ライフサイエンスコーパス: tubular atrophy

1 ted with increased interstitial fibrosis and tubular atrophy.

2 nterstitial area, interstitial fibrosis, and tubular atrophy.

3 n scores, including inflammation in areas of tubular atrophy.

4 for some of them, near foci of fibrosis and tubular atrophy.

5 xhibited more tubular proliferation and less tubular atrophy.

6 reduced tubular proliferation and increased tubular atrophy.

7 ents had near-normal histology, with minimal tubular atrophy (20%) and/or <20% interstitial fibrosis

8 ioning graft = 73, and interstitial fibrosis/tubular atrophy = 59) from 168 unique kidney allograft r

9 rstitial fibrosis (67% vs. 45%, P=0.003) and tubular atrophy (82% vs., 66%, P=0.01).

10 Renal tubular atrophy accompanies many proteinuric renal disea

11 significantly less interstitial fibrosis and tubular atrophy after ischemia-reperfusion injury.

12 r may contribute to excessive cell death and tubular atrophy after obstructive injury.

13 omerulosclerosis, interstitial fibrosis, and tubular atrophy) all increase with age.

14 sulin-injected BB rats showed moderate focal tubular atrophy and an increased mesangial matrix.

15 nificantly reduced interstitial fibrosis and tubular atrophy and associated with improved renal funct

16 Development of proximal tubular atrophy and atubular glomeruli was determined in

17 infiltration is not required for progressive tubular atrophy and increased interstitial fibrosis afte

18 thies (P = 0.002), interstitial fibrosis and tubular atrophy and inflammation (P = 0.04), borderline

19 tion was examined by comparing the degree of tubular atrophy and interstitial fibrosis and the nature

20 n was markedly depressed and linear zones of tubular atrophy and interstitial fibrosis had developed

21 pathologic diagnosis as well as the percent tubular atrophy and interstitial fibrosis on renal biops

22 of diabetic glomerulosclerosis, and greater tubular atrophy and interstitial fibrosis predicted ESRD

23 The degree of tubular atrophy and interstitial fibrosis was graded as

24 Recipients with chronic rejection exhibited tubular atrophy and interstitial fibrosis with an increa

25 ent accelerated recovery, reduced postinjury tubular atrophy and interstitial fibrosis, and increased

26 ut a period of 14 days, in areas of cortical tubular atrophy and interstitial fibrosis, loss of VEGFR

27 e graft, concomitant with the development of tubular atrophy and interstitial fibrosis.

28 ed deterioration in chronic Banff components tubular atrophy and interstitial fibrosis.

29 ontributes to renal dysfunction by promoting tubular atrophy and interstitial fibrosis.

30 damage in the obstructed kidney, with marked tubular atrophy and interstitial fibrosis.

31 erihilar lesions, and seven showed > or =40% tubular atrophy and interstitial fibrosis.

32 rate of graft loss to acute rejection or to tubular atrophy and interstitial fibrosis.

33 ition of peritubular capillaries in areas of tubular atrophy and interstitial fibrosis; VEGF-A down-r

34 Wild-type and SCID mice developed tubular atrophy and interstitial volume expansion in the

35 the development of interstitial fibrosis and tubular atrophy and kidney graft deterioration by preven

36 wk, regeneration of simplified tubules with tubular atrophy and loss with focal, mild interstitial f

37 nd exhibited severe pathological injury with tubular atrophy and necrosis.

38 at a deficiency in Glis2 expression leads to tubular atrophy and progressive fibrosis, similar to nep

39 fusion, inflammation, interstitial fibrosis, tubular atrophy and tissue levels of tumor necrosis fact

40 ead to less severe interstitial fibrosis and tubular atrophy and to significantly better graft surviv

41 ant outcome, such as age-related fibrosis or tubular atrophy and tubular loss.

42 ant outcome, such as age-related fibrosis or tubular atrophy and tubular loss.

43 s associated with higher glomerulosclerosis, tubular atrophy, and arteriosclerosis.

44 ge in body mass index, interstitial fibrosis/tubular atrophy, and change in renal function.

45 The histologic score for CI, tubular atrophy, and CV and the total Banff score were i

46 t formation, necrosis, wire loops, fibrosis, tubular atrophy, and epimembranous deposits.

