ライフサイエンスコーパス: acute rejection

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

2 seem to protect renal allografts from fatal acute rejection.

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

4 wis rats to investigate fatal and reversible acute rejection.

5 2 patients with acute tubular injury without acute rejection.

6 57; I=8%; Pheterogeneity=0.36), but not with acute rejection.

7 eeks after nonarterialized OLT due to severe acute rejection.

8 ) compared with those who did not experience acute rejection.

9 transplant patients compared with those with acute rejection.

10 despite a nearly threefold increased risk of acute rejection.

11 antly increased in C3(-/-) recipients during acute rejection.

12 itis obliterans syndrome (fBOS) and rates of acute rejection.

13 and incidence and severity of biopsy-proven acute rejection.

14 lity, bacterial translocation, and possibly, acute rejection.

15 between patients with borderline changes and acute rejection.

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

17 of alloreactive T effector cells and delayed acute rejection.

18 the alloreactive T cell response that causes acute rejection.

19 o the recipient is intrinsically involved in acute rejection.

20 All of them developed episodes of acute rejection.

21 nterstitial inflammatory response similar to acute rejection.

22 standing diabetes might increase the risk of acute rejections.

23 tions than within those from T cell-mediated acute rejections.

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

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

26 Preemptive recipients had less acute rejection (12% vs. 16%; P<0.0001) and delayed graf

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

28 kidney biopsy samples covering 41 cases with acute rejection (15 vascular rejection, 15 interstitial

29 e with CsA; higher rates of biopsy-confirmed acute rejection (21.4% vs. 6.1%; P<0.001); and higher ra

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

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

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

33 e patients ever experienced acute and severe acute rejections (A>/=2; both P<0.0001) and lymphocytic

34 Acute rejection, a common complication of lung transplan

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

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

37 (AMR) is responsible for up to 20% to 30% of acute rejection after kidney transplantation.

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

39 Three LuTX recipients had a mild acute rejection after one to three months after LuTX, an

40 was significantly worse in 23 patients with acute rejection after randomization.

41 The risk of acute rejection after transplantation may be reduced in

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

43 (adjusted hazard ratio [AHR], 2.03; P=0.05), acute rejection (AHR, 5.4; P<0.001), and mycophenolic ac

44 splantation associates with higher risks for acute rejection and 1-year graft survival in adults, but

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

46 nth 3 in non-African Americans, but rates of acute rejection and adverse events (including gastrointe

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

48 points included development of biopsy-proven acute rejection and analysis of graft survival and funct

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

50 00 s increased with T cells from mice during acute rejection and decreased with T cells from mice ren

51 IS protects allografts from acute rejection and early graft loss.

52 cy defined as the incidence of biopsy-proven acute rejection and estimated creatinine clearance.

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 ney injury (AKI) that increases the risk for acute rejection and graft loss after kidney transplantat

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

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

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

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

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

61 Although acute rejection and lymphocytic bronchiolitis have been

62 ped infiltrates on CT and classic histologic acute rejection and lymphocytic bronchiolitis.

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 cohort demonstrated the highest incidence of acute rejection and missed clinic appointments.

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

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

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

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 This report characterizes acute rejection and rejection outcomes in subjects rando

72 with standard A and BR pathology scores for acute rejection and small-airway lymphocytic bronchiolit

73 cells in BKVN and viremia samples resembling acute rejection and suggested the involvement of both ad

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

75 in (Hsp)-27 in mouse hearts protects against acute rejection and the mechanisms of such protection.

76 Recipients who experienced acute rejection and treated with T-cell-depleting antibo

77 termine whether there was a correlation with acute rejection and with transplant function and surviva

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

79 d inflammation, necrosis, vascular reaction (acute rejection) and in parallel improved capillary dens

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

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

82 f respiratory tract infection, colonization, acute rejection, and lymphocytic bronchiolitis were comp

83 tasol were effective in treating episodes of acute rejection, and the best outcomes were achieved whe

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

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

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

87 ents with dDSA were more likely to suffer an acute rejection (AR) (35% vs. 10%, P<0.001), an antibody

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

89 nes that were significantly overexpressed in acute rejection (AR) across all transplanted organs.

