sensory urgency, sphincteric incontinence, polyuria or nocturnal polyuria.

61 ated a significant polydipsia (P < 0.03) and polyuria (P < 0.04), with a lower urine osmolality (P <

62 eversal of clinical diabetes markers such as polyuria, polydipsia, and polyphagia.

63 l characteristic symptoms of XNDI, including polyuria, polydipsia, and resistance to the antidiuretic

64 tation is acute, with a few days to weeks of polyuria, polydipsia, and weight loss and lack of a prec

65 ease in mice included lethargy, dehydration, polyuria, polydypsia, and death.

66 r two had transient massive salt-wasting and polyuria reminiscent of antenatal Bartter's syndrome.

67 te the presence of persistent hyperglycemia, polyuria, renal hypertrophy, and hyperfiltration.

68 In addition, these mice suffered from marked polyuria resistant to desmopressin administration.

69 ategorized into organized subsets: nocturnal polyuria, storage or reduced bladder capacity, 24-h poly

70 Thus absence of NKCC2 in the mouse causes polyuria that is not compensated elsewhere in the nephro