ライフサイエンスコーパス: graft dysfunction

1 brosis, vascular neointimal development, and graft dysfunction.

2 ossible role of antibodies in a patient with graft dysfunction.

3 lux disease (GERD) are at increased risk for graft dysfunction.

4 tudied 92 patients who had been biopsied for graft dysfunction.

5 Function (MEAF) grades the severity of liver graft dysfunction.

6 directly related to the severity of primary graft dysfunction.

7 HR for identifying patients at risk of early graft dysfunction.

8 jects who died by 30 days, 43.6% had primary graft dysfunction.

9 ted with renal allograft rejection and early graft dysfunction.

10 etween the production of DSA, AHR, and early graft dysfunction.

11 tion must be considered in all patients with graft dysfunction.

12 r is not yet on dialysis but has significant graft dysfunction.

13 is for the marginal liver to minimize early graft dysfunction.

14 thin 30 days and a 48% reduced odds of early graft dysfunction.

15 s are the gold standard for evaluating renal graft dysfunction.

16 yroxine also significantly reduced prolonged graft dysfunction.

17 afts and may be a critical factor in chronic graft dysfunction.

18 is necessary for accurate classification of graft dysfunction.

19 mmune hepatitis (score > 15) at the onset of graft dysfunction.

20 ography with doppler studies at the onset of graft dysfunction.

21 platelet counts (P = 0.05) and showed early graft dysfunction.

22 on or with infection, rejection, and chronic graft dysfunction.

23 ansplantation developed this unusual form of graft dysfunction.

24 either for routine surveillance or for acute graft dysfunction.

25 as been implicated in both acute and chronic graft dysfunction.

26 re, tumor, and postOLT complications causing graft dysfunction.

27 ntially valuable adjunct in the diagnosis of graft dysfunction.

28 iations between subclinical inflammation and graft dysfunction.

29 ion and differentiation from other causes of graft dysfunction.

30 rd in the differential diagnosis of pancreas graft dysfunction.

31 differentiate rejection from other causes of graft dysfunction.

32 surveillance or to diagnose the etiology of graft dysfunction.

33 ess the value of UFC in the setting of acute graft dysfunction.

34 FC should be considered in the evaluation of graft dysfunction.

35 1 hr after reperfusion is a risk factor for graft dysfunction.

36 allograft survival only when associated with graft dysfunction.

37 ue in pancreas transplantation patients with graft dysfunction.

38 nother valuable tool for diagnosing pancreas graft dysfunction.

39 s a safe and effective method for diagnosing graft dysfunction.

40 characterized by fever, lymphadenopathy, and graft dysfunction.

41 ings were the most common sole indication of graft dysfunction.

42 onic rejection remains a major cause of late graft dysfunction.

43 potency and attenuates long-term Tac-induced graft dysfunction.

44 y associated with the development of chronic graft dysfunction.

45 e already undergone retransplantation due to graft dysfunction.

46 kidney transplant recipients still face late graft dysfunction.

47 eloping in tolerant animals without signs of graft dysfunction.

48 ney transplantation (KTx) and increases with graft dysfunction.

49 tatively associated with each other and with graft dysfunction.

50 evelopment of allograft fibrosis and chronic graft dysfunction.

51 at the time of biopsies performed because of graft dysfunction.

52 rmed in the absence of any clinical signs of graft dysfunction.

53 ventilation, renal insufficiency and primary graft dysfunction.

54 y prompt tissue biopsy, to diagnose cause of graft dysfunction.

55 ts/year, p < 0.001) and rejection-associated graft dysfunction (+0.37 events/year, p = 0.002).

56 ease 21 months after PTLD treatment (liver), graft dysfunction 25 months after PTLD (heart).

57 21.7%) were related to infection, 24 (20.9%) graft dysfunction, 25 (21.7%) gastrointestinal, 25 (21.7

58 year survival rate after re-OLT was 61 % for graft dysfunction, 50% for chronic rejection, 60% for he

59 In patients with graft dysfunction, a low IL-10/TNF-alpha ratio in TrBs a

60 lular rejection, hemodynamically significant graft dysfunction, a second transplantation, or death or

61 In a patient with minor graft dysfunction, a strain with an archetype-like nonco

62 r program and graded the severity of primary graft dysfunction according to the International Society

63 Chronic rejection is a major cause of graft dysfunction after kidney transplantation.

64 e hepatitis must be considered as a cause of graft dysfunction after liver transplantation.

