ライフサイエンスコーパス: graft dysfunction

1 accelerated cardiac allograft rejection and graft dysfunction .

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

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

4 ventilation, renal insufficiency and primary graft dysfunction.

5 ole in antibody-mediated rejection (AMR) and graft dysfunction.

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

7 brosis, vascular neointimal development, and graft dysfunction.

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

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

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

11 directly related to the severity of primary graft dysfunction.

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

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

14 ted with renal allograft rejection and early graft dysfunction.

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

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

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

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

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

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

21 yroxine also significantly reduced prolonged graft dysfunction.

22 ole in antibody-mediated rejection (AMR) and graft dysfunction.

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

24 is necessary for accurate classification of graft dysfunction.

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

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

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

28 ansplantation developed this unusual form of graft dysfunction.

29 either for routine surveillance or for acute graft dysfunction.

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

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

32 ntially valuable adjunct in the diagnosis of graft dysfunction.

33 iations between subclinical inflammation and graft dysfunction.

34 ion and differentiation from other causes of graft dysfunction.

35 rd in the differential diagnosis of pancreas graft dysfunction.

36 differentiate rejection from other causes of graft dysfunction.

37 surveillance or to diagnose the etiology of graft dysfunction.

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

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

40 1 hr after reperfusion is a risk factor for graft dysfunction.

41 allograft survival only when associated with graft dysfunction.

42 ue in pancreas transplantation patients with graft dysfunction.

43 nother valuable tool for diagnosing pancreas graft dysfunction.

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

45 characterized by fever, lymphadenopathy, and graft dysfunction.

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

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

48 oach was applied to assess for mortality and graft dysfunction.

49 ntilation or the incidence of severe primary graft dysfunction.

50 that HOPE was beneficial in reducing primary graft dysfunction.

51 evelopment of allograft fibrosis and chronic graft dysfunction.

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

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

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

55 y associated with the development of chronic graft dysfunction.

56 e already undergone retransplantation due to graft dysfunction.

57 kidney transplant recipients still face late graft dysfunction.

58 eloping in tolerant animals without signs of graft dysfunction.

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

60 tatively associated with each other and with graft dysfunction.

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

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

63 21.7%) were related to infection, 24 (20.9%) graft dysfunction, 25 (21.7%) gastrointestinal, 25 (21.7

64 oints); recipient age >=70 years and chronic graft dysfunction (5 points); cytomegalovirus mismatch (

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

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

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

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

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

70 culatory support have been achieved, primary graft dysfunction after cardiac transplantation continue

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

72 Although many prognostic factors of primary graft dysfunction after liver transplantation (LT) are a

73 on injury (IRI) is believed to contribute to graft dysfunction after liver transplantation (LT).

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

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

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

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

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

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

80 Late graft dysfunction after orthotopic liver transplantation

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

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

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

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

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

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

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

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

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

90 Primary graft dysfunction and allograft rejection represent majo

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

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

93 % of renal transplant biopsies performed for graft dysfunction and capillary C4d deposition in heart

94 The incidence of primary graft dysfunction and cardiac allograft vasculopathy-fre

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

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

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

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

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

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

101 d with (late) (sub)clinical acute rejection, graft dysfunction and graft loss, development of donor-s

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

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

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

105 jection (AR) remains a major risk factor for graft dysfunction and loss.

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

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

108 No graft dysfunction and no rejection were observed.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

126 Among the 351 survivors, 19% sustained renal graft dysfunction, and there were 13 (4%) graft losses.

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

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

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

130 Graft dysfunction as a result of preservation injury rem

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

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

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

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

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

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

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

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

139 he Spiesser Group) included patients without graft dysfunction biopsied because of the presence of de

140 he Spiesser group) included patients without graft dysfunction biopsied because of the presence of dn

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

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

143 , there was no echocardiographic evidence of graft dysfunction, clinically significant rejection, or

144 sed rates of biliary complications and early graft dysfunction compared to DBD LT.

