ライフサイエンスコーパス: plasma creatinine

1 eatinine clearance <60 ml/min or doubling of plasma creatinine).

2 drofolate reductase (DHFR) genotype and cord plasma creatinine.

3 al changes in peritubular capillary flow and plasma creatinine.

4 tion along with decreased levels of ngal and plasma creatinine.

5 peptide (NT-proBNP), urine output (UOP), and plasma creatinine.

6 hil and macrophage infiltration, and rise in plasma creatinine.

7 arance with elevated blood urea nitrogen and plasma creatinine.

8 f allografts are still functioning with mean plasma creatinine 1.5 mg/dL.

9 ing kidney injury, as reflected by 40% lower plasma creatinine (1.17 +/- 0.03 mg/dl) in the electric

10 e HO inhibitor had no effect on the level of plasma creatinine 24 h after reperfusion after treatment

11 ed with a ninefold increase in the levels of plasma creatinine 24 h after reperfusion as compared wit

12 chemia significantly decreased the levels of plasma creatinine 24 h after reperfusion as compared wit

13 ere collected once a week after grafting for plasma creatinine, allo-specific antibodies, and protein

14 ed a significant increase in albuminuria and plasma creatinine and a concurrent decrease in circulati

15 miology Collaboration equation based on both plasma creatinine and cystatin C.

16 cisions of the thymus induced an increase in plasma creatinine and histological rejection in 1 of 3 a

17 NP) significantly reduced CKD as assessed by plasma creatinine and histology.

18 Adenine diet significantly increased plasma creatinine and kidney fibrosis; this was suppress

19 es between groups were apparent in both mean plasma creatinine and mean creatinine clearance; mean (S

20 5 +/- 147 pg/ml; plasma potassium was lower; plasma creatinine and proteinuria (78 +/- 7 mg/d) were g

21 um fused to the remnant kidney and had lower plasma creatinine and urea nitrogen levels; less glomeru

22 nduced renal insufficiency with increases in plasma creatinine and urea, along with increased urinary

23 c nephropathy (mesangial expansion, elevated plasma creatinine and urea, decreased creatinine clearan

24 ral morphometry and the utility of measuring plasma creatinine and urinary albumin, has been almost e

25 sion injury was confirmed by measurements of plasma creatinine and urinary protein excretion.

26 h the highest kidney Ca(2+) content, highest plasma creatinine, and greatest amount of nephrocalcinos

27 d MWF-CKD rats showed proteinuria, increased plasma creatinine, and hypercholesterolemia (all P<0.05)

28 ne systolic blood pressure, urinary albumin, plasma creatinine, and Indian-Asian ethnicity.

29 health and in a CKD model, we examined GFR, plasma creatinine, and kidney histology in mice when gut

30 bleeding were age >75 years, anemia, raised plasma creatinine, and planned long-term anticoagulation

31 orrelated to the degree of tubular fibrosis, plasma creatinine, and urea levels.

32 Using plasma creatinine as outcome could reduce the sample siz

33 al impairment as reflected by an increase in plasma creatinine, associated with acute tubular damage

34 ated with the glomerular filtration rate and plasma creatinine but not with mean arterial pressure.

35 ance rate was 22.7 (5.2) mL/min and the mean plasma creatinine clearance rate was 20.7 (4.8) mL/min.

36 Estimated GFR and 24-hr plasma creatinine clearance underestimate GFR with great

37 content as well as a significant increase in plasma creatinine concentration and a reduced capacity o

38 with the risk of renal outcomes (doubling of plasma creatinine concentration and/or progression to en

39 Dogs were killed when the plasma creatinine concentration exceeded 7 mg/dL.

40 en of 13 grafts were surviving with a median plasma creatinine concentration of 185 mumol/L (range 10

41 -proven idiopathic membranous nephropathy, a plasma creatinine concentration of less than 300 mumol/L

42 gorized on the basis of their peak (maximum) plasma creatinine concentration recorded in the first 24

43 loss and kidney function reduction (rise in plasma creatinine concentration); albuminuria was also g

44 alphaT completely prevented the increase in plasma creatinine concentration, the decrease in urinary

45 is or peritoneal dialysis), and missing peak plasma creatinine concentration.