90 Acute rejection (AR) and development of chronic rejectio

91 Both acute rejection (AR) and major infection events (MIE) ca

92 may be associated with an increased risk of acute rejection (AR) and worse overall outcomes after in

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

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

95 and with de novo DQ plus other DSAs had more acute rejection (AR) episodes (22%, P=0.005; and 36%, P=

96 sis also showed clear separation between the acute rejection (AR) group (N=3) and the no AR group (N=

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

98 free DNA (dd-cfDNA) in blood correlates with acute rejection (AR) in heart transplantation.

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

100 es, including donor age, on the incidence of acute rejection (AR) in the first year after deceased-do

101 In renal transplantation, acute rejection (AR) increases the risk for chronic graf

102 Acute pyelonephritis (APN) versus acute rejection (AR) is a frequently encountered diagnos

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

104 on, redundancy in the molecular diversity of acute rejection (AR) often results in incomplete resolut

105 However, acute rejection (AR) rates are over twice those of HIV-n

106 Freedom from acute rejection (AR) was significantly higher in TAC-MMF

107 r TL to determine the association of TL with acute rejection (AR), chronic graft dysfunction (CGD), a

108 r TL to determine the association of TL with acute rejection (AR), chronic graft dysfunction (CGD), a

109 In the absence of acute rejection (AR), rapamycin was withdrawn after mont

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

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

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

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

114 analyzed in overall transplantations, in the acute rejection (AR; n=110) and non-AR (n=292) groups.

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

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

117 Adjustment for acute rejection as a time-varying covariate significantl

118 in pretransplant panel reactive antibodies, acute rejection at 1-year nor in 10-year transplant or p

119 Biopsy-confirmed acute rejection (BCAR) was grade 1A or higher by Banff c

120 Acute rejection before hospital discharge was lowest amo

121 ion, induction with antithymocyte globulins, acute rejection before month 3 (M3), tacrolimus trough l

122 Incidence of acute rejection, BK nephropathy and renal function at 1

123 e compared among patients with biopsy-proven acute rejection, borderline changes, and in rejection-fr

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

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

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

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

128 The 1-year incidence of biopsy-proven acute rejection (BPAR) was 14.1% in African Americans ve

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

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

131 PPI use on the 1-year rates of biopsy-proven acute rejection (BPAR).

132 h, graft failure, locally read biopsy-proven acute rejection [BPAR], or loss to follow-up) within 12

133 s that DSA-SPA increases the overall risk of acute rejection but does not appear to adversely impact

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

135 The rate of biopsy-proven acute rejection by 12 months was lower in the alemtuzuma

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

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

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

139 reas the best graft survival was among early acute rejection cases (85% 10-year survival; P<0.01).

140 is associated with an increased incidence of acute rejection, chronic rejection, and slightly worse g

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

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

143 sociated with high rates of biopsy-confirmed acute rejection compared with CsA-based immunosuppressio

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

145 tion from transplant to BOS was increased by acute rejection, CXCL5, and the interaction between pseu

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

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

148 Acute rejection develops frequently in the early postgra

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

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

151 h stroke (3.30 [1.31-8.28]), and one or more acute rejection episode (13.89 [4.78-40.37]).

152 ually effective in reducing the incidence of acute rejection episodes in SPKT recipients.

153 Three acute rejection episodes occurred in the intervention gr

154 Biopsy-proven acute rejection episodes occurred in three patients (two

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

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

157 During acute rejection episodes, CD8(+) T cells can contribute

158 apeutic tacrolimus concentrations may induce acute rejection episodes.

159 ore frequent (P=0.034) and earlier (P=0.065) acute rejection episodes.

160 erapy resulted in a significant reduction in acute rejection episodes.

