ライフサイエンスコーパス: graft loss

1 rst 4 months after infusion (2 with an early graft loss).

2 experienced AMR, and 4 of 80 had experienced graft loss.

3 sible to explore the mechanism of late islet graft loss.

4 ated with an increased risk of mortality and graft loss.

5 ions remain difficult to treat, causing late graft loss.

6 a to find out the potential cause(s) of late graft loss.

7 th antibody-mediated rejection and long-term graft loss.

8 0% in fact is an independent risk factor for graft loss.

9 uld unveil the cause of insidious late islet graft loss.

10 e-mediated injury, the leading cause of late graft loss.

11 (NHPs) enabled us to investigate on the late graft loss.

12 P=0.007) were associated with lower risk of graft loss.

13 outcome is the combined endpoint of death or graft loss.

14 infection and rejection are major causes of graft loss.

15 riability in modeling and reduced by 40% for graft loss.

16 graft vasculopathy, remains a major cause of graft loss.

17 ausing antibody-mediated rejection (AMR) and graft loss.

18 all renal graft loss, but not death-censored graft loss.

19 n risk factor for graft thrombosis and early graft loss.

20 ication by race for acute rejection, but not graft loss.

21 ciated with either overall or death-censored graft loss.

22 have significantly increased rates of early graft loss.

23 ociated with both overall and death-censored graft loss.

24 is an independent risk factor for long-term graft loss.

25 ed rates of delayed graft function and early graft loss.

26 vity and therapeutic intervention to prevent graft loss.

27 experience disproportionately high rates of graft loss.

28 e of great importance in prevention of total graft loss.

29 ociated with antibody-mediated rejection and graft loss.

30 ontribute to antibody-mediated rejection and graft loss.

31 was independently associated with subsequent graft loss.

32 R episode, 2 of these were associated with a graft loss.

33 = 0.007) were associated with lower risk of graft loss.

34 78%, with inferior survival of patients with graft loss.

35 ed strongly with inferior graft function and graft loss.

36 was a composite of estimated GFR halving and graft loss.

37 biopsies, can lead to chronic rejection and graft loss.

38 fter cDCD is associated with higher rates of graft loss.

39 r risk of ongoing acute rejection and future graft loss.

40 biopsies, can lead to chronic rejection and graft loss.

41 ) and worse than a 100% risk of dying before graft loss (0.17: 0.12-0.23).

42 5% confidence interval, 0.53-0.75) for total graft loss, 0.69 (0.55-0.86) for death, and 0.62 (0.49-0

43 r prediction of posttransplant mortality and graft loss, 10 predictors were used (recipients' age, ca

44 . 32% for non-NRP livers, P = .0076), 30-day graft loss (2% NRP livers vs. 12% non-NRP livers, P = .0

45 dney injury (26% versus 33%; P = 0.49), 90-d graft loss (2% versus 5%; P = 0.66), and arterial (4% ve

46 27%; difference, 2% [95% CI, -14% to 10%]), graft loss (2% vs 2%; difference, <1% [95% CI, -4% to 4%

47 Among 3657 patients with first graft loss, 2472 died and were not retransplanted.

48 In total, 365 graft losses (36.5%) were identified, of which 211 (57.8

49 We found no differences in death-censored graft loss (5.0% versus 4.8%, aHR: 1.06; 95% CI, 0.51-2.

50 acute rejection (11% versus 22%, P=0.05) and graft loss (9% versus 22%, P=0.01) along with better tra

51 sociated with an increased risk of all-cause graft loss (ACGL) in kidney transplant (KT) recipients.

52 eceiving cyclosporine A had a higher risk of graft loss (adjusted hazard ratio = 1.26; P = 0.046).

53 ificant differences in the risk of all-cause graft loss (adjusted hazard ratio [HR], 1.16; 95% confid

54 ctomy time was independently associated with graft loss [adjusted hazard ratio (HR) 1.03 for every 10

55 vasculopathy (TV) is a major cause for late graft loss after cardiac transplantation.

56 significant differences in 1-year or 3-year graft loss after LDKT or DDKT in the most recent cohorts

57 r V as a biomarker of EAD and a predictor of graft loss after liver transplantation (LT).

58 and is a continuous predictor of short-term graft loss after LT.

59 e (CS) is a major cause of injury leading to graft loss after LT.

60 t risk factor for graft thrombosis and early graft loss after renal transplantation.

61 quent influence on mortality, morbidity, and graft loss after SPK transplantation.

62 ncreasingly recognized as a leading cause of graft loss after transplantation.