65 on injury (IRI) significantly contributes to graft dysfunction after liver transplantation.

66 AIH must be considered in all patients with graft dysfunction after liver transplantation.

67 erfusion injury is the main cause of primary graft dysfunction after lung transplantation and results

68 ion injury is a major determinant of primary graft dysfunction after lung transplantation, an approac

69 ovel therapeutic strategy to prevent primary graft dysfunction after lung transplantation.

70 Late graft dysfunction after orthotopic liver transplantation

71 he gold standard for diagnosing rejection or graft dysfunction after pancreas transplantation.

72 y 1, 2006 and underwent biopsy for new onset graft dysfunction after that date (mean creatinine at bi

73 w years: the role of antibodies in mediating graft dysfunction after transplantation, ABO-incompatibl

74 ions and therapies for variant syndromes and graft dysfunction after transplantation.

75 actor contributing to reperfusion injury and graft dysfunction after transplantation.

76 Methods of assessing graft dysfunction alone may not be accurate enough in th

77 pathy is an increasingly recognized cause of graft dysfunction among kidney transplant recipients, an

78 IRI) represents a major risk factor of early graft dysfunction and a key obstacle to expanding the do

79 er, there was no association between primary graft dysfunction and acute rejection or lymphocytic bro

80 y help to predict the development of primary graft dysfunction and avoid the need for retransplantati

81 mens from 21 renal allograft recipients with graft dysfunction and biopsy-confirmed acute rejection a

82 % of renal transplant biopsies performed for graft dysfunction and capillary C4d deposition in heart

83 as identified by the presence of biochemical graft dysfunction and concurrent liver biopsy showing di

84 major complications including severe primary graft dysfunction and early mortality rates were similar

85 Differences in outcomes (time-to-graft dysfunction and failure) were compared using Kapla

86 of reduced-size livers, which contributes to graft dysfunction and failure.

87 N) can recur in kidney allografts leading to graft dysfunction and failure.

88 lograft recipients with acute and/or chronic graft dysfunction and from 22 controls.

89 ificantly higher incidence of severe primary graft dysfunction and higher short- and long-term mortal

90 ate aminotransferase (AST) peak value; early graft dysfunction and histological I/R injury were secon

91 Graft dysfunction and loss in 30% to 45% of polyomavirus

92 Ischemia/reperfusion (I/R) injury leads to graft dysfunction and may contribute to alloimmune respo

93 or contributor to early post-lung transplant graft dysfunction and mortality.

94 poor prognosis, independent of the level of graft dysfunction and other chronic histologic changes.

95 cted late (up to 4 years after biopsy) renal graft dysfunction and proteinuria.

96 The long-term effect of viral infections on graft dysfunction and rejection after renal transplantat

97 in renal allograft biopsies obtained during graft dysfunction and rejection has been proposed to be

98 antation and is a major contributor to early graft dysfunction and subsequent graft immunogenicity.

99 In contrast, if RCE is of donor origin, graft dysfunction and subsequent graft loss are common.

100 operatively, the incidence of severe primary graft dysfunction and the incidence of acute renal insuf

101 allograft rejection depend upon detection of graft dysfunction and the presence of a mononuclear leuk

102 ta were analyzed before development of islet graft dysfunction and while insulin independent.

103 reased estimated glomerular filtration rate (graft dysfunction), and reduced lean tissue index (P</=0

104 plication cohort; 81% had rejection, 51% had graft dysfunction, and 13% had vasculopathy, 7% died and

105 isk of rejection, graft cytokine expression, graft dysfunction, and a higher mortality after cardiac

106 vated aminotransferase levels, coagulopathy, graft dysfunction, and either fever or leukocytosis with

107 nts, is an important risk factor for chronic graft dysfunction, and is linked to reduced graft surviv

108 coronary atherosclerosis (21.2% vs. 12.3%), graft dysfunction, and loss after transplantation.

109 hospital stay, peak glucose, inotropic dose, graft dysfunction, and survival after HTx were similar b

110 re performed in all children to evaluate the graft dysfunction, and the histologic findings were inte

111 gher intraoperative blood use, postoperative graft dysfunction, and, in some cases, graft loss.

