ライフサイエンスコーパス: acute tubular necrosis

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

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

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

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

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

6 ne and ameliorated the histological score of acute tubular necrosis.

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

8 finding at autopsy in patients with ischemic acute tubular necrosis.

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

10 pitalized patients with AKI and COVID-19 was acute tubular necrosis.

11 shown to differentiate acute rejection from acute tubular necrosis.

12 inflammatory response in the pathogenesis of acute tubular necrosis.

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

14 t this previously underappreciated aspect of acute tubular necrosis.

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

16 There were no cases of acute tubular necrosis.

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

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

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

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

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

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

23 15 patients with acute renal failure due to acute tubular necrosis (12), bilateral renal cortical ne

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

25 tubular degenerative changes consistent with acute tubular necrosis (73%).

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

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

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

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

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

31 prerenal AKI, 64 (39.5%) HRS-AKI, 27 (16.7%) acute tubular necrosis-AKI (ATN-AKI), and 36 (22.2%) a m

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

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

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

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

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

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

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

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

40 lso showed utility in the early detection of acute tubular necrosis and rejection.

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

42 Simultaneous acute tubular necrosis and tubular cell apoptosis was ra

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

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

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

46 All biopsy samples showed varying degrees of acute tubular necrosis, and one patient had associated w

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

48 Acute tubular necrosis, apoptosis, urinary kidney damage

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

50 .4%); BK virus nephropathy (BKVAN) 9.9%; and acute tubular necrosis (ATN with i-INT) in 5.9% of cases

51 Cases included patients with acute tubular necrosis (ATN) (n = 10), hepatorenal syndr

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

53 the highest recovery rates of recovery were acute tubular necrosis (ATN) and acute interstitial neph

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

55 r main diagnostic groups-SAGN, primary IgAN, acute tubular necrosis (ATN) and normal kidney (baseline

56 be useful in differential diagnosis between acute tubular necrosis (ATN) and other types of acute ki

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

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

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

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

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

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

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

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

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

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

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

68 arly AMR, acute cellular rejection (ACR), or acute tubular necrosis (ATN).

69 pecific section of a nephron, referred to as acute tubular necrosis (ATN).

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

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

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

73 s was obtained for 77 patients (96.3%), with acute tubular necrosis being the most frequent: 23 (29.9

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

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

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

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

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

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

80 itrate is used primarily for differentiating acute tubular necrosis from interstitial nephritis and a

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

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

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

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

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

86 who died with severe COVID-19 in China found acute tubular necrosis in the kidney, a few patient repo

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

88 Acute tubular necrosis involves dynamic cell death propa

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

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

91 Differential diagnosis with AKI-acute tubular necrosis may be challenging and kidney bio

92 Acute tubular necrosis mediates acute kidney injury (AKI

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

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

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

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

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

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

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

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

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

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

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

104 nd blood-perfused kidneys had vastly reduced acute tubular necrosis scores and degrees of terminal de

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

106 Acute tubular necrosis secondary to ischemic acute renal

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

108 In acute tubular necrosis, there are early transient increa

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

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

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

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

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

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

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

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

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

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

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

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

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