ライフサイエンスコーパス: acute tubular necrosis

1 y reduced scores of acute tubular injury and acute tubular necrosis.

2 y or prevent recovery from ischemic or toxic acute tubular necrosis.

3 shown to differentiate acute rejection from acute tubular necrosis.

4 inflammatory response in the pathogenesis of acute tubular necrosis.

5 anges as significant novel findings in human acute tubular necrosis.

6 t this previously underappreciated aspect of acute tubular necrosis.

7 entirely new approaches for the treatment of acute tubular necrosis.

8 There were no cases of acute tubular necrosis.

9 sis in kidneys of rats with ischemia-induced acute tubular necrosis.

10 ecipients who develop delayed graft function/acute tubular necrosis.

11 l or accidental overdose of OP can result in acute tubular necrosis.

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

13 used to estimate risk early in the course of acute tubular necrosis.

14 ree survival in critically ill patients with acute tubular necrosis.

15 naritide in 504 critically ill patients with acute tubular necrosis.

16 sen it in patients without oliguria who have acute tubular necrosis.

17 picture was consistent with the diagnosis of acute tubular necrosis.

18 n molecule-1 (ICAM-1) in the pathogenesis of acute tubular necrosis.

19 e cyclosporine or tacrolimus toxicity (58%), acute tubular necrosis (12%), and urinary obstruction (1

20 15 patients with acute renal failure due to acute tubular necrosis (12), bilateral renal cortical ne

21 uses of AKI were prerenal azotemia (68.6 %), acute tubular necrosis (25.7 %), hepatorenal syndrome (5

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

23 ture similar to the human condition known as acute tubular necrosis, a process that resolved by cellu

24 the steatotic rats was associated with renal acute tubular necrosis after 24 hours of reperfusion in

25 gand also exacerbated kidney dysfunction and acute tubular necrosis after subthreshold ischemia.

26 The HLA B49, acute tubular necrosis after transplantation, previous t

27 prolonged CI followed by WI and reperfusion, acute tubular necrosis and apoptosis did not occur in hi

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

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

30 esponse was associated with higher scores of acute tubular necrosis and chronic allograft nephropathy

31 injury, shown by the increased incidence of acute tubular necrosis and consequent delayed graft func

32 f ASKs into infants has an increased risk of acute tubular necrosis and graft loss from vascular thro

33 ge in the kidneys and liver, consistent with acute tubular necrosis and multifocal necrosis, and chan

34 Histologic examination revealed acute tubular necrosis and neutrophilic infiltration, bo

35 e clinical course was further complicated by acute tubular necrosis and renal failure requiring long-

36 Simultaneous acute tubular necrosis and tubular cell apoptosis was ra

37 tion of hepatic steatosis and kidney injury, acute tubular necrosis, and apoptotic cell death by the

38 l azotemia (volume-responsive prerenal AKI), acute tubular necrosis, and hepatorenal syndrome (HRS),

39 angiopathies, necrotizing and crescentic GN, acute tubular necrosis, and infective pyelonephritis or

40 vascular and tubular damage consistent with acute tubular necrosis, apoptosis, and renal tubular cel

41 dysfunction, antibody-mediated rejection or acute tubular necrosis, as compared with normal biopsy r

42 dysfunction due to acute rejection (n = 12), acute tubular necrosis (ATN) (n = 8), chronic rejection

43 kidney, lower serum creatinine, and reduced acute tubular necrosis (ATN) and apoptosis.