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

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

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

164 mmune diseases and is associated with severe acute rejection following renal transplantation, leading

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

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

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

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

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

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

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

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

173 these outcomes-delayed graft function (DGF), acute rejection, graft or patient survival at 1 or 5 yea

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

175 Late acute rejection (>2 years) occurred more often in Africa

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

177 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

178 pared with recipients who did not experience acute rejection (HR 2.20, 95% CI 1.33-3.66, P=0.007).

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

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

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

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

184 n provides improved protection against early acute rejection in black renal transplant recipients, wh

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

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

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

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

189 The standard test for the diagnosis of acute rejection in kidney transplants is the renal biops

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

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

192 05 and 15 December 2012 in the Assessment of Acute Rejection in Renal Transplantation (AART) study.

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

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

195 1.11; P = 0.20) despite an increased risk of acute rejection in the first year posttransplant (odds r

196 Acute rejection in the year before nocardiosis was assoc

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

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

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

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

201 Pathological changes associated with acute rejection, including T-cell, macrophage, and fibro

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

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

204 Acute rejection is a systemic inflammatory state and may

205 y improved over the past two decades, though acute rejection is common.

206 Because the most common type of acute rejection is distinguished by inflammatory cells e

207 tential of targeting monocyte/macrophages in acute rejection is unknown.

208 Late acute rejection (LAR) after liver transplantation is oft

209 Late acute rejection (LAR) has been associated with inferior

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

211 Acute rejection, lymphocytic bronchiolitis, colonization

212 Protection against acute rejection may involve increased accumulation of CD

213 However, acute rejection may predispose to chronic rejection.

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

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

216 ith either CNI or rapamycin in six patients (acute rejection [n=2], progression to end-stage renal di

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

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

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

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 ocusing on the presentation and treatment of acute rejection of the abdominal wall vascularized compo

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

228 3 (subhazard ratio [SHR] = 1.95, P = 0.009), acute rejection (one vs. none) (SHR = 1.93, P = 0.033),

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

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

231 ity was excellent; there were no episodes of acute rejection or opportunistic infection.

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

233 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

234 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

235 .17-3.21; P = .679; Q = 4.48; I(2) = 55.3%), acute rejection (OR = 0.93; 95% CI, .70-1.24; P = .637;

236 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),

237 was defined as graft loss, biopsy-confirmed acute rejection, or graft dysfunction at week 24.

238 ndpoint was graft loss, death, biopsy-proven acute rejection, or lost to follow-up.

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

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

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

242 sociated with significantly higher risks for acute rejection (P=0.02), chronic graft injury (P=0.02),

243 ate aABMR was also inferior to late non-ABMR acute rejections (P=0.008).

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

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

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

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

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

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

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

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

252 We analyzed patient and graft outcomes, acute rejection rate, HIV progression, BKV replication,

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

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

255 months but terminated early because of high acute rejection rates in the sirolimus arm.

256 Cumulative acute rejection rates of 11% in the DSA+ group and 12% i

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

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

259 Acute rejection requiring T-cell-depleting antibody is a

260 The acute rejection response has been attributed to donor de

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

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

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

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

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

266 C5 abrogated the development of OB, reduced acute rejection severity, lowered systemic and local lev

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

268 e aimed to determine the association between acute rejection, T-cell-depleting antibody use and cance

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

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

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

272 llaries and glomeruli from antibody-mediated acute rejections than within those from T cell-mediated

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 organ quality, ischemia-reperfusion injury, acute rejection, tolerance and chronic allograft dysfunc

279 no significant differences in biopsy-proven acute rejection (two trials, n=1093; risk ratio [RR; con

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

281 geneic transplantation, such as incidence of acute rejections, very much depends on the individual's

282 Incidence of biopsy proven acute rejection was 18.5%.

283 The incidence of acute rejection was 9% at 1 year and the patient and all

284 Acute rejection was compared with Student's t test.

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

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

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

288 Acute rejection was reversible in two patients.

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

290 In patients with no signs of acute rejection, we observed an immediate reduction of C

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

292 Rates of acute rejection were less in SSc-ILD (P = 0.05).

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

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

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

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

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

298 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

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

300 RATG was protective against 6- and 12-month acute rejection, without an increased risk of infection.