ライフサイエンスコーパス: urine volume

1 feeling of needing to urinate regardless of urine volume.

2 e for automated and continuous monitoring of urine volume.

3 urinary Na+ excretion and lead to increased urine volume.

4 lution resulting from changes in the overall urine volume.

5 nor with a substantial increase in residual urine volume.

6 d not correlate with creatinine clearance or urine volume.

7 bed to urinary stasis from elevated residual urine volumes.

8 the absence of significant postvoid residual urine volumes.

9 within- and between-person variabilities in urine volume, 24-hour UICs, and spot UICs were higher th

10 women, we observed no seasonal effect on the urine volume, 24-hour UIE, 24-hour UIC, spot UIC, spot U

11 g/mL/h, p = 0.03), resulting in higher total urine volume (299 vs. 80 mL, p < 0.001) and creatinine c

12 LDD caused a significant increase in urine volume (88 +/- 58 to 115 +/- 70 ml/h, p = 0.02, 95

13 BG9719 was given in addition to furosemide, urine volume additionally increased and there was no det

14 a vasopressin-dependent manner, allowing for urine volume adjustment.

15 The persistent high urine volume after AVP administration was traced to a re

16 er handling, with decreased water intake and urine volume, alongside higher urine osmolality.

17 control mice, Dot1l(AC) mice had 40% higher urine volume and 18% lower urine osmolarity with relativ

18 esulting in an approximately sixfold greater urine volume and a fivefold greater fluid requirement, c

19 In the kidney, SLC14A1 regulates urine volume and concentration whereas in erythrocytes i

20 pared with placebo, KW-3902 increased hourly urine volume and estimated CrCl with peak effects occurr

21 sponded to 24-h dehydration with a decreased urine volume and increased urine osmolality.

22 is diuresis was compensated for by a drop in urine volume and nitrogen excretion after the epinephrin

23 tes, creatinine, plasma renin concentration, urine volume and osmolality, ability to concentrate and

24 Knockout mice had increased urine volume and reduced urine sodium concentration, but

25 roup, WAS exposure decreased the single void urine volume and shortened the post-contrast T(1) relaxa

26 ion of the PGI(2) receptor agonist increased urine volume and sodium excretion in mice.

27 Mean 24-h urine volume and sodium excretion were 1964 +/- 1228 mL

28 The coprimary end points were cumulative urine volume and the change in serum cystatin-C in 72 ho

29 Twenty-four-hour urine volume and total uric acid did not differ among th

30 on PP was associated with an improvement in urine volume and urinary excretion of sodium during the

31 5-6), luseogliflozin significantly increased urine volume and urinary glucose excretion (P < 0.001) w

32 re collected for assessing furosemidePK, and urine volume and urine sodium excretion for PD analyses.

33 Urine volume and urine sodium excretion increased signif

34 ithout ibuprofen), a significant increase in urine volume and water intake was observed; urine volume

35 Urine volume and water intake were unchanged in all othe

36 Postvoid residual urine volumes and urine flow rates were not significantl

37 ollection duration, 2) normalization by mean urine volume, and 3) multivariable linear regression mod

38 d using Ringer's lactate to replace excreted urine volume, and 8 kidneys were perfused using urine re

39 eficient mice had lower BP (11 mmHg), higher urine volume, and increased sodium excretion despite mil

40 es as assessed by plasma glucose level, 24-h urine volume, and levels of glycated hemoglobin.

41 trast, are indistinguishable from +/+ in BP, urine volume, and osmolality.

42 stment for treatment order, baseline 24-hour urine volume, and percentage change in loop diuretic dos

43 ng arterial pressure, food and water intake, urine volume, and sodium and potassium excretion.

44 ater intake, food consumption, stool weight, urine volume, and sodium excretion are not significantly

45 g high intravesical pressure, large residual urine volume, and voiding difficulty.

46 Sensitivity analyses using urine volume as another index of RKF yielded consistent

47 NAs quantification by qPCR was possible with urine volume as low as 0.5 mL.

48 ccompanied by reduced daily water intake and urine volume, as well as increased urine osmolality last

49 icantly affect body weight, fluid intake, or urine volume, but the 10 mg x kg(-1) x day(-1) dose redu

50 tial kidney response: There was no effect on urine volume, but there was a significant increase of ur

51 collecting duct principal cells and reduced urine volume by 45% after 5 days of treatment in mice wi

52 The ability to determine adequacy of urine volume by creatinine excretion rate (UVcr) was exa

53 an associated increase in postvoid residual urine volume by the combinations, but not a significantl

54 mitations via the normalization of extracted urine volume by the ratio of absorbance at 300 nm to an

55 ntake of caffeine was associated with higher urine volume, calcium, and potassium and with lower urin

56 for accurate bladder region segmentation and urine volume calculation.

57 multiple abnormalities, including increased urine volume, changes in the circadian rhythm of urinary

58 The total urine volume, creatinine clearance, and change in plasma

59 imary end points included 72-hour cumulative urine volume (decongestion end point) and the change in

60 After 4 d of water restriction, urine volume decreased to the same level as in the rats

61 Therefore, urine volume did not significantly increase with dapagli

62 me), the nocturnal polyuria index (nocturnal urine volume divided by 24-hour volume), and nocturnal u

63 data included the nocturia index (nocturnal urine volume divided by maximal voided volume), the noct

64 no significant effect on 72-hour cumulative urine volume (dopamine, 8524 mL; 95% CI, 7917-9131 vs pl

65 ermeable barrier despite large variations in urine volume during bladder filling and voiding.

