ライフサイエンスコーパス: acute rejection

1 enal function, proteinuria, or biopsy-proven acute rejection.

2 despite a nearly threefold increased risk of acute rejection.

3 suppression (SIS) without rejection and with acute rejection.

4 of alloreactive T effector cells and delayed acute rejection.

5 the alloreactive T cell response that causes acute rejection.

6 o the recipient is intrinsically involved in acute rejection.

7 All of them developed episodes of acute rejection.

8 nterstitial inflammatory response similar to acute rejection.

9 cipient T cell infiltration, the hallmark of acute rejection.

10 seem to protect renal allografts from fatal acute rejection.

11 DSAs) have been associated with a history of acute rejection.

12 wis rats to investigate fatal and reversible acute rejection.

13 rmed 12 months postweaning or at concern for acute rejection.

14 2 patients with acute tubular injury without acute rejection.

15 nistration of corticosteroid boluses used in acute rejection.

16 5 to an increased incidence of biopsy-proven acute rejection.

17 iratory tract infectious disease (LRTID), or acute rejection.

18 promise, despite their higher rates of early acute rejection.

19 ween DGF duration and DCGL were explained by acute rejection.

20 ess whether this association was mediated by acute rejection.

21 ated recipients within 10 days due to severe acute rejection.

22 standing diabetes might increase the risk of acute rejections.

23 r outcomes of delayed graft function, 1-year acute rejection, 1-year BK virus or patient death.

24 ared with those taking cyclosporin, had less acute rejection (11% versus 22%, P=0.05) and graft loss

25 idence of DGF (29.3% versus 29.2%, P = 0.9), acute rejection (11.2% versus 11.7%, P = 0.8), and media

26 e incidence of DGF (29.3% vs. 29.2%, p=0.9), acute rejection (11.2% vs. 11.7%, p=0.8), and median LOS

27 LP use was associated with a similar rate of acute rejection (13% vs 9%, P = 0.08) but increased rate

28 SLK-HCC patients had similar rates of acute rejection (13.3% vs 10.5%, P = 0.36) and liver gra

29 ] vs 17 [21.9%], P = .007) and biopsy-proven acute rejections (15 [23.4%] vs 31 [48.4%], P = .002).

30 52 patients with biopsy specimens indicating acute rejection (26 acute T cell-mediated rejection and

31 was significantly increased in patients with acute rejection: 3.89 (1.36) versus 2.32 (1.82), P = 0.0

32 Rates of biopsy-proven acute rejection (5.7% vs 7.9%), adverse events, and seri

33 converted to SRL showed higher incidence of acute rejection (7.3% vs 0%), proteinuria (59.6% vs 25%;

34 Next, among patients diagnosed with acute rejection, a similar statistical approach identifi

35 transplantation, with specific reference to acute rejection, acute kidney injury in allografts, chro

36 0.99, 95% confidence interval 0.62-1.58) or acute rejection (adjusted odds ratio 0.89, 95% confidenc

37 ients experienced more early rejection, more acute rejection after 90 days, and a clinically signific

38 ients experienced more early rejection, more acute rejection after 90 days, and a clinically-signific

39 igh-dose corticosteroids effectively combats acute rejection after kidney transplantation, but at the

40 TPN22 polymorphisms are also associated with acute rejection after liver transplantation.

41 , and 57 patients who suffered from multiple acute rejections after transplantation.

42 rejection, biopsy proven, and suspected late acute rejection) after month 6.

43 68 [1.08-2.62]; P = 0.022) and biopsy-proven acute rejection (aHR, 1.71 [1.13-2.60]; P = 0.012).

44 nted into Brown Norway recipients to trigger acute rejection (allogeneic untreated group).