112 At the time of biopsies performed because of graft dysfunction, antibody-mediated rejection or acute

113 t time that T cells of patients with chronic graft dysfunction are primed to recognize and respond to

114 Graft dysfunction as a result of preservation injury rem

115 We hypothesize that severity of graft dysfunction assessed by either the MELD score or t

116 nt, rejection with hemodynamic compromise or graft dysfunction at 18 months post transplant.

117 ransplantation correlated with the degree of graft dysfunction at 3 days after transplantation.

118 ic allograft nephropathy was associated with graft dysfunction at 3 years.

119 sies in the absence of any clinical signs of graft dysfunction at the time of biopsy (i.e., "true sur

120 Usually, it is not known whether there is graft dysfunction at the time of biopsy.

121 ne hepatitis or any other form of persistent graft dysfunction at the time of last follow-up.

122 t loss, biopsy-confirmed acute rejection, or graft dysfunction at week 24.

123 to decreased in PS or GS, or an increase in graft dysfunction but as associated with reduced complic

124 ion of TL with acute rejection (AR), chronic graft dysfunction (CGD), and graft failure of kidney all

125 ion of TL with acute rejection (AR), chronic graft dysfunction (CGD), and graft failure of kidney all

126 Primary graft dysfunction contributes to nearly half of the shor

127 0.831 (0.789-0.867) compared to the UK early graft dysfunction criteria of 0.674 (0.624-0.721).

128 nsulin independence with A1c reduction below graft dysfunction criteria.

129 rlapping histologic features, and persistent graft dysfunction despite antibiotics are frequently enc

130 Graft dysfunction due to chronic rejection appears to be

131 me of rejection with hemodynamic compromise, graft dysfunction due to other causes, death, or retrans

132 e scenario could explain the higher rates of graft dysfunction due to primary nonfunction traditional

133 ed that platelet thrombi might contribute to graft dysfunction during development of hyperacute rejec

134 allograft vascular patency in patients with graft dysfunction, either delayed or slow graft function

135 Graft dysfunction (estimated glomerular filtration rate

136 oss, biopsy-proven acute rejection or severe graft dysfunction: estimated glomerular filtration rate

137 as loss, and the number of episodes of acute graft dysfunction evaluated by biopsy (multivariate anal

138 on, which may have contributed to the severe graft dysfunction experienced by this group.

139 ed an unexplained but characteristic form of graft dysfunction (five boys, two girls; median age at p

140 8 of 12 cases, whereas 10 of 11 episodes of graft dysfunction from other causes (infection, drug tox

141 Progressive graft dysfunction (GDF) and loss of insulin independence

142 the 334 recipients, 65 did not have primary graft dysfunction (grade 0), 130 had grade 1, 69 had gra

143 currence of late adverse events (>6 months): graft dysfunction, graft loss, death, and immunosuppress

144 d graft damage in the form of either chronic graft dysfunction (group 1, n=20) or a recent previous a

145 iving at least 1 year, those who had primary graft dysfunction had significantly worse survival over

146 lished, although a characteristic pattern of graft dysfunction has been observed in our patients who

147 histologic acute rejection in the absence of graft dysfunction, has been suggested as a cause of chro

148 Survivors of primary graft dysfunction have increased risk of death extending

149 Long-term outcomes of subjects with primary graft dysfunction have not been studied.

150 notypes was associated with a higher risk of graft dysfunction (hazard ratio [HR]: 1.5, p = 0.02) and

151 The presence of graft dysfunction identified patients at greater risk fo

152 lantation can develop severe immune-mediated graft dysfunction (IGD) characterized by plasma cell hep

153 for type 1 diabetes is limited by long-term graft dysfunction, immunosuppressive drug toxicity, need

154 were used to identify 106 cases of suspected graft dysfunction in 57 patients (56 men, one woman; age

155 ger increase (DeltaMFI>50%) were followed by graft dysfunction in almost all patients and could signi

156 nephropathy (BKVN) is a significant cause of graft dysfunction in kidney transplant recipients, but i

157 e H-NMR based metabolomics to diagnose early graft dysfunction in liver transplantation.

158 uable tool for the differential diagnosis of graft dysfunction in lung transplantation.