66 Parenteral support was reduced if 48-hour urine volumes exceeded baseline values by >/= 10%.

67 d imaging of the bladder is used to estimate urine volume for early diagnosis and management of urine

68 oses of desmopressin (dDAVP) which decreased urine volume from 10 to 4 I/day.

69 Balance studies revealed increased urine volume, hypertonic plasma, polydipsia, and impaire

70 inine in high-risk patients, and documenting urine volume in acutely ill people to achieve early diag

71 re frequent voiding facilitated by increased urine volume in hydrated patients may be offset by incre

72 increasing fluid intake or reducing residual urine volume in the bladder may help prevent infection,

73 A significant increase in urine volume in the water-loaded rats was observed by th

74 Larger plasma and urine volumes in contrived and patient samples showed a

75 concentration (and creatinine to correct for urine volume) in stored samples from 1040 first-trimeste

76 ncreasing salt intake increases drinking and urine volume is widely accepted.

77 Urinary function was assessed by residual urine volume, maximal flow rate (MFR), and International

78 ncentrated urine, and methods to correct for urine volume may be considered.

79 Urine volumes measured by a bladder scanner correlated h

80 by a bladder scanner correlated highly with urine volumes measured by bladder catheterization (summa

81 The second was the correlation between urine volumes measured with a bladder scanner and those

82 h 2014) were searched to identify studies of urine volumes measured with a bladder scanner vs those m

83 ing urinary retention, incontinence, wounds, urine volume measurement, urine sample collection, and c

84 Free water reserve [FWR; urine volume (mL/24 h) minus obligatory urine volume (mL

85 FWR; urine volume (mL/24 h) minus obligatory urine volume (mL/24 h)] served as an HS biomarker.

86 no significant effect on 72-hour cumulative urine volume (nesiritide, 8574 mL; 95% CI, 8014-9134 vs

87 PS volume was equivalently reduced if mean urine volume of a 48-hour balance period exceeded baseli

88 ereby prevented a glucose-driven increase in urine volume of approximately 10 mL/kg/d . 75 kg = 750 m

89 on (preREL), voiding parameters and residual urine volume of preREL+future rapa, preREL+future veh gr

90 om based, aimed at either reducing nocturnal urine volume or targeting autonomic receptors within the

91 her genotype nor IR affected BP, heart rate, urine volume, or albumin excretion.

92 d a significant and dose-related increase in urine volume over 4 h, compared with placebo.

93 In HF, this was associated with increases in urine volume (p < 0.01), sodium excretion (p < 0.01), an

94 ), and nocturnal urine production (nocturnal urine volume per hours slept).

95 children, because of the age-related smaller urine volumes producing spuriously higher iodine concent

96 During 24 h, increases in urine volume ranged from 1.8 l with placebo to 3.9 l aft

97 Intravenous bumetanide increased urine volume, regardless of the diluent used.

98 urine volume and water intake was observed; urine volume rose from 9.5+/-1.0 to 22.9+/-1.1 ml/d in r

99 A bladder scan for urine volume should be performed to assess patients with

100 BPE increases urine volume, sodium, and magnesium compared to the cont

101 analysis (postacquisition normalization) to urine volume, specific gravity and median fold change ar

102 Hot climate conditions may reduce urine volume, thus leading to overestimations of UIC and

103 We measured the urine volume, UIC, and urinary creatinine concentration

104 Hemodynamics, gastric intramucosal pH (pHi) urine volumes, urinary sodium excretion, and cimetidine-

105 Urine volume, urine osmolality, and urinary excretion of

106 After we measured the total urine volume (Uvol), the aliquot was stored for the late

107 001) and nesiritide (interaction P=0.039) on urine volume varied by EF group.

108 ified their self-assessed diuretic response (urine volume) via a standardized survey.

109 k women was 0.11 units higher (P = 0.03) and urine volume was 0.24 L less (P = 0.001).

110 In South African women, the median 24-hour urine volume was 1.40 L (IQR, 0.96-2.05 L) in the winter

111 In heart failure with reduced EF, urine volume was higher with active treatment versus pla

112 e, whereas relationship between eGFR and 6-h urine volume was linear (r = 0.61, p < 0.001).

113 whereas in heart failure with preserved EF, urine volume was lower with active treatment.

114 Urine volume was measured 3 hours after administration o

115 An increase in urine volume was observed with tolvaptan when compared w

116 PVR bladder urine volume was quantified as the largest cross-section

117 Voiding parameters and residual urine volume were measured prior to sacrifice of sham an

118 However, 6-hour urine sodium and 6-hour urine volume were not different between the two groups.

119 These increases in urine volumes were accompanied by significant increases

120 or were invasive urodynamic studies, and if urine volumes were measured with a bladder scanner and b

121 onditions, plasma and urine osmolalities and urine volumes were similar between CD-KO mice and contro

122 ttern of relationship between UNa(+) and 6-h urine volume, whereas relationship between eGFR and 6-h

123 iuria, hyperoxaluria, hypocitraturia and low urine volume, whereas the formation of uric acid and cal

124 h the assessment of sodium concentration and urine volume, which are also treatment goals themselves.

125 Luseogliflozin significantly increased urine volume, which was associated with significantly in

126 decrease in water intake and an increase in urine volume with surplus osmolyte excretion.

127 V2 receptor blockade increased urine volume without affecting protein excretion.

128 zin caused a significant increase in 24-hour urine volume without an increase in urinary sodium when

129 Hydrochlorothiazide increases urine volume without enhancing FDG excretion.