45 Biopsy-proven acute rejection and acute rejection were significantly h

46 The adjusted hazard ratio for acute rejection and all-cause mortality at 3 years in re

47 table graft function, histologic features of acute rejection and borderline changes that are associat

48 munosuppression regimens effectively control acute rejection and decrease graft loss in the first yea

49 00 s increased with T cells from mice during acute rejection and decreased with T cells from mice ren

50 ensored graft survival using Cox regression, acute rejection and delayed graft function (DGF) using l

51 tter allograft survival in the BK group over acute rejection and disease recurrence remained after ad

52 tified individuals at higher risk of ongoing acute rejection and future graft loss.

53 in Renal Disease-4) <30 mL/min per 1.73 m), acute rejection and graft and patient survival.

54 estigated the association of DSA features to acute rejection and graft failure.

55 scores were associated with a lower risk of acute rejection and graft loss in AA kidney transplant r

56 ion immunosuppression decreases the risk for acute rejection and improves graft outcomes in kidney tr

57 clinical outcome, including the incidence of acute rejection and infection after lung transplantation

58 The primary composite endpoint included acute rejection and infection at 12 months after transpl

59 the presence of allograft injury, including acute rejection and infection, and return to baseline af

60 enabled noninvasive diagnosis of subclinical acute rejection and inflammation in the graft and may re

61 sociation between threshold duration of DGF, acute rejection and long-term allograft loss remains und

62 se that results in spontaneous resolution of acute rejection and long-term graft protection.

63 ioles and vessels at day 14, consistent with acute rejection and lymphocytic bronchitis, to subepithe

64 ction after 1 year but increases the risk of acute rejection and may be poorly tolerated.

65 +) lymphocytes and was sufficient to prevent acute rejection and OB.

66 hat is >15-fold higher than that seen during acute rejection and occurs >45 d postengraftment at the

67 The LFA-1 blockade prevented acute rejection and preserved palpable beating quality w

68 ver transplantation (LT) was associated with acute rejection and prevented further attempts of IS wit

69 splantation and the impact of early dnDSA on acute rejection and protocol biopsy findings.

70 A 1-mg TAC resulted in acute rejection and recipient death; 3 mg and 5 mg prolo

71 the first 72 hours (in the absence of hyper acute rejection and technical surgical factors, such as

72 portion of corneal transplants, the rates of acute rejection and/or graft failure are comparable to o

73 ne in renal graft function, a higher risk of acute rejections and more renal grafts lost due to acute

74 Acute rejections and the biopsy-proven findings disquali

75 ndary endpoints that included blood viremia, acute rejection, and chronic lung allograft dysfunction

76 ntation/solitary pancreatic transplantation, acute rejection, and CT findings of peripancreatic edema

77 ensored graft survival using Cox regression, acute rejection, and delayed graft function (DGF) using

78 older, male sex, HLA mismatch or 4 greater, acute rejection, and depleting antibody induction had a

79 t to graft and patient survival, episodes of acute rejection, and its response to treatment.

80 Postoperative hemodynamics, biopsy-proven acute rejections, and mortality were similar.

81 He experienced 6 acute rejections, and none were resistant to steroids.

82 model for end-stage liver disease score, and acute rejection; and donor age and race, cold ischemia t

83 CI, 1.50-2.65; P < 0.001), respectively, for acute rejection; and were 1.10 (95% CI< 0.73-1.67; P = 0

84 In cases of acute rejection, animals also received steroids.

85 cells) were associated with protection from acute rejection (any Banff grade; HR: 0.60; 95% CI: 0.37

86 ed odds ratio [aOR]: 0.580.861.27, P = 0.4), acute rejection (aOR: 0.610.941.43, P = 0.8), and LOS (a

87 sted odds ratio [aOR]: 0.580.861.27, p=0.4), acute rejection (aOR: 0.610.941.43, p=0.8), and LOS (adj

88 ESW was associated with increased acute rejection (aOR=(1.09)1.16(1.23)), slightly increas

89 Less biopsy-proven acute rejection (AR) (p = 0.005), cytomegalovirus (CMV)

90 assay was developed to noninvasively detect acute rejection (AR) after kidney transplantation.