46 rgement, medullary congestion, and a reduced plasma creatinine concentration.

47 critically ill patients, low admission peak plasma creatinine concentrations are independently assoc

48 splantation (n=20) had significantly greater plasma creatinine concentrations at posttransplant days

49 Regression analysis identified that peak plasma creatinine concentrations less than 60 mumol/L me

50 Elevated plasma creatinine concentrations were associated with ma

51 greater mortality and prolonged elevation of plasma creatinine correlating with less tubular epitheli

52 l; change in kidney weight; 0, 24, and 72 hr plasma creatinine (CR); urea nitrogen (BUN); thromboxane

53 as assessed 24 h later (blood urea nitrogen, plasma creatinine [Cr], and renal histology).

54 ly reduced multiple markers of renal injury (plasma creatinine, cystatin C, FGF23, and TMAO), reduced

55 s later, there was no subsequent increase in plasma creatinine, decrease in glomerular filtration rat

56 evelop kidney damage, evidenced by increased plasma creatinine, decreased kidney weight/body weight r

57 Plasma creatinine did not change with diabetes or SU5416

58 using reported plasma levels and urinary and plasma creatinine estimates.

59 tients surviving one year after trial entry, plasma creatinine exceeded the baseline by more than 25%

60 rated by its analysis of GFRs underlying the plasma creatinine fluctuations in several scenarios of A

61 a dose-dependent decrease in proteinuria and plasma creatinine for the entire 90-day period after tra

62 A2A-KO-->WT chimera, but reduced the rise in plasma creatinine from IRI by 75% in WT mice and by 60%

63 MSCs did not affect plasma creatinine, glomerular filtration rate, neutrophi

64 rsening renal function, defined as a rise in plasma creatinine >/=26.5 mumol/l or 50% higher than the

65 Plasma creatinine had strong longitudinal correlations w

66 Control animals had a stable plasma creatinine, had donor-specific unresponsiveness i

67 renal function showed a significantly higher plasma creatinine in HO-1(-/-) mice compared with HO-1(+

68 mocysteine are significantly correlated with plasma creatinine in patients.

69 ure-induced sepsis was effective in reducing plasma creatinine in this model of AKI.

70 Plasma creatinine, inflammation markers (e.g., TNF-alpha

71 Plasma creatinine is a predictor of survival in amyotrop

72 Plasma creatinine is an inexpensive and easily accessibl

73 creatinine is stable, but do not work if the plasma creatinine is changing rapidly.

74 equations estimate kidney function when the plasma creatinine is stable, but do not work if the plas

75 ity to estimate the kidney function when the plasma creatinine is varying acutely.

76 defined as stage 2 or 3 acute kidney injury (plasma creatinine level >/=2 times the baseline level or

77 ment of acute kidney injury according to the plasma creatinine level alone failed to identify acute k

78 onset diabetes mellitus, skin allergy, and a plasma creatinine level exceeding 150% of the baseline l

79 e >=60 years, cardiac involvement, increased plasma creatinine level, and total plasma exchange volum

80 al 20-HETE levels after ischemia and reduced plasma creatinine levels (+/-SEM) 24 hours after IR from

81 Increased MDA and plasma creatinine levels also became evident after 4 hou

82 Renal graft function was assessed by plasma creatinine levels and histologic analyses.

83 Plasma creatinine levels and renal inflammation, necrosi

84 alt protoporphyrin prevented the increase in plasma creatinine levels and tubulointerstitial and micr

85 fter slow BD induction, superoxide, MDA, and plasma creatinine levels increased further, whereas GPx

86 Plasma creatinine levels rose transiently with complete

87 d heme-oxygenase 1 expression, and increased plasma creatinine levels were evident.

88 herapy also reduced kidney and liver injury, plasma creatinine levels, and messenger RNA expressions

89 on of cisplatin-induced blood urea nitrogen, plasma creatinine levels, kidney injury markers, and tub

90 xygenase 1 expression, and increased MDA and plasma creatinine levels.