47 ed significantly with interstitial fibrosis, tubular atrophy, and glomerulosclerosis and associated i

48 Interstitial fibrosis, tubular atrophy, and glomerulosclerosis associated signi

49 iated with increasing cellular infiltration, tubular atrophy, and glomerulosclerosis in the grafts.

50 actors, the result is interstitial fibrosis, tubular atrophy, and graft failure.

51 es after treatment were observed for g, C4d, tubular atrophy, and interstitial fibrosis scores in ear

52 d glomerulosclerosis, vascular obliteration, tubular atrophy, and interstitial fibrosis.

53 h extensive focal global glomerulosclerosis, tubular atrophy, and interstitial fibrosis.

54 common changes such as glomerular sclerosis, tubular atrophy, and interstitial fibrosis.

55 frequently develop interstitial fibrosis and tubular atrophy, and these pathologic changes are the ha

56 lomerulosclerosis, interstitial fibrosis and tubular atrophy, and vascular disease; specimens with a

57 nsition, including interstitial fibrosis and tubular atrophy, and with an ameliorated inflammatory in

58 Albuminuria and tubular atrophy are among the highest risks for CKD prog

59 ccumulation of myofibroblasts and subsequent tubular atrophy are considered key determinants of renal

60 al damage of which interstitial fibrosis and tubular atrophy are dominant features.

61 Interstitial fibrosis and tubular atrophy are major contributors to late graft los

62 ualed the sum of interstitial fibrosis (CI), tubular atrophy, arteriolar hyaline thickening, fibrous

63 The degrees of interstitial fibrosis, tubular atrophy, arteriosclerosis, and arteriolar hyalin

64 e and accumulation of LC-CoAs contributes to tubular atrophy by severing the NHE1-PI(4,5)P2 interacti

65 al animals had severe interstitial fibrosis, tubular atrophy, chronic transplant glomerulopathy, and

66 ar cell quality (defined by a higher rate of tubular atrophy) combined with the reduced potential of

67 te of inflammatory cells in association with tubular atrophy, epithelial mesenchymal transdifferentia

68 elial-mesenchymal transition, with resultant tubular atrophy, fibrosis and renal failure.

69 bular apoptosis is a major factor leading to tubular atrophy following unilateral ureteral obstructio

70 educed chronic histologic changes, including tubular atrophy, glomerulosclerosis, fibrointimal hyperp

71 splants developing interstitial fibrosis and tubular atrophy; however, whether WISE contributes to ch

72 Interstitial fibrosis/tubular atrophy (IF/TA) contributes to the loss of kidne

73 ical rejection and interstitial fibrosis and tubular atrophy (IF/TA) in protocol biopsies are associa

74 itium or ESRD from interstitial fibrosis and tubular atrophy (IF/TA) in the Angiotensin II Blockade f

75 damage, defined by interstitial fibrosis and tubular atrophy (IF/TA), is a leading cause of allograft

76 18S rRNA diagnostic of interstitial fibrosis/tubular atrophy (IF/TA).

77 Interstitial fibrosis and tubular atrophy (IFTA) associated with interstitial infl

78 tions accompanying interstitial fibrosis and tubular atrophy (IFTA) in kidney allografts may point to

79 is a predictor of interstitial fibrosis and tubular atrophy (IFTA) on 24-month biopsy and death-cens

80 iopsy diagnosis of interstitial fibrosis and tubular atrophy (IFTA) was based on random, cause-indica

81 is, 23.9% abnormal interstitial fibrosis and tubular atrophy (IFTA), 4.8% abnormal mesangial matrix i

82 is associated with interstitial fibrosis and tubular atrophy (IFTA).

83 r to the origin of interstitial fibrosis and tubular atrophy (IFTA).

84 opathologic entity interstitial fibrosis and tubular atrophy (IFTA).

85 ole for Bmf in regulating RPTC apoptosis and tubular atrophy in diabetes.

86 increased tubular proliferation and reduced tubular atrophy in the late repair phase.

87 ted rejection, Banff-5 interstitial fibrosis/tubular atrophy, in samples from stable patients and in

88 sion model, both CD3(+) T cell tubulitis and tubular atrophy independently associated with estimated

89 perimental animal models is characterized by tubular atrophy, infiltration of mononuclear inflammator

90 n renal biopsy by global glomerulosclerosis, tubular atrophy, interstitial fibrosis, and arterioscler

91 sclerosis, podocyte foot process effacement, tubular atrophy, interstitial fibrosis, and casts, were

92 lar hypertrophy, diffuse glomerulosclerosis, tubular atrophy, interstitial fibrosis, and decreased re

93 he primary etiology, CKD is characterized by tubular atrophy, interstitial fibrosis, and glomeruloscl

94 ic and functional features of CAN, including tubular atrophy, interstitial fibrosis, glomeruloscleros

95 rosis and total glomerulosclerosis, and more tubular atrophy/interstitial fibrosis.