91 ion to compare the risk of CMV infection and acute rejection (AR) among KT recipients by ATG dose.

92 Acute rejection (AR) and development of chronic rejectio

93 Declining rates of acute rejection (AR) and the high rate of 1-year graft s

94 ortal hypoplasia in biliary atresia (BA) and acute rejection (AR) are still major concerns in this fi

95 Classification of acute rejection (AR) based on etiology and timing may pr

96 allograft recipients who are predisposed to acute rejection (AR) could allow for optimization of cli

97 ive biomarker that could accurately diagnose acute rejection (AR) in heart transplant recipients coul

98 ed graft function (DGF) is a risk factor for acute rejection (AR) in renal transplant recipients, and

99 Prognostic biomarkers of acute rejection (AR) in solid organ transplantation have

100 Glucocorticoid (GC)-refractory acute rejection (AR) is a risk factor for inferior renal

101 V-infected (HIV+) persons are excellent, yet acute rejection (AR) is common and optimal immunosuppres

102 geneous cohorts showed unacceptable rates of acute rejection (AR), we hypothesized that we could iden

103 (n = 120) central histology for Banff scored acute rejection (AR), were transcriptionally profiled fo

104 ively on biopsies in patients that developed acute rejection (AR).

105 nt recipients with (n=21) and without (n=22) acute rejection (AR).

106 med 12 months post-weaning or at concern for acute rejection (AR).

107 irculatory death (DCD) have a higher risk of acute rejection (AR).

108 ts surviving at least 90 days, early events (acute rejection [AR] and delayed graft function [DGF] be

109 tion and postliver transplant infections and acute rejection are evolving.

110 Noninvasive biomarkers of subclinical acute rejection are needed to avoid the risks and costs

111 n those without ACR-3 of subsequent clinical acute rejection at 12 and 24 months, faster decline in g

112 sociation between quartiles of DGF duration, acute rejection at 6 months and death-censored graft los

113 derwent PAK retransplantation diagnosed with acute rejection at day 180.

114 The primary endpoint was biopsy-confirmed acute rejection (BCAR) within 60 weeks after transplanta

115 erm survival and secondary outcomes included acute rejection before discharge and need for extracorpo

116 Acute rejection before hospital discharge was lowest amo

117 tients who experienced treated biopsy-proven acute rejection (BPAR) during the first year posttranspl

118 Cumulative rates of biopsy-proven acute rejection (BPAR) from first randomization to year

119 entration and the incidence of biopsy-proven acute rejection (BPAR) in 216 moderately sensitized rena

120 At that time, the rate of biopsy-proven acute rejection (BPAR) of the pancreas was low in both g

121 Biopsy-proven acute rejection (BPAR) rates and types were compared bet

122 Biopsy-proven acute rejection (BPAR) rates and types were compared bet

123 ugh concentration [mug/L]) and biopsy-proven acute rejection (BPAR) the first 90 days posttransplanta

124 st follow-up, the incidence of biopsy-proven acute rejection (BPAR) was 77% (37/48) and 66% (31/47) (

125 eakthrough CMV, resistant CMV, biopsy-proven acute rejection (BPAR), graft loss, opportunistic infect

126 ing delayed graft function and biopsy-proven acute rejection (BPAR).

127 co-primary efficacy end point (biopsy-proven acute rejection [BPAR], graft loss, or death from random

128 of composite efficacy failure (biopsy-proven acute rejection [BPAR], graft loss, or death) at month 3

129 significant effect modification by race for acute rejection, but not graft loss.

