ライフサイエンスコーパス: tubular necrosis

1 al anesthesia (Cr, 2.8 +/- 0.3 mg/dl; severe tubular necrosis).

2 ccidental overdose of OP can result in acute tubular necrosis.

3 may play a role in the pathogenesis of acute tubular necrosis.

4 o estimate risk early in the course of acute tubular necrosis.

5 rvival in critically ill patients with acute tubular necrosis.

6 de in 504 critically ill patients with acute tubular necrosis.

7 in patients without oliguria who have acute tubular necrosis.

8 e was consistent with the diagnosis of acute tubular necrosis.

9 cule-1 (ICAM-1) in the pathogenesis of acute tubular necrosis.

10 ced scores of acute tubular injury and acute tubular necrosis.

11 emarkable pathologic renal injury, including tubular necrosis.

12 revent recovery from ischemic or toxic acute tubular necrosis.

13 cecal luminal fluid accumulation, and renal tubular necrosis.

14 to differentiate acute rejection from acute tubular necrosis.

15 matory response in the pathogenesis of acute tubular necrosis.

16 as significant novel findings in human acute tubular necrosis.

17 previously underappreciated aspect of acute tubular necrosis.

18 ly new approaches for the treatment of acute tubular necrosis.

19 There were no cases of acute tubular necrosis.

20 d urea nitrogen, serum creatinine, and renal tubular necrosis.

21 kidneys of rats with ischemia-induced acute tubular necrosis.

22 nts who develop delayed graft function/acute tubular necrosis.

23 site of vascular leak and the kidneys suffer tubular necrosis.

24 osporine or tacrolimus toxicity (58%), acute tubular necrosis (12%), and urinary obstruction (12%).

25 tients with acute renal failure due to acute tubular necrosis (12), bilateral renal cortical necrosis

26 f AKI were prerenal azotemia (68.6 %), acute tubular necrosis (25.7 %), hepatorenal syndrome (5.7 %),

27 from mice infected with C227-11 showed acute tubular necrosis, a finding seen in mice infected with t

28 imilar to the human condition known as acute tubular necrosis, a process that resolved by cellular re

29 eatotic rats was associated with renal acute tubular necrosis after 24 hours of reperfusion in the fa

30 lso exacerbated kidney dysfunction and acute tubular necrosis after subthreshold ischemia.

31 The HLA B49, acute tubular necrosis after transplantation, previous transpl

32 kade during the early injury phase prevented tubular necrosis and AKI, TLR4 blockade during the heali

33 ged CI followed by WI and reperfusion, acute tubular necrosis and apoptosis did not occur in hibernat

34 Ischemic injury to the kidney produces acute tubular necrosis and apoptosis followed by tubular regen

35 corresponding to the morphologic evidence of tubular necrosis and cell detachment; quite surprisingly

36 survival rate, and significantly less acute tubular necrosis and cellular infiltrates.

37 e was associated with higher scores of acute tubular necrosis and chronic allograft nephropathy (P<0.

38 y, shown by the increased incidence of acute tubular necrosis and consequent delayed graft function.

39 into infants has an increased risk of acute tubular necrosis and graft loss from vascular thrombosis

40 d serum creatinine) and histologic criteria (tubular necrosis and in situ DNA fragmentation assessed

41 )C(2)]fumarate allows the detection of early tubular necrosis and its distinction from glomerular inf

42 the kidneys and liver, consistent with acute tubular necrosis and multifocal necrosis, and changes in

43 Histologic examination revealed acute tubular necrosis and neutrophilic infiltration, both of

44 ies in two patients at 70 mg/m(2) were renal tubular necrosis and proteinuria (both grade 3).

45 ical course was further complicated by acute tubular necrosis and renal failure requiring long-term h

46 e shows little correlation between the renal tubular necrosis and the degree of OP-induced acetylchol

47 eys from surviving wild-type mice had severe tubular necrosis and tubular cell apoptosis 24 hours aft

48 Simultaneous acute tubular necrosis and tubular cell apoptosis was rare (55

49 al injury, as assessed by plasma creatinine, tubular necrosis, and apoptosis.