159 d a 2-fold higher risk (P=0.06) of long-term graft dysfunction in patients who had increased levels o

160 filling-pressure thresholds to discriminate graft dysfunction in pediatric patients.

161 tant and treatable cause of hypertension and graft dysfunction in renal allograft recipients.

162 w alternative for histological evaluation of graft dysfunction in selected patients with contraindica

163 -OLT was required in 42 (11.2%) patients for graft dysfunction in the initial 30 days after OLT.

164 for ischemia reperfusion injury and primary graft dysfunction in the recipient.

165 igh-dose IVIG may reduce the risk of chronic graft dysfunction in those with an acute AMR event.

166 f cardiopulmonary bypass, and severe primary graft dysfunction increased the risk for death in patien

167 The correlation between clinical evidence of graft dysfunction (increased serum enzymes and glucose),

168 Primary graft dysfunction is a common complication after lung tr

169 Primary graft dysfunction is a severe acute lung injury syndrome

170 Primary graft dysfunction is associated with an increased risk o

171 Progressive graft dysfunction is commonly observed in recipients of

172 re now discarded because the risk of primary graft dysfunction is considered too great.

173 ated whether differential diagnosis of acute graft dysfunction is feasible using urinary cell mRNA pr

174 Intestinal graft dysfunction is sometimes irreversible and requires

175 ney injury but its utility for prediction of graft dysfunction is unknown.

176 In cases of irreversible intestinal graft dysfunction, isolated allograft enterectomy succes

177 n renal allograft recipients presenting with graft dysfunction, it is critical to determine the paten

178 Post-HTx outcomes included graft dysfunction, length of intensive care unit stay, l

179 sis, biliary and vascular complications, nor graft dysfunction/loss or death at 3 and 5 years after L

180 re not suitable for early diagnosis of islet graft dysfunction, magnetic resonance imaging (MRI) has

181 ssociated with an increased risk for chronic graft dysfunction manifested as bronchiolitis obliterans

182 was correlated with the incidence of severe graft dysfunction manifested as pulmonary infiltrates an

183 n ligand to prevent donor-associated chronic graft dysfunction may be of special clinical interest in

184 Graft dysfunction may result from damage inflicted on tu

185 As a continuous score grading graft dysfunction, MEAF provides additional, granulated

186 s 3.5+/-0.7 L/min per m(2); P=0.02) and mild graft dysfunction measured by echocardiography-derived l

187 c diagnoses of TxCAD and had symptoms and/or graft dysfunction (n = 10) or positive stress studies (n

188 tions were protocol graft monitoring (n=73), graft dysfunction (n=17), enteric hemorrhage (n=9), or o

189 tudied recipients with new onset late kidney graft dysfunction (n=173) to determine the importance of

190 16) from 10 patients with AHR who had acute graft dysfunction, neutrophils in peritubular capillarie

191 One patient died of graft dysfunction, noncompliance with immunosuppressant

192 Neither graft dysfunction nor vascular complications occurred.

193 the presence of basal or persistent PRA+ and graft dysfunction occurred also in the absence of PRA+.

194 Early graft dysfunction occurred in 5.6% of 3HR donor hearts a

195 t last follow-up 10 children have persistent graft dysfunction, of whom 5 have progressed to de novo

196 We evaluated the impact of primary graft dysfunction on acute rejection, lymphocytic bronch

197 We examined the impact of primary graft dysfunction on bronchiolitis obliterans syndrome.

198 Vehicle-treated recipients developed graft dysfunction on day 1 which rapidly worsened by day

199 GS-492429 did not affect graft dysfunction on day 1, but treatment reduced allogr

200 Two treated patients developed graft dysfunction, one of who had histological evidence

201 in GS, is a powerful predictor of subsequent graft dysfunction or end-stage graft failure.

202 ificant associations were observed with late graft dysfunction or graft loss.

203 samples, but unless this was associated with graft dysfunction or serious immune destruction, treatme

204 Higher BKV viremia correlated with graft dysfunction (P=0.01), more advanced histological p

205 s in plasma would be associated with primary graft dysfunction (PGD) after lung transplantation.

206 e associated with the development of primary graft dysfunction (PGD) after lung transplantation.