130 rease in tacrolimus CV augmented the risk of acute rejection by 20% (adjusted hazard ratio, 1.20, 1.1

131 olytic induction therapy reduced the risk of acute rejection by 32% (OR 0.68, 0.62-0.75), graft loss

132 These include a higher risk of acute rejection, cardiac allograft vasculopathy after he

133 etional induction experience higher rates of acute rejection compared to patients treated with conven

134 anted for AILD are more likely to experience acute rejection compared to those transplanted for non-A

135 ients who received ATG were at lower risk of acute rejection compared to those who received IL2RA (1-

136 ients who received ATG were at lower risk of acute rejection compared to those who received IL2RA (1-

137 e therapy resulted in higher and more severe acute rejection compared with tacrolimus-based therapy.

138 in biopsies that would be classified as mild acute rejection correlates with troughs in immunosuppres

139 tively assessed clinical variables including acute rejection, cytomegalovirus pneumonia, upper and lo

140 ondary outcomes included treated episodes of acute rejection, de novo anti-HLA antibodies (including

141 condary endpoints including the incidence of acute rejection, degree of renal function recovery, and

142 Acute rejection develops frequently in the early postgra

143 lians, but it is unknown whether the type of acute rejection differs between these patient groups or

144 lians, but it is unknown whether the type of acute rejection differs between these patient groups, or

145 was superior to other surrogates, including acute rejection, doubling of serum creatinine level, and

146 Data about acute rejection, DSA, and renal function were collected.

147 The first patient had several episodes of acute rejection during the 7-year follow-up.

148 inical factors associated with biopsy-proven acute rejection during the first post-transplant year in

149 cumulative probabilities of infection, first acute rejection episode, malignancy, de novo donor speci

150 Of the 196, 37 (18.9%) had a previous acute rejection episode; 96 (49%) had concurrent i score

151 um HLA-G levels were higher in patients with acute rejection episodes than nonrejectors.

152 During the first posttransplant year the acute rejection episodes were characterized by reversibl

153 apeutic tacrolimus concentrations may induce acute rejection episodes.

154 worsen LT outcomes, such as the incidence of acute rejection, Epstein-Barr virus infection, sepsis, b

155 arget of rapamycin immunosuppression, and an acute rejection event were independent risk factors for

156 t effect between DGF duration and DCGL, with acute rejection explaining less than 10% of the effects

157 obtained from animals undergoing reversible acute rejection expressed increased levels of ApoE mRNA,

158 ssful transplants without having experienced acute rejection (follow-up, 18 months).

159 survival (GS), death-censored GS (DCGS), and acute rejection-free survival (ARFS) rates for RDP compa

160 ars after transplantation, the biopsy-proven acute rejection-free survival was worse in the Cw/DP and

161 nt factor B, and vimentin that distinguishes acute rejection from acute tubular injury; 10-fold cross

162 splantation, and clinical outcomes including acute rejection, graft and patient survival were examine

163 ent and associated with (late) (sub)clinical acute rejection, graft dysfunction and graft loss, devel

164 , and quantified the association of ESW with acute rejection, graft failure, and mortality using mult

165 IL-2 receptor antibody (IL-2RA) induction on acute rejection, graft loss and death in African-America

166 sion were utilized to assess the outcomes of acute rejection, graft loss, and mortality, with interac

167 in renal function or rates of biopsy-proven acute rejection, graft loss, opportunistic infections, o

168 e efficacy endpoint of treated biopsy-proven acute rejection, graft loss, or death was 10.9%, 14.1%,

169 points were treatment failure (biopsy-proven acute rejection, graft loss, or death), delayed graft fu

170 Rates of technical failure, 1 year acute rejection, graft survival, and patient survival we

171 or more early rejections (<1 y) or any late acute rejection (>1 y) have been associated with coronar

172 ical endpoint (renal function, biopsy-proved acute rejection, >=grade 2 interstitial fibrosis, and tu

173 significantly more mild/moderate episodes of acute rejection have been reported, favored by the fact

174 r mTORi versus MPA in terms of biopsy-proven acute rejection (hazard ratio [confidence interval], 0.3