63 lity (aHR = 51.43, 95% CI, 16.00-165.43) and graft loss (aHR = 33.57, 95% CI, 11.25-100.21) in the fi

64 1.38-1.83, respectively) and death-censored graft loss (aHR, 1.41; 95% CI, 1.24-1.60 and aHR, 1.38;

65 more likely than whites to experience 5-year graft loss (aHR, 1.53; 95% CI, 1.27 to 1.83; P<0.001), b

66 after adjustment for time-varying covariate graft loss (aHR, 1.68 [1.08-2.62]; P = 0.022) and biopsy

67 re (aHR, 2.29; 95% CL, 1.59-3.32), all-cause graft loss (aHR, 2.09; 95% CL, 1.50-2.91), and death (aH

68 mortality (aHR=51.43,95%CI:16.00-165.43) and graft loss (aHR=33.57,95%CI:11.24-100.21) in the first y

69 ated with higher risks for patient death and graft loss, although SRL + MPA was associated with a low

70 ssociated with an increased risk of death or graft loss, although there was a trend toward a greater

71 % of graft failures and only 7.4% of overall graft losses, although 72.7% of cases with chronic injur

72 The increased risk of 1-y graft loss among en bloc recipients only appeared in the

73 There were no differences in terms of graft loss among low versus optimal and high IS groups (

74 0 (95% CI, 1.50-4.51; P = 0.001) for overall graft loss and 2.49 (95% CI, 1.39-4.47; P = 0.002) for D

75 ce interval, 1.39 to 1.68) increased risk of graft loss and a 2.38-fold (95% confidence interval, 2.2

76 lication and is an important risk factor for graft loss and adverse cardiovascular outcomes in pediat

77 GF-D, the adjusted hazard ratios for overall graft loss and DCGL in recipients who have experienced D

78 ibody (IL-2RA) induction on acute rejection, graft loss and death in African-American (AA) kidney tra

79 ost-transplant and subsequent cause-specific graft loss and death were determined using Cox models ad

80 recipients with DGF had experienced overall graft loss and death-censored graft loss at 3 years comp

81 mpaired renal function have a higher risk of graft loss and death.

82 ence of IgA-aB2GP1 was associated with early graft loss and delayed graft function.

83 Graft loss and EAD rate were 2% (n = 1) and 26% (n = 13)

84 stage approach to joint modelling of time to graft loss and longitudinal SAI did not predict graft lo

85 to be an independent risk factor of AMR and graft loss and may be a useful tool to stratify the immu

86 main cause for functional decline and kidney graft loss and may only be assessed through surveillance

87 We estimated the risk of death-censored graft loss and mortality after developing dementia or th

88 rch efforts should explore the mechanisms of graft loss and mortality associated with cognitive impai

89 Additionally, a subgroup analysis for graft loss and mortality at 3 years (study period Januar

90 readmission is most strongly associated with graft loss and mortality during the readmission hospital

91 To examine death-censored graft loss and mortality for KT recipients with and with

92 CV, and cross-sectionally compared long-term graft loss and mortality rates between those who were tr

93 bserved-to-expected outcome ratios (O:E) for graft loss and mortality using the Scientific Registry o

94 readmission is independently associated with graft loss and mortality.

95 umonia was associated with high incidence of graft loss and patient death (30% and 17% respectively,

96 .9%]; and class D, one of 41 [2.4%]); 30-day graft loss and patient mortality were zero.

97 e 13% and 5.7%, respectively, with no 30-day graft loss and patient mortality.

98 ratio (aHR) of patient death, death-censored graft loss and posttransplant malignancy associated with

99 s been associated with an increased risk for graft loss and reduced host survival.

100 r, affecting 30% of patients, predicted both graft loss and rejection, independent of immunologic sta

101 shortly after transplantation, resulting in graft loss and the need for a second transplant.

102 with IL-2RA, reduces the risk of rejection, graft loss, and death in adult AA KTX recipients, partic

103 d by recurrent rejection in 35.3%, increased graft loss, and greater patient mortality.

104 whereby the associations between induction, graft loss, and incident cancer were examined using adju

105 here were no associations between induction, graft loss, and incident cancer.

106 recipients, we estimated risk of mortality, graft loss, and length of stay (LOS) by recurrent falls

107 recipients, we estimated risk of mortality, graft loss, and length of stay by recurrent falls before

108 d to assess the outcomes of acute rejection, graft loss, and mortality, with interaction terms to ass

109 There was no HBV-related graft loss, and no retransplantation or deaths due to HB

110 Primary endpoint was death-censored graft loss, and secondary endpoint was all-cause mortali

111 ccording to their long-term risk of death or graft loss, and thus facilitate a personalization of lon

112 ding 71,845 patient-years of follow-up, 1121 graft losses, and 1192 deaths.