96 of unilateral ureteral obstruction, proximal tubular atrophy leads to formation of atubular glomeruli

97 , characterized by interstitial fibrosis and tubular atrophy, leads to a progressive decline in graft

98 aft glomerulopathy and interstitial fibrosis/tubular atrophy lesions (P<0.001 for all comparisons).

99 histology (n = 5), interstitial fibrosis and tubular atrophy (n = 6), subclinical (n = 6) and clinica

100 , 4.2], normal and interstitial fibrosis and tubular atrophy, n = 52), and borderline tubulitis (3.3,

101 ey allografts with interstitial fibrosis and tubular atrophy not otherwise specified (IFTANOS), in th

102 thy, now defined as interstital fibrosis and tubular atrophy not otherwise specified, is a near unive

103 ot the pronephric ducts, consistent with the tubular atrophy observed in the affected individuals.

104 moderate to severe interstitial fibrosis and tubular atrophy (odds ratio, 2.50; 95% confidence interv

105 ndocrine defects that include testicular and tubular atrophy, oligospermia, Leydig cell hyperprolifer

106 filtration rate or creatinine clearance and tubular atrophy on biopsy were concurrently assessed.

107 us level, and grade of interstitial fibrosis/tubular atrophy or graft loss.

108 iginally found to have evidence of fibrosis, tubular atrophy, or CD3gamma transcription had worsening

109 iated with interstitial fibrosis (P<0.0001), tubular atrophy (P<0.0001), and upregulation in gal-3 ex

110 0.001) and presence of interstitial fibrosis/tubular atrophy (P=0.003) at diagnosis and changes in GF

111 nd higher risk for interstitial fibrosis and tubular atrophy (P=0.01).

112 cortex and outer medulla accompanied by mild tubular atrophy particularly in the distal convoluted tu

113 , while those with interstitial fibrosis and tubular atrophy plus inflammation (ci>0, cg = 0, i>0) ha

114 Tubular atrophy predicts chronic kidney disease progress

115 ified, what drives interstitial fibrosis and tubular atrophy progression in individual patients is of

116 Tubular atrophy remained an independent predictor at 24

117 Progressive renal interstitial fibrosis and tubular atrophy represent the final injury pathway for a

118 Tubular atrophy resulting from epithelial cell loss is o

119 oint was the change in interstitial fibrosis/tubular atrophy score between implantation and 24-month

120 After 1 year, interstitial fibrosis and tubular atrophy score was significantly greater (1.5+/-0

121 Interstitial fibrosis and tubular atrophy score, interstitial inflammation score,

122 tic regression analysis revealed that higher tubular atrophy scores (ct) together with a lower expres

123 nction due to interstitial fibrosis (IF) and tubular atrophy (TA) is the most common cause of kidney

124 Interstitial fibrosis (IF) and tubular atrophy (TA) was present in 7 (28%) of 25 ABOi c

125 The incidence of (interstitial fibrosis) IF/(tubular atrophy) TA at month 24 was 57.6%, higher in SRL

126 In an attempt to explain the tubular atrophy that is observed in advanced glomerulone

127 The severity of tubular atrophy, tubular casts, and interstitial fibrosi

128 nal function with less interstitial fibrosis/tubular atrophy versus calcineurin inhibitor therapy.

129 on of the previous interstitial fibrosis and tubular atrophy was noted in two patients, suggesting a

130 ing interstitial inflammation, fibrosis, and tubular atrophy were found in the kidney tissue of the D

131 days later, renal interstitial fibrosis and tubular atrophy were quantitated.

132 sion can be predicted based on the degree of tubular atrophy, which is the result of proximal tubule

133 crolimus group for interstitial fibrosis and tubular atrophy with a trend toward higher estimated per

134 aled small dysplastic kidneys with cysts and tubular atrophy with secondary glomerular sclerosis, res

135 Extensive interstitial fibrosis and tubular atrophy without a clear cause was identified as