175 As (OR 2.05, 95% CI 1.28-3.30, P = .003) and acute rejection (hazard ratio [HR] 4.18, 95% CI 2.31-7.5

176 I, 1.01-1.18), and a higher risk for treated acute rejection (hazard ratio, 1.63; 95% CI, 1.43-1.86).

177 r mTORi versus MPA in terms of biopsy-proven acute rejection [Hazard Ratio (HR)(Confidence Interval)

178 h prevalence of DSA and the correlation with acute rejection highlight the need for optimizing immuno

179 (HR, 2.30; 95% CI, 1.06-5.01; P = 0.03), and acute rejection (HR, 1.49; 95% CI, 0.99-2.24; P = 0.05)

180 idence interval {CI}, 1.52-5.91]; P = .002), acute rejection (HR, 2.97 [95% CI, 1.51-5.83]; P = .002)

181 ), whereas it was a significant predictor of acute rejection in AAs (HR, 0.89; 95% CI, 0.80-0.99).

182 imus variability is strongly associated with acute rejection in AAs and graft loss in all patients.

183 sparities in AAs; the crude relative risk of acute rejection in AAs was reduced by 46% when including

184 (IL-2RAb) induction in reducing the risk of acute rejection in adult kidney transplant recipients is

185 ntithymocyte globulin (ATG) reduces rates of acute rejection in adult kidney transplant recipients, y

186 been shown to protect liver recipients from acute rejection in an allogeneic model of liver transpla

187 ciate with both circulating endothelin-1 and acute rejection in cardiac transplant patients (sensitiv

188 L10 as a noninvasive biomarker for detecting acute rejection in children and to extend these findings

189 inical outcomes using clinical trial data on acute rejection in kidney transplantation and response t

190 g two clinically relevant phenotypes, namely acute rejection in kidney transplantation and response t

191 was no association between baseline SAI and acute rejection in non-AAs (hazard ratio [HR], 0.92; 95%

192 evaluate the efficacy of IL-2RAb in reducing acute rejection in pediatric and adolescent recipients a

193 05 and 15 December 2012 in the Assessment of Acute Rejection in Renal Transplantation (AART) study.

194 r IF/TA were azathioprine, a drug to prevent acute rejection in renal transplantation, and kaempferol

195 Modern era retransplants had more acute rejection in the first year after transplantation.

196 1.11; P = 0.20) despite an increased risk of acute rejection in the first year posttransplant (odds r

197 no hyperacute rejections and very infrequent acute rejection in the first year suggesting no evidence

198 Acute rejection in the year before nocardiosis was assoc

199 Given the higher rates of acute rejection in this population, ATG appears to be sa

200 D leads to better graft function and reduced acute rejection in untreated renal allograft recipients

201 Histologic criteria for diagnosing acute rejection in vascularized composite tissue allogra

202 immunosenescence is linked to lower rates of acute rejections in older recipients, whereas the engraf

203 rejections and more renal grafts lost due to acute rejection.In patients with a functional renal graf

204 One-year acute rejection incidence was higher in DSA-positive gro

205 ng the first year following transplantation, acute rejections increase the risk of developing dnDSA,

206 with at least a 40% reduction in the odds of acute rejection, independent of age, era, immunological

207 The secondary endpoints were incidence of acute rejections, infections, treatment failure and kidn

208 Acute rejection is a systemic inflammatory state and may

209 factor was associated with patient survival, acute rejection, liver function test results, recurrence

210 Rationale: Acute rejection, manifesting as lymphocytic inflammation

211 ly analyzed for early and late AMR and mixed acute rejection (MAR).

212 Protection against acute rejection may involve increased accumulation of CD

213 aft loss, graft function, chronic rejection, acute rejection, mortality, infection, cancer (excluding

214 and MMF/MPA-CNI did not show differences in acute rejection, mortality, or graft loss rates.