113 archers should focus on using death-censored graft loss as the primary outcome of interest to facilit

114 Transplant recipients regarded graft loss as worse than death and showed minimal willin

115 Graft loss at 1 month and 1 year was similar between gro

116 ed glomerular filtration rate < 30 mL/min or graft loss at 1 y, n = 66) were analyzed by using a mult

117 Graft loss at 1 year was the least desirable outcome (me

118 transplantation (LT) that is associated with graft loss at 3 months after LT.

119 In this cohort of 131 patients, graft loss at 3 months occurred in 14 patients (11.9%).

120 OR for graft loss at 3 months was 70.211 (p<0.001, 95% CI 10.87

121 yielded an AUC of 0.95 for association with graft loss at 3 months.

122 glycomic signature is highly associated with graft loss at 3 months.

123 ienced overall graft loss and death-censored graft loss at 3 years compared with those without DGF (1

124 t DGF, the adjusted hazard ratio for overall graft loss at 3 years for recipients with DGF was 4.31 (

125 Graft loss at 6 months posttransplantation was higher in

126 groups according to hazard ratio for 1-year graft loss at each PF value, which was standardized with

127 6 recipients (21.4%) and was associated with graft loss attributed to chronic allograft nephropathy (

128 r severe allograft dysfunction and for early graft loss (AUROC 0.93, 95% CI, 0.84-1.0).

129 ded incidence of composite efficacy failure (graft loss, biopsy-proven acute rejection or severe graf

130 There were no graft losses but there were 2 deaths in the control grou

131 itus (PTDM) is associated with overall renal graft loss, but not death-censored graft loss.

132 pients experience a substantial disparity in graft loss, but not mortality.

133 Only 1 episode was associated with graft loss, but this was in the context of a mixed rejec

134 AMR is highly associated with graft loss, but unfortunately there are few efficacious

135 1.20, 1.13-1.28; P < 0.001) and the risk of graft loss by 30% (adjusted hazard ratio, 1.30, 1.23-1.3

136 = 2.02-12.06, P < 0.001) and death-censored graft loss by 5 years (adjusted HR = 4.00, 95% confidenc

137 % CI 2.02-12.06, p<0.001) and death-censored graft loss by 5 years (aHR 4.00, 95% CI 1.31-12.24, p=0.

138 8, P < .001) by 12 months and death-censored graft loss by 5 years (HR 3.12, 95% CI 1.53-6.37, P = .0

139 opsy specimens independently correlated with graft loss by 5 years.

140 acute rejection by 32% (OR 0.68, 0.62-0.75), graft loss by 9% (HR 0.91, 0.86-0.97), and death by 12%

141 We calculated adjusted risk of graft loss by means of competing-risks regression, consi

142 the presence of CD47 on islets will minimize graft loss by mitigating IBMIR.

143 tibodies, acute rejection, or death-censored graft loss by non dosed corrected TAC CV and TAC TTR dur

144 of dnDSA, acute rejection, or death-censored graft loss by non-dosed-corrected TAC CV and TAC TTR dur

145 s of BMI had variable risks for mortality vs graft loss by recipient characteristics in competing ris

146 d on the current public reporting of overall graft loss by US regulatory organizations for transplant

147 gher incidence of overall and death-censored graft loss compared with those without DGF.

148 st-transplant period, the initiation of late graft loss could rarely be detected before the overt gra

149 ation exists in mortality and death-censored graft loss (DCGL) after transplantation.

150 tween DGF status, overall and death-censored graft loss (DCGL) were examined using adjusted Cox regre

151 ute rejection at 6 months and death-censored graft loss (DCGL).

152 g too sick to transplant) or post-transplant graft loss (death/re-HT).

153 oved grade II/III AMR (Banff 2007 criteria), graft loss, death, or loss to follow-up, within 9 weeks

154 III; assessed by blinded central pathology); graft loss; death; or loss to follow-up.

155 nical acute rejection, graft dysfunction and graft loss, development of donor-specific anti-HLA antib

156 All control animals (n = 6) experienced graft loss due to antibody-mediated rejection (AMR) afte

157 was observed only in HCV patients with first graft loss due to disease recurrence (HR: 0.31; P = .002

158 Graft loss due to rejection was significantly more frequ

159 There were only 3 graft losses due to abdominal complications, all after r

160 se of technically successful graft survival, graft losses due to technical problems in the first 60 d

161 All 3 graft losses, due to rejection, occurred in the belatace

162 ted with a consistently lower hazard rate of graft loss-due-to-infection (P = 0.003).