145 ng number of an organ's demand and long-term graft dysfunction constitute some of the major problems.

146 Primary graft dysfunction contributes to nearly half of the shor

147 0.831 (0.789-0.867) compared to the UK early graft dysfunction criteria of 0.674 (0.624-0.721).

148 nsulin independence with A1c reduction below graft dysfunction criteria.

149 The odds of initial graft dysfunction (delayed graft function/primary nonfun

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

151 ent endoscopy and biopsy without evidence of graft dysfunction does not appear to confer survival adv

152 Graft dysfunction due to chronic rejection appears to be

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

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

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

156 y outcomes [primary nonfunction (PNF), early graft dysfunction (EAD)].

157 Secondary endpoints included primary graft dysfunction, early posttransplant bleeding, reject

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

159 Graft dysfunction (estimated glomerular filtration rate

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

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

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

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

164 subunit alpha [COPA] syndrome), and primary graft dysfunction following lung transplantation, the me

165 8 of 12 cases, whereas 10 of 11 episodes of graft dysfunction from other causes (infection, drug tox

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

167 iety for Heart & Lung Tranplantation primary-graft dysfunction grade 3 (PGD3) within 72 h post-transp

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

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

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

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

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

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

174 ers correlating with allograft rejection and graft dysfunction have been described, evaluation of the

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

195 mes such as hospital length of stay, primary graft dysfunction, inotrope score, mechanical circulator

196 Primary graft dysfunction is a common complication after lung tr

197 Primary graft dysfunction is a severe acute lung injury syndrome

198 Primary graft dysfunction is associated with an increased risk o

199 Progressive graft dysfunction is commonly observed in recipients of

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

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

202 Intestinal graft dysfunction is sometimes irreversible and requires

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

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

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

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

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

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

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

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

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

212 Graft dysfunction may result from damage inflicted on tu

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

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

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

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

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

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

219 One patient died of graft dysfunction, noncompliance with immunosuppressant

220 Neither graft dysfunction nor vascular complications occurred.

221 ecipients and increases the risk for chronic graft dysfunction.Objectives: To evaluate clinical facto

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

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

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

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

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

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

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

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

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

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

232 early posttransplant course, such as primary graft dysfunction or hyperacute rejection.

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

234 -human leukocyte antigen antibody (P=0.001), graft dysfunction (P=0.004), and prior history of defini

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

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

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

238 Primary graft dysfunction (PGD) continues to be a potentially li

239 predispose to the fatal syndrome of primary graft dysfunction (PGD) following lung transplantation.

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

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

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

243 Severe primary graft dysfunction (PGD) is the leading cause of early de

244 Rationale: Primary graft dysfunction (PGD) is the leading cause of early mo

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

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

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

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

249 We sought to determine if primary graft dysfunction (PGD), a syndrome of acute lung injury

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

251 ptability for transplant and risk of primary graft dysfunction (PGD).

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

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

254 significantly reduced risk of severe primary graft dysfunction, postbypass severe right ventricular d

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

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

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

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

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

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

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

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

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

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

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

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

267 Late graft dysfunction that does not result from recognised c

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

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

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

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

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

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

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

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

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

277 Graft dysfunction was defined as estimated glomerular fi

278 Graft dysfunction was defined as significant systolic dy

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

280 Acute graft dysfunction was more frequent in MVI score 3 (P <

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

282 Renal graft dysfunction was seen in 11 of 25 (44%) cases.

283 Graft dysfunction was the most common cause of operative

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

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

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

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

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

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

290 t exhibited biventricular failure along with graft dysfunction while the remaining four exhibited no

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

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

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

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

295 , 2 to chronic rejection, one has persistent graft dysfunction with recurrent cytomegalovirus activat

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

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

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

299 HLA donor-specific Abs who experienced acute graft dysfunction within 3 months after transplantation

300 is generally well preserved, with transitory graft dysfunction without negative impact after 3 months