215 Six episodes of acute rejection (n = 2 KT, 4 LT) occurred, during hepati

216 ies (EMBs) of both patients who developed an acute rejection necessitating therapy (rejectors; Intern

217 an all solid organs, such as graft survival, acute rejection, new onset of diabetes after transplanta

218 No acute rejections, no differences in renal function in al

219 quency of endoscopic evaluation, episodes of acute rejection, nutritional therapy, and renal function

220 s associated with an increased risk of early acute rejection occurring within the first 6 months afte

221 Biopsy-proven acute rejection (odds ratio [OR] 2.32, 95% confidence in

222 withdrawal/avoidance was not associated with acute rejection (odds ratio [OR], 0.87; P = 0.63), graft

223 s greater than 80% were at increased risk of acute rejection (odds ratio, 1.81, 95% confidence interv

224 ble for sustained tolerance, as evidenced by acute rejection of allografts in established chimeric re

225 IDO) has been previously proposed to predict acute rejection of human kidney transplants.

226 - and MHC class II-specific IgE was found on acute rejection of skin and heart grafts in several muri

227 Despite aggressive immunosuppression, acute rejection of the lung allograft occurs in over hal

228 However, acute rejection of the skin is frequently observed and u

229 onsented; 6 were excluded due to subclinical acute rejection on baseline biopsy or other reasons, and

230 7 who were nontolerant (non-TOL), 6 had mild acute rejection on biopsy near the end of weaning or at

231 unction on echocardiogram and no evidence of acute rejection on discharge.

232 3 (subhazard ratio [SHR] = 1.95, P = 0.009), acute rejection (one vs. none) (SHR = 1.93, P = 0.033),

233 transplantation, including the incidence of acute rejection or chronic allograft vasculopathy.

234 owed better growth with no adverse impact on acute rejection or graft survival.

235 biopsy for cause did not show biopsy-proven acute rejection or microinflammation score).

236 efficacy failure (graft loss, biopsy-proven acute rejection or severe graft dysfunction: estimated g

237 cidence of both AMR (OR 4.6, P=0.009) and of acute rejection (OR 3.57, P=0.02) as compared to those w

238 .17-3.21; P = .679; Q = 4.48; I(2) = 55.3%), acute rejection (OR = 0.93; 95% CI, .70-1.24; P = .637;

239 DGF (OR, 1.22; 95% CI, 0.96-1.56; P = 0.11), acute rejection (OR, 0.95; 95% CI, 0.76-1.19; P = 0.63),

240 e risk of de novo donor-specific antibodies, acute rejection, or death-censored graft loss by non dos

241 We analyzed the risk of dnDSA, acute rejection, or death-censored graft loss by non-dos

242 There was no difference in the incidence of acute rejection, or in graft or patient survival between

243 iation was found with chronic rejection, LB, acute rejection, or respiratory infections, although sig

244 o had prior allograft failure as a result of acute rejection (P < .001) or disease recurrence (P = .0

245 in death-censored graft survival (P = .11), acute rejection (P = .49), and patient survival (P = .13

246 during IS minimization was a risk factor for acute rejection (P = 0.015).

247 pients with cancer had a higher incidence of acute rejection (P = 0.02) and cytomegalovirus (CMV) inf

248 icant difference in the overall incidence of acute rejection (P = 0.754) and the number of treated in

249 cipient (R)- serostatus(P = 0.04) and recent acute rejection(P = 0.02).

250 f immunosuppression used in the treatment of acute rejection, particularly the use of T-cell-depletin

251 ons have been associated with higher risk of acute rejection, particularly within African American (A

252 Incidence of acute rejection per 1000 patient-years was significantly

253 actors were associated with PJP development: acute rejection (pooled odds ratio (pOR) = 2.35 (1.69, 3

254 city, renal function, proteinuria, and prior acute rejection) predicted death-censored and overall gr

255 e assessed in the Evaluation of Sub-Clinical Acute rejection PrEdiction (ESCAPE) Study in 75 consecut

256 tacept has been associated with an increased acute rejection rate after kidney transplantation.