163 ted with a consistently lower hazard rate of graft loss-due-to-infection(P=0.003).

164 months posttransplant for the hazard rate of graft loss-due-to-rejection (P = 0.01 and P = 0.003), rA

165 st 6mo posttransplant for the hazard rate of graft loss-due-to-rejection(P=0.01 and 0.003), rATG/ritu

166 ping any ACR, severe ACR, and cause-specific graft loss during the first 60 months posttransplant amo

167 ping any ACR, severe ACR, and cause-specific graft loss during the first 60mo posttransplant among 44

168 orrelations of PP with graft factors, 90-day graft loss, early allograft dysfunction (EAD), L-GrAFT s

169 as they are associated with a higher risk of graft loss, even though candidates may wait an indefinit

170 as they are associated with a higher risk of graft loss, even though candidates may wait an indefinit

171 There were very few graft loss events documented in this study.

172 tis obliterans syndrome (BOS), mortality and graft loss for up to 15 years posttransplant, controllin

173 ecur frequently after liver transplantation, graft loss from disease recurrence after transplantation

174 effective in preventing HBV reactivation and graft loss from recurrent hepatitis B after liver transp

175 Area under the curve of ALP in predicting graft loss from rejection was 0.81 (95% CI 0.71-0.90) an

176 Studies report that the incidence of graft loss (GL) during pregnancy is low, but less data a

177 Studies report that the incidence of graft loss (GL) during pregnancy is low, but less data i

178 >/=8; proportion, >85%) in both groups were graft loss, graft function, chronic rejection, acute rej

179 plantation is associated with a high risk of graft loss, graft-versus-host disease (GvHD), and transp

180 Although early graft loss has been well studied and controlled, the mec

181 e estimated overall and death-censored renal graft loss hazard ratios in patients diagnosed with PTDM

182 end toward increased risk of post-transplant graft loss (hazard ratio 1.4; 95% confidence interval 1.

183 on were independently associated with higher graft loss (hazard ratio = 1.729, P = 0.029 and hazard r

184 l, 1.54-5.06]; P = 0.001) and death-censored graft loss (hazard ratio = 4.65 [95% confidence interval

185 use of induction of was not associated with graft loss (hazard ratio [HR], 0.88; 95% confidence inte

186 sociated with a 0.9% increase in the risk of graft loss (hazard ratio [HR], 1.009; P < 0.001).

187 re significantly more likely to have overall graft loss (hazard ratio [HR], 1.19; 95% confidence inte

188 .13-1.88; P < 0.001), but not death-censored graft loss (hazard ratio, 1.25; 95% confidence interval,

189 s associated with slightly increased risk of graft loss (hazard ratio, 1.3; 95% confidence interval,

190 plantation, PTDM was associated with overall graft loss (hazard ratio, 1.46; 95% confidence interval,

191 sociated with a 0.9% increase in the risk of graft loss, hazard ratio (HR) 1.009, P < 0.001.

192 nterval [95% CI], 1.07-1.33), death-censored graft loss (HR, 1.67; 95% CI, 1.45-1.92), and lower mort

193 urrence of PBC significantly associated with graft loss (HR, 2.01; 95% CI, 1.16-3.51; P = .01) and de

194 (hazard ratio [HR]: 0.921.041.16, p=0.5) or graft loss (HR: 0.931.031.15, p=0.5) with steatotic vers

195 hazard ratio [HR]: 0.921.041.16; P = 0.5) or graft loss (HR: 0.931.031.15; P = 0.5) with steatotic ve

196 1.411.70, p<0.001) and 39% increased risk of graft loss (HR: 1.161.391.66, p<0.001) with steatotic ve

197 411.70; P < 0.001) and 39% increased risk of graft loss (HR: 1.161.391.66; P < 0.001) with steatotic

198 ficant (HR, 1.38; 95% CI, 1.12-1.71; overall graft loss [HR, 1.08; 95% CI, 0.91-1.28]; mortality [HR,

199 One graft loss in 4 years was avoided for every 14.3 patient

200 d the association between nsSNP mismatch and graft loss in a Cox proportional hazard model, adjusting

201 dehiscence are significantly correlated with graft loss in a maxillary FFBA augmentation.