50 f hepatic steatosis and kidney injury, acute tubular necrosis, and apoptotic cell death by the endopl

51 rial rods, proliferative glomerulonephritis, tubular necrosis, and fibrin thrombi within small vessel

52 emia (volume-responsive prerenal AKI), acute tubular necrosis, and hepatorenal syndrome (HRS), a func

53 athies, necrotizing and crescentic GN, acute tubular necrosis, and infective pyelonephritis or sepsis

54 tects against ischemic AKI by reducing renal tubular necrosis, apoptosis, and inflammation, and that

55 lar and tubular damage consistent with acute tubular necrosis, apoptosis, and renal tubular cell desq

56 nction, antibody-mediated rejection or acute tubular necrosis, as compared with normal biopsy results

57 A renal biopsy showed massive tubular necrosis associated with a prominent granulomato

58 ction due to acute rejection (n = 12), acute tubular necrosis (ATN) (n = 8), chronic rejection (n = 6

59 y, lower serum creatinine, and reduced acute tubular necrosis (ATN) and apoptosis.

60 Acute tubular necrosis (ATN) is a syndrome of intrinsic renal

61 Acute tubular necrosis (ATN) is common in hospitalized patient

62 tained in these recipients demonstrate acute tubular necrosis (ATN) occasionally associated with tubu

63 the influence of donor tissue mass and acute tubular necrosis (ATN) on graft survival and incidence o

64 ics are used successfully to alleviate acute tubular necrosis (ATN) produced by chemotherapeutic agen

65 significant reduction in morphological acute tubular necrosis (ATN) score compared with vehicle-treat

66 welling resulted in varying degrees of acute tubular necrosis (ATN) that slowed the recovery of the d

67 opsies were diagnosed as no rejection, acute tubular necrosis (ATN), acute rejection (AR), chronic re

68 d patient survival rates, incidence of acute tubular necrosis (ATN), acute rejection episodes, and ca

69 s setting are prerenal azotemia (PRA), acute tubular necrosis (ATN), and hepatorenal syndrome (HRS).

70 Histologic analysis at 24 h revealed acute tubular necrosis (ATN), and intravital two-photon micros

71 -intoxicated mice revealed multifocal, acute tubular necrosis (ATN).

72 The most frequent cause of AKI is acute tubular necrosis (ATN).

73 sy-proven acute allograft dysfunction (acute tubular necrosis [ATN, n=5] and acute rejection [n=13] i

74 In ischemic allografts, eg, with acute tubular necrosis but no cellular rejection, DR3 was indu

75 Kidneys of moribund wt mice revealed tubular necrosis, but no histopathologic changes were ob

76 enal function, renal inflammation, and acute tubular necrosis compared with mice receiving isotype co

77 Most patients with acute tubular necrosis-delayed graft function that resolved la

78 Renal transplant biopsies with acute tubular necrosis demonstrated high levels of CtsD in dam

79 vious acute rejection episode, initial acute tubular necrosis, diastolic blood pressure above 85 mmHg

80 Three patients with tubular necrosis died after seven, 11 and 26 days of oli

81 The clinical syndrome known as acute tubular necrosis does not actually manifest the morpholo

82 Other lesions included progressive renal tubular necrosis, glomerular fibrin thrombosis, and red

83 k, previously thought to contribute to acute tubular necrosis, has now emerged as a potentially benef

84 l models of toxin and ischemia-induced acute tubular necrosis, human studies have not shown any clini

85 m cells ameliorates the acute phase of acute tubular necrosis in animals by promoting proliferation o

86 Transplant kidney biopsy showed acute tubular necrosis in patient 2.

87 sted in eight additional patients with acute tubular necrosis in the absence of hypovolemia.