44 Acute tubular necrosis (ATN) is a syndrome of intrinsic

45 Acute tubular necrosis (ATN) is common in hospitalized p

46 ies obtained in these recipients demonstrate acute tubular necrosis (ATN) occasionally associated wit

47 uates the influence of donor tissue mass and acute tubular necrosis (ATN) on graft survival and incid

48 diuretics are used successfully to alleviate acute tubular necrosis (ATN) produced by chemotherapeuti

49 ighly significant reduction in morphological acute tubular necrosis (ATN) score compared with vehicle

50 cell swelling resulted in varying degrees of acute tubular necrosis (ATN) that slowed the recovery of

51 nal biopsies were diagnosed as no rejection, acute tubular necrosis (ATN), acute rejection (AR), chro

52 val and patient survival rates, incidence of acute tubular necrosis (ATN), acute rejection episodes,

53 in this setting are prerenal azotemia (PRA), acute tubular necrosis (ATN), and hepatorenal syndrome (

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

55 Stx2a-intoxicated mice revealed multifocal, acute tubular necrosis (ATN).

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

57 d biopsy-proven acute allograft dysfunction (acute tubular necrosis [ATN, n=5] and acute rejection [n

58 In ischemic allografts, eg, with acute tubular necrosis but no cellular rejection, DR3 wa

59 s of renal function, renal inflammation, and acute tubular necrosis compared with mice receiving isot

60 Most patients with acute tubular necrosis-delayed graft function that resol

61 Renal transplant biopsies with acute tubular necrosis demonstrated high levels of CtsD

62 a previous acute rejection episode, initial acute tubular necrosis, diastolic blood pressure above 8

63 The clinical syndrome known as acute tubular necrosis does not actually manifest the mo

64 eedback, previously thought to contribute to acute tubular necrosis, has now emerged as a potentially

65 animal models of toxin and ischemia-induced acute tubular necrosis, human studies have not shown any

66 id stem cells ameliorates the acute phase of acute tubular necrosis in animals by promoting prolifera

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

68 ts existed in eight additional patients with acute tubular necrosis in the absence of hypovolemia.

69 al scan was consistent with an area of focal acute tubular necrosis in the newly transplanted kidney.

70 nsplant biopsies, acute CsA toxicity but not acute tubular necrosis is associated with elevated level

71 radigm for recovery of the renal tubule from acute tubular necrosis is that surviving cells from the

72 In the folic acid nephrotoxicity model of acute tubular necrosis, mice expressing KCP survived hig

73 utrophil influx in an in vivo renal ischemic acute tubular necrosis model.

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

75 few mice, while histology showed multifocal acute tubular necrosis of the kidney and edema in the lu

76 r urinary YKL-40 concentration (P<0.001) and acute tubular necrosis on procurement biopsies (P=0.05).

77 No differences were seen in rates of acute tubular necrosis or overall acute rejection incide

78 sed caspase-3 activation, tubular apoptosis, acute tubular necrosis, or BBI, and reduced renal functi

79 01) and clinical rejection (P = 0.0006), and acute tubular necrosis (P < 0.0001).

80 lassical "prerenal acute kidney injury" and "acute tubular necrosis" paradigm might be of limited int

81 n HLA matching, occurrence of posttransplant acute tubular necrosis, presence versus absence of previ

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

83 Furthermore, acute tubular necrosis scores were also similar in IL-1R

84 Acute tubular necrosis secondary to ischemic acute renal

85 in human biopsy specimens from patients with acute tubular necrosis showed similar increases in Nogo-

86 In acute tubular necrosis, there are early transient increa

87 All patients developed acute tubular necrosis; two required a brief period of h

88 intrinsic graft failure comprised rejection, acute tubular necrosis, urinary tract infection/pyelonep

89 d to avoid low-flow states that could induce acute tubular necrosis, vascular thrombosis, or primary

90 and CAD organ recipients, the occurrence of acute tubular necrosis was a significnat risk factor for

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

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

93 cute kidney injury in contemporary articles, acute tubular necrosis was relatively uncommon and, when

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

95 ill patients with acute renal failure due to acute tubular necrosis, we evaluated 256 patients enroll

96 Glomerulonephritis and acute tubular necrosis were present in 28 (68%) and 16 (

97 Untreated animals had significant cortical acute tubular necrosis, which was almost completely prev

98 ermore, patients with delayed graft function/acute tubular necrosis who were treated with tacrolimus+

99 ative response that follows glycerol-induced acute tubular necrosis worsened peak renal injury in viv