202 P mismatch was independently associated with graft loss in a multivariable model adjusted for HLA epl

203 ), whereas it was a significant predictor of graft loss in AAs (HR, 0.23; 95% CI, 0.06-0.93).

204 DGF) is associated with an increased risk of graft loss in adult kidney transplant recipients but the

205 y associated with acute rejection in AAs and graft loss in all patients.

206 nic rejection were the most common causes of graft loss in both arms.

207 yte antigen (HLA) is a major risk factor for graft loss in cardiac transplantation.

208 1.51; 95% CI, 0.78-2.93) and death-censored graft loss in everolimus versus control (adjusted HR, 1.

209 d nephropathy is the second leading cause of graft loss in kidney transplant recipients.

210 ft loss and longitudinal SAI did not predict graft loss in non-AAs (HR, 1.01; 95% CI, 0.28-3.62), whe

211 Finally, gDSA predicted subsequent graft loss in patients who showed a stable renal functio

212 Finally, gDSA predicted subsequent graft loss in patients who showed a stable renal functio

213 s to examine the association between DGF and graft loss in pediatric and adolescent deceased donor ki

214 risk of overall but not death-censored renal graft loss in renal transplant recipients with PTDM.

215 ecific anti-HLA antibodies (dnDSA) may cause graft loss in renal transplant recipients.

216 Tac) is widely used to prevent rejection and graft loss in solid organ transplantation.

217 l thrombosis was the most important cause of graft loss in the 3 time periods, irrespective of demogr

218 ctively control acute rejection and decrease graft loss in the first year after transplantation; howe

219 ) may be 1 of the factors that contribute to graft loss in the long run.

220 such treatment is a major cause of premature graft loss in these patients.

221 hat poverty is more strongly associated with graft loss in women, targeted efforts are needed to spec

222 Thrombosis caused 1.3% of the graft losses in open kidney transplant and 0% in the RKT

223 loss within 30 days of transplantation, and graft losses in the first-year posttransplant and assess

224 se variables to the model for death-censored graft loss increased predictability (c statistic =0.90),

225 ociated with an increased risk of functional graft loss independently of HLA incompatibility.

226 Although graft loss is a primary endpoint in many studies in kidn

227 udied and controlled, the mechanisms of late graft loss largely remains obscure.

228 One graft loss, mediated by non-HLA IgM and IgA antibodies,

229 pproach, we investigated the 10-year risk of graft loss, mortality and graft function in 349 particip

230 ere used to estimate the association between graft loss, mortality, and readmission for 2 periods: re

231 recipient death (n = 540) or death-censored graft loss (n = 353).When the observational time started

232 ss could rarely be detected before the overt graft loss observed via uncontrolled blood glucose level

233 Uncensored and death-censored graft loss occurred in 263 and 46 recipients, respective

234 cluded, at 1 year, no deaths occurred, but 1 graft loss occurred in each group.

235 No graft losses occurred, and at last follow-up (median [IQ

236 d 329 graft failures before death (638 total graft losses) occurred during a median of 5.4 years of f

237 ose with de novo DSA experienced accelerated graft loss once DSA was detected, reaching a 28% failure

238 Graft loss or death occurred in about one third of recip

239 The primary endpoint was a composite of graft loss or no improvement in renal function at day 12

240 ardiovascular outcome in KTRs independent of graft loss or rejection.

241 as a continuous predictor for 3- and 6-month graft losses (OR, 0.96; 95% CI, 0.94-0.99 and OR, 0.97;

242 point (biopsy-proven acute rejection [BPAR], graft loss, or death from randomization to month 12) was

243 nt of treated biopsy-proven acute rejection, graft loss, or death was 10.9%, 14.1%, and 14.1% for EVR

244 ilure (biopsy-proven acute rejection [BPAR], graft loss, or death) at month 36 was 9.8% vs 9.6% (diff

245 ment failure (biopsy-proven acute rejection, graft loss, or death), delayed graft function, patient a

246 There were no cases of chronic rejection, graft loss, or death.

247 any TASC II lesion was not a risk factor for graft loss (overall P = 0.282).

248 rejection (P < .0001), as well as all-cause graft loss (P = .0012) and each of these correlations pe

249 iated with eightfold increased risk of early graft loss (P = 0.001; odds ratio, 8.4) and a 2.9-fold i

250 sk factor for both mortality (P = 0.031) and graft loss (P = 0.034).

251 between total ischemic time, donor age, and graft loss (P value for interaction = 0.03).

