ライフサイエンスコーパス: tubular atrophy

1 ion, and extensive interstitial fibrosis and tubular atrophy.

2 osis, hyalinosis, interstitial fibrosis, and tubular atrophy.

3 of cast formation and interstitial fibrosis/tubular atrophy.

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

5 ted with increased interstitial fibrosis and tubular atrophy.

6 nterstitial area, interstitial fibrosis, and tubular atrophy.

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

8 xhibited more tubular proliferation and less tubular atrophy.

9 reduced tubular proliferation and increased tubular atrophy.

10 rejection (67.4%); interstitial fibrosis and tubular atrophy (14.4%); BK virus nephropathy (BKVAN) 9.

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

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

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

14 Renal tubular atrophy accompanies many proteinuric renal disea

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

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

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

18 stigated modifying interstitial fibrosis and tubular atrophy allowing semiquantitative reporting.

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

20 l glomerulosclerosis, interstitial fibrosis, tubular atrophy and arteriolosclerosis.

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

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

23 to inflammation in interstitial fibrosis and tubular atrophy and chronic active T cell-mediated rejec

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

45 of biomarkers with interstitial fibrosis and tubular atrophy and progression to end-stage kidney dise

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

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

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

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

50 58% had under 5% interstitial fibrosis with tubular atrophy, and 46% versus 25% had no vascular dise

51 biopsies showed mild interstitial fibrosis, tubular atrophy, and a resolution of bile casts.

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

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

54 lary hypercellularity, interstitial fibrosis/tubular atrophy, and crescents ( P < 0.05 each).

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

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

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

58 Interstitial fibrosis, tubular atrophy, and glomerulosclerosis associated signi

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

60 logic changes such as interstitial fibrosis, tubular atrophy, and glomerulosclerosis may represent ch

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

62 Interstitial fibrosis, tubular atrophy, and inflammation are major contributors

63 sclerotic glomeruli, interstitial fibrosis, tubular atrophy, and inflammation within both nonatrophi

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

65 glomerulopathy, fibrous intimal thickening, tubular atrophy, and interstitial fibrosis scores were a

66 with mild interstitial inflammation, minimal tubular atrophy, and interstitial fibrosis.

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

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

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

70 i, accompanied by interstitial inflammation, tubular atrophy, and interstitial fibrosis.

71 f DKD, such as basement membrane thickening, tubular atrophy, and podocyte cytoskeletal impairment.

72 riolar hyalinosis, interstitial fibrosis and tubular atrophy, and the percentage of renal sclerotic g

73 , segmental sclerosis, interstitial fibrosis/tubular atrophy, and the presence of crescents (MEST-C)

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

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

76 kidney aging, including glomerulosclerosis, tubular atrophy, and vascular rarefaction.

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

78 omerulosclerosis, interstitial fibrosis with tubular atrophy, and/or vascular disease was non-inferio

79 egmental sclerosis and interstitial fibrosis/tubular atrophy-and novel features, including adhesion,

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

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

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

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

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

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

86 al glomerulosclerosis, interstitial fibrosis/tubular atrophy, artery luminal stenosis, and arteriolar

87 ection, >=grade 2 interstitial fibrosis, and tubular atrophy), as well as with de novo donor-specific

88 ion diagnoses were interstitial fibrosis and tubular atrophy, ascending pyelonephritis, and calcineur

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

90 ivity of angiogenesis, interstitial fibrosis tubular atrophy, CA-AMR, and DSA-related pathways when c

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

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

93 racterized by greater interstitial fibrosis, tubular atrophy, complement degradation split-product 4d

94 x was the sum of interstitial fibrosis (ci), tubular atrophy (ct), chronic vasculopathy (cv), and chr

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

96 ted with augmented interstitial fibrosis and tubular atrophy eventually leading to CKD.

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

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

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

100 Interstitial fibrosis and tubular atrophy >1% is also associated with graft failur

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

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

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

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

105 y luminal stenosis and interstitial fibrosis/tubular atrophy (IF/TA) of the cortex.

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

107 centage of cortex with interstitial fibrosis/tubular atrophy (IF/TA).

108 18S rRNA diagnostic of interstitial fibrosis/tubular atrophy (IF/TA).

109 were determined by interstitial fibrosis and tubular atrophy (IFTA) and by transplant glomerulopathy.

110 12 mos), premature interstitial fibrosis and tubular atrophy (IFTA) and decreased seven-year graft su

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

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

113 Interstitial fibrosis and tubular atrophy (IFTA) is a strong indicator of decline

114 Interstitial fibrosis/tubular atrophy (IFTA) is an important cause of kidney a

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

116 Interstitial fibrosis and tubular atrophy (IFTA) on a renal biopsy are strong indi

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

118 grafts, pathologic interstitial fibrosis and tubular atrophy (IFTA) was scored and eGFR was calculate

119 limeter, and degree of interstitial fibrosis/tubular atrophy (IFTA) were independently associated wit

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

121 d glomeruli (GSG), interstitial fibrosis and tubular atrophy (IFTA), and arteriosclerosis (luminal st

122 nd the severity of interstitial fibrosis and tubular atrophy (IFTA), glomerulosclerosis, arteriolar s

123 lomeruli (GSG) and interstitial fibrosis and tubular atrophy (IFTA), is a pathology of both kidney ag

124 regions of mature interstitial fibrosis and tubular atrophy (IFTA), pre-IFTA, and non-IFTA.

125 erulosclerosis and interstitial fibrosis and tubular atrophy (IFTA).

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

127 disease (CKD) are interstitial fibrosis and tubular atrophy (IFTA).

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

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

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

131 easing severity of interstitial fibrosis and tubular atrophy in the Boston Kidney Biopsy Cohort.

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

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

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

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

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

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

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

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

140 ng to common nonspecific end points ( e.g ., tubular atrophy, interstitial fibrosis, and glomeruloscl

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

142 ercellularity, segmental glomerulosclerosis, tubular atrophy/interstitial fibrosis, crescents score,

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

144 omerulosclerosis, interstitial fibrosis, and tubular atrophy) is the defining pathology of both kidne

145 histologically by interstitial fibrosis and tubular atrophy, is the major cause of kidney allograft

146 aracteristics included interstitial fibrosis/tubular atrophy, larger cortical nephron size (but not n

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

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

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

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

151 , 4.2], normal and interstitial fibrosis and tubular atrophy, n = 52), and borderline tubulitis (3.3,

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

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

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

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

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

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

158 higher fraction of interstitial fibrosis and tubular atrophy on histology.

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

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

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

162 0.001) and presence of interstitial fibrosis/tubular atrophy (P=0.003) at diagnosis and changes in GF

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

164 erosis, P=0.001 or interstitial fibrosis and tubular atrophy, P<0.001) on kidney biopsy.

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

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

167 Tubular atrophy predicts chronic kidney disease progress

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

169 Tubular atrophy remained an independent predictor at 24

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

171 Tubular atrophy resulting from epithelial cell loss is o

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

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

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

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

176 ly associated with interstitial fibrosis and tubular atrophy severity.

177 glomeruli (N) and interstitial fibrosis and tubular atrophy (T) were reweighted (N0: >25%=0, N1: 10%

178 lerosis [S] and interstitial fibrosis and/or tubular atrophy [T]) is useful in helping assess prognos

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

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

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

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

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

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

185 The parameter interstitial fibrosis and tubular atrophy was modified to allow wider access, risk

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

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

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

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

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

191 on coefficients of interstitial fibrosis and tubular atrophy with mean SWE score stood at 0.667 and 0

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

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