257 In this randomized-controlled trial, acute rejection rate was compared between belatacept- an

258 their objectives remain focused on improving acute rejection rates and graft survival in the first 12

259 Similar patient and graft survival, and acute rejection rates can be achieved in DSA+ patients c

260 One-year acute rejection rates were low and similar between group

261 Acute rejection, re-transplant and CV greater than 30% (

262 The acute rejection response has been attributed to donor de

263 n renal function during the first 5 years or acute rejection risk during the first year after renal t

264 nsplantation but is associated with a higher acute rejection risk than ciclosporin.

265 o mTORi was associated with a higher risk of acute rejection (RR, 1.76; 95% CI, 1.33-2.34; I, 0%) and

266 Unlike allograft samples showing acute rejection, samples from FCRx recipients did not sh

267 Subclinical acute rejection (sc-AR) is a main cause for functional d

268 st-heart-transplant events, with and without acute rejection (six participants with moderate-to-sever

269 kidney transplant (KT), because subclinical acute rejection (subAR), currently detectable only with

270 ue to a higher rate of treated biopsy-proven acute rejection (tBPAR) during TAC withdrawal.

271 experienced more delayed graft function and acute rejection than did elderly recipients of young DBD

272 bjects with antibodies to FN/Col-IV had more acute rejection than did those without these antibodies

273 t for patient 3, who presented 6 episodes of acute rejection, the latest 2 treated with Campath-1H.

274 There have been 4 acute rejections: the fourth was treated with methylpred

275 self-antigens that may increase the risk for acute rejection through unclear mechanisms.

276 isteria monocytogenes infection precipitates acute rejection, thus abrogating transplantation toleran

277 mug/mL) versus low Ficolin-3 (<33.3 mug/mL), acute rejection (time-dependent), age, basiliximab induc

278 tion (one vs. none) (SHR = 1.93, P = 0.033), acute rejection (two vs. none) (SHR = 5.45, P < 0.001),

279 Incidence of biopsy proven acute rejection was 18.5%.

280 analysis was conducted to determine whether acute rejection was a causal intermediate between DGF an

281 Biopsy-proven acute rejection was diagnosed in 21 patients (12.9%).

282 iation between IL-2RAb induction and risk of acute rejection was examined using adjusted logistic reg

283 The 1-year incidence of biopsy-proven acute rejection was monitored.

284 Early acute rejection was noted after day 5 that was histologi

285 Subclinical acute rejection was observed in 22 (29.3%) patients (17

286 A lower incidence of biopsy-proven acute rejection was seen in patients receiving corticost

287 rate at 12 months and rates of biopsy-proven acute rejection were also similar between groups.

288 ed patients and immunological biomarkers for acute rejection were investigated.

289 retransplantations, the rate and severity of acute rejection were markedly de creased in liver-inclus

290 Biopsy-proven acute rejection and acute rejection were significantly higher in arm 2 versu

291 e score pretransplantation and the number of acute rejections were identified as independent predicto

292 Patient survival and biopsy-proven acute rejections were statistically similar among HbA1c

293 tacrolimus levels predispose to episodes of acute rejection, whereas supratherapeutic levels may cau

294 ation, dnDSA development was associated with acute rejection, which prevented further IS withdrawal a

295 recipients experienced at least 1 episode of acute rejection, which was easily reversed by increasing

296 showed an HR of 0.51 (95% CI, 0.25-1.02) for acute rejection with group B versus group A, and 0.54 (9

297 It is unclear if the category of acute rejection with intimal arteritis (ARV) is relevant

298 Two were biopsy-proven acute rejections with subsequent graft failures.

299 des of T cell-mediated and antibody-mediated acute rejection, with high negative predictive values.

300 as compared to IL2RA, may lower the risk of acute rejection without increasing hepatic complications