252 verage, a 9% increase in the overall risk of graft loss per hour increase in the total ischemic time

253 The increase in the risk of graft loss per year rise in donor age was 1.4% for 18 to

254 The increase in the risk of graft loss per year rise in donor age was 1.4% for 18- t

255 antation and identify new factors to improve graft loss prediction in DSA+ patients.

256 24.2% in 3 years, 33.0% in 5 years) and the graft loss rate (2.2% in 1 year, 4.8% in 3 years, 7.5% i

257 Mortality and graft loss rates at 90 days were 42.5% and 46.6%, respec

258 Mortality and graft loss rates at 90 days were set as primary and seco

259 ifferences in acute rejection, mortality, or graft loss rates.

260 A composite definition of graft loss reduced the magnitude of disparities in black

261 n fully adjusted models, only death-censored graft loss remained significant (HR, 1.38; 95% CI, 1.12-

262 After readmission, the hazard of graft loss remained, but decreased 19% per year for DDKT

263 tation in children is associated with a high graft loss risk and no survival benefit, whereas > 85 KD

264 The 10-year graft loss risk was 28.8% for those who did not develop

265 hronic lung allograft dysfunction (CLAD) and graft loss, severe infection would.

266 ansplants from donors 5-30 kg had first-year graft loss similar to ECK.

267 1.14-1.40) neighborhoods had higher risk of graft loss than men, but there were no differences in we

268 ological advantage against rejection-related graft loss, this protective effect was lost among recipi

269 .001) and a lower overall predicted risk for graft loss (UK-DCD-risk score 6 vs 9 points, P < 0.001).

270 e impact of donor steatosis on mortality and graft loss using interaction analysis, classifying recip

271 erulonephritis and determined if the risk of graft loss varied with donor source within each glomerul

272 ith a significant reduction in mortality and graft loss versus no prophylaxis, particularly in high-r

273 Adjusted risk of graft loss was 41% higher in HIV-infected versus HIV-uni

274 Adjusted risk of graft loss was 41% higher in HIV-infected vs. uninfected

275 ying Cox regression, no crude association to graft loss was found for rs3811321 on chromosome 14 (haz

276 Graft loss was low (2.1% vs 3.8%) with no deaths.

277 [CI], 0.93-1.20]; P = 0.40), death-censored graft loss was lower (HR, 0.63; 95% CI, 0.47-0.84; P = 0

278 The risk of graft loss was not increased by asymptomatic CARV infect

279 chemic cholangiopathy were diagnosed, and no graft loss was observed over a medium follow-up period o

280 In the whole population, graft loss was only significantly associated with longer

281 ren had CMV disease; no CMV-related death or graft loss was recorded.

282 9), whereas in the Tac subgroup, the risk of graft loss was significantly higher in recipient CYP3A5*

283 cipients without prior nkSOT, death-censored graft loss was similar (adjusted hazard ratio [aHR]: 1.1

284 5% CI, 0.47-0.84; P = 0.002), and uncensored graft loss was similar (HR, 0.99; 95% CI, 0.87-1.12; P =

285 During the readmission hospitalization, graft loss was substantially higher (deceased donor kidn

286 The most frequent cause of early graft loss was vessel thrombosis, especially in group 1

287 -survival models including histology predict graft loss well, both in DSA+ cohorts as well as DSA- pa

288 Associations of cancers with mortality and graft loss were estimated by time-varying Cox regression

289 Ratios for mortality and graft loss were similar between VA centers and their res

290 The 3 graft losses were caused at least in part by nonadherenc

291 (aHR, 1.83; P < 0.001) were associated with graft loss, whereas more recent period of LT 2012-2015 (

292 cers had similar associations with death and graft loss, whereas NMSC was associated with 33% higher

293 P = 0.006) were independent risk factors for graft loss, while heart failure (HR 3.77, 95% CI: 1.79-7

294 HCV (aHR,1.83; P<0.001) were associated with graft loss, while more recent period of LT 2012-2015 (aH

295 2) 3.57(4.88) , P < .001) and death-censored graft loss (wHR = (1.15) 4.01(13.95) ,P = .03).

296 risk profile with elevated risks for overall graft loss with low BMI and obesity.

297 We compared mortality and graft loss with steatotic versus nonsteatotic livers in

298 The primary outcome was graft loss within 1, 3, and 6 months.

299 09 to December 31, 2017) and quantified PNF, graft loss within 30 days of transplantation, and graft

300 The risk of graft loss within the first 90 days was 5.2 times higher