91 g/hr [95% CI, 0.4-1.2], p = 0.001) and lower plasma creatinine levels.

92 h after reperfusion as compared with normal plasma creatinine levels; however, administration of CO

93 features of moderate CKD, including elevated plasma creatinine, lower hematocrit, and increased intac

94 Plasma creatinine may, therefore, increase the power to

95 ance technique and adds the convenience of a plasma creatinine measurement.

96 thout albuminuria (n = 4,031) or with normal plasma creatinine (n = 5,032) at diagnosis.

97 t of WRF, defined as a sustained increase in plasma creatinine of 0.5 mg/dl or >/=50% above first val

98 for 92 (87) months (mean [median]) and has a plasma creatinine of 178 (161) micromol/L, whereas the n

99 as AKI, defined as postoperative increase of plasma creatinine of 50% or more, corresponding to the R

100 id not improve renal function as measured by plasma creatinine or blood urea nitrogen.

101 o effect on hematologic changes, the rise in plasma creatinine, or lung myeloperoxidase content.

102 quantitative difference between consecutive plasma creatinines over a given time.

103 slightly attenuated after adjusting for cord plasma creatinine (P = 0.05).

104 Specifically, plasma creatinine (pCr) 2.6 +/- 0.70 mg/dL for KO, n = 1

105 However, in these patients plasma creatinine (Pcr) is inaccurate and the place of s

106 IRI produced a rise in plasma creatinine (PCr) levels in mice receiving no cell

107 time were detected between groups regarding plasma creatinine, plasma neutrophil gelatinase-associat

108 ce demonstrated improvements in albuminuria, plasma creatinine, plasma urea, plasma cholesterol, hist

109 Renal function as determined by plasma creatinine, proteinuria, and glomerular structura

110 PSTR was defined as the four-hour dialysate/plasma creatinine ratio from the first peritoneal equili

111 The mean four-hour dialysate/plasma creatinine ratio in participants was 0.70.

112 was positively correlated with the dialysate/plasma creatinine ratio.

113 Plasma creatinine remained high during hospitalization i

114 decreased creatinine clearance and increased plasma creatinine, renal blood flow (+46% +/- 6%) and co

115 lectomy did not show changes in body weight, plasma creatinine, sodium and potassium, and daily urina

116 amely: creatinine clearance (CrCl) and serum plasma creatinine (SPCr), are integrated into the propos

117 Proteinuria and plasma creatinine strongly associated with plasma choles

118 een patients in rate of decline was lower in plasma creatinine than in ALS functional rating scale-Re

119 ormula variables needed are any steady-state plasma creatinine, the corresponding eGFR by an empirica

120 rawal patients showed a further rise in mean plasma creatinine to 160 (44) and 161 (65) mumol/L at tw

121 AKI attenuated renal injury, as assessed by plasma creatinine, tubular necrosis, and apoptosis.

122 fusion significantly attenuated increases in plasma creatinine, tubular necrosis, macrophage infiltra

123 After 24 hours of reperfusion, we measured plasma creatinine, urea, and histological kidney injury.

124 ifested by increases in blood urea nitrogen, plasma creatinine, urinary N-acetyl-beta-(d)-glucosamini

125 ine and mean creatinine clearance; mean (SD) plasma creatinine values at entry, immediately after wit

126 Plasma creatinine values were lower in the hyperoxia gro

127 Postoperatively, peak plasma creatinine was 1230 and 1274 umol/L (Tx-controls

128 e clearance as estimated from mass, age, and plasma creatinine was a significant predictor of BFI on

129 Plasma creatinine was higher in diabetic CTGF+/+ group (

130 Twenty-four h later, plasma creatinine was measured.

131 Plasma creatinine was significantly greater in A2A-KO th

132 l decline, muscle strength and survival with plasma creatinine were assessed.

133 In line with these findings, increases in plasma creatinine were no different between WT and P2X7(

134 e rejection episodes, insidious increases in plasma creatinine were observed more frequently in this

135 fraction of total glomerular tuft area, and plasma creatinine were significantly higher in D-WT but