207 Primary graft dysfunction (PGD) is a major complication followin

208 Primary graft dysfunction (PGD) is a significant cause of early

209 Primary graft dysfunction (PGD) is a significant contributor to

210 Primary graft dysfunction (PGD) is the main cause of early morbi

211 Primary graft dysfunction (PGD) is the most important cause of e

212 (LT), early prediction of grade 3 pulmonary graft dysfunction (PGD) remains a research gap for clini

213 Twenty-three patients with Grade 3 primary graft dysfunction (PGD) were frequency matched with cont

214 afts may be at an increased risk for primary graft dysfunction (PGD), the leading cause of early mort

215 phics may influence the incidence of primary graft dysfunction (PGD).

216 with good early outcome [absence of primary graft dysfunction- (PGD) grade 3]; (II) PGD3: bilateral

217 In conclusion, graft dysfunction predicts poor graft survival only when

218 in perfusates of kidneys with posttransplant graft dysfunction (primary nonfunction and delayed graft

219 Early graft dysfunction rate was similar in both groups (20% v

220 dysfunction versus 6.1% in patients without graft dysfunction (relative risk = 6.95; 95% CI, 5.98, 8

221 ult patient because of the high incidence of graft dysfunction (right graft) when placed in an emerge

222 e care unit stay (P = 0.74), highest primary graft dysfunction score (P = 0.67) and hospital stay (P

223 nit stay, hospital stay, and highest primary graft dysfunction score within 72 hours) and long-term (

224 had undergone liver transplantation and had graft dysfunction secondary to recurrent nonalcoholic st

225 ential recipients of organs at high risk for graft dysfunction should be carefully screened for medic

226 ctors and analyzed treatment and outcomes of graft dysfunction subtypes.

227 n solution in grafts with subsequent primary graft dysfunction, suggesting a slower recovery of bile

228 Patients with new early DSA but without graft dysfunction that are treated with IVIG and Rituxim

229 Late graft dysfunction that does not result from recognised c

230 nvestigated a particular type of unexplained graft dysfunction that is associated with autoimmune fea

231 torage influences the development of chronic graft dysfunction, the major clinical problem in solid o

232 Among the 23 patients with graft dysfunction, the ratios were also compared with gr

233 tation also is associated with rejection and graft dysfunction, this study sought to determine whethe

234 Furthermore, it may cause graft dysfunction through the development of recurrent n

235 rus tubulo-interstitial nephritis-associated graft dysfunction usually calls for judicious decrease i

236 e mortality at 30 days was 42.1% for primary graft dysfunction versus 6.1% in patients without graft

237 The overall incidence of primary graft dysfunction was 10.2% (95% confidence intervals [C

238 atric liver transplant patients in whom late graft dysfunction was associated with autoimmune markers

239 Graft dysfunction was defined as estimated glomerular fi

240 Graft dysfunction was defined as significant systolic dy

241 obliterans syndrome associated with primary graft dysfunction was independent of acute rejection, ly

242 A higher rate of graft dysfunction was observed in modulated vs. unmodula

243 Graft dysfunction was the most common cause of operative

244 n multivariable regression analysis, primary graft dysfunction was the predominant perioperative risk

245 donor biopsies for their ability to predict graft dysfunction, we used a proportional odds model tha

246 univariable analysis, all grades of primary graft dysfunction were associated with a significantly i

247 n June 1997 and March 2001, 67 patients with graft dysfunction were found to have biopsy-proven PVN.

248 Death within 30 days and early graft dysfunction were used as endpoints.

249 CMV disease was a significant cause of early graft dysfunction, whereas the presence of chronic allog

250 fication of transplant recipients with acute graft dysfunction who are at high risk for future graft

251 e sought to test the relationship of primary graft dysfunction with both short- and long-term mortali

252 only 4 (5%) had severe but reversible early graft dysfunction with pulmonary infiltrates and hypoxem

253 Three patients (50%) developed severe graft dysfunction with pulmonary infiltrates and hypoxem

254 , 2 to chronic rejection, one has persistent graft dysfunction with recurrent cytomegalovirus activat

255 the remaining kidneys had mild but transient graft dysfunction with reversible, mild microangiopathic

256 T cell antibody group, one patient had early graft dysfunction, with extensive hepatic necrosis and h

257 ent a risk factor for severe early pulmonary graft dysfunction, with the potential to progress to hyp