88 Hypoxic injury is a major cause of tubular necrosis in the corticomedullary junction of iso

89 n was consistent with an area of focal acute tubular necrosis in the newly transplanted kidney.

90 orrelated with the degree of single cell and tubular necrosis in the S(3)-M segment of the proximal t

91 erum creatinine/urea, caspase-3 protein, and tubular necrosis induced by rhabdomyolysis in wild-type

92 t biopsies, acute CsA toxicity but not acute tubular necrosis is associated with elevated levels of r

93 for recovery of the renal tubule from acute tubular necrosis is that surviving cells from the areas

94 ter cisplatin administration revealed marked tubular necrosis localized to the outer stripe of the ou

95 y attenuated increases in plasma creatinine, tubular necrosis, macrophage infiltration, oxidative str

96 the folic acid nephrotoxicity model of acute tubular necrosis, mice expressing KCP survived high dose

97 il influx in an in vivo renal ischemic acute tubular necrosis model.

98 rfusion, Slit2 significantly inhibited renal tubular necrosis, neutrophil and macrophage infiltration

99 Thus, acute kidney injury is not acute tubular necrosis, nor is it renal failure.

100 reactions, thromboembolic events, and renal tubular necrosis occurred rarely.

101 ice, while histology showed multifocal acute tubular necrosis of the kidney and edema in the lungs of

102 ary YKL-40 concentration (P<0.001) and acute tubular necrosis on procurement biopsies (P=0.05).

103 No differences were seen in rates of acute tubular necrosis or overall acute rejection incidence, a

104 spase-3 activation, tubular apoptosis, acute tubular necrosis, or BBI, and reduced renal function.

105 phase of IRI had no impact on organ atrophy, tubular necrosis, or fibrosis.

106 d clinical rejection (P = 0.0006), and acute tubular necrosis (P < 0.0001).

107 mild renal damage (Cr, 0.9 +/- 0.1, minimal tubular necrosis; P < 0.01).

108 al "prerenal acute kidney injury" and "acute tubular necrosis" paradigm might be of limited interest

109 matching, occurrence of posttransplant acute tubular necrosis, presence versus absence of previous al

110 There was a 4.2% acute tubular necrosis rate for the kidney.

111 Somewhat worse azotemia, but comparable tubular necrosis, resulted with desflurane use.

112 creatinine levels and a lower morphological tubular necrosis score than did wild-type mice with isch

113 Furthermore, acute tubular necrosis scores were also similar in IL-1Ra-trea

114 Acute tubular necrosis secondary to ischemic acute renal failu

115 an biopsy specimens from patients with acute tubular necrosis showed similar increases in Nogo-B in c

116 In acute tubular necrosis, there are early transient increases in

117 All patients developed acute tubular necrosis; two required a brief period of hemodia

118 sic graft failure comprised rejection, acute tubular necrosis, urinary tract infection/pyelonephritis

119 void low-flow states that could induce acute tubular necrosis, vascular thrombosis, or primary nonfun

120 AD organ recipients, the occurrence of acute tubular necrosis was a significnat risk factor for the d

121 any renal histopathologic changes, but acute tubular necrosis was found in 184 (17.4%).

122 The prevalence of acute tubular necrosis was not related to animal size or model

123 idney injury in contemporary articles, acute tubular necrosis was relatively uncommon and, when prese

124 e in two patients, with one developing acute tubular necrosis, was dose-limiting at 6.0 mg/m(2).

125 tients with acute renal failure due to acute tubular necrosis, we evaluated 256 patients enrolled in

126 l failure, glomerular capillary collapse and tubular necrosis were observed.

127 Glomerulonephritis and acute tubular necrosis were present in 28 (68%) and 16 (39%) o

128 eated animals had significant cortical acute tubular necrosis, which was almost completely prevented

129 , patients with delayed graft function/acute tubular necrosis who were treated with tacrolimus+MMF ex

130 response that follows glycerol-induced acute tubular necrosis worsened peak renal injury in vivo.