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1                                              DGF has a much more detrimental impact in DSApos-patient
2                                              DGF is a relevant problem after kidney transplantation;
3                                              DGF occurred in 137 of 375 patients (37%), and DSA were
4                                              DGF occurred in 23 (24%) kidney recipients from deceased
5                                              DGF rates increase with donor AKI stage (p < 0.005), and
6                                              DGF severity and functional recovery dynamics were asses
7                                              DGF was associated with a 2.6-fold increase in kidney gr
8                                              DGF was diagnosed in 4/6 (67%) G1 recipients, 3/3 (100%)
9                                              DGF-ESW interaction was statistically significant for gr
10 survival in DBD grafts (HR 1.67; P < 0.001), DGF did not impact graft survival in DCD grafts (HR 1.08
11 cipients (n=53) were divided into AKI (n=37; DGF, n=10; SGF, n=27) and immediate graft function (n=16
12 PNF (OR, 0.82; 95% CI, 0.46-1.46; P = 0.50), DGF (OR, 1.22; 95% CI, 0.96-1.56; P = 0.11), acute rejec
13  graft failure (aHR: 0.521.001.91, P > 0.9), DGF (adjusted odds ratio [aOR]: 0.580.861.27, P = 0.4),
14 ed graft failure (aHR: 0.521.001.91, p>0.9), DGF (adjusted odds ratio [aOR]: 0.580.861.27, p=0.4), ac
15       Among recipients who had experienced a DGF duration of 1 to 4 days, the adjusted hazard ratio f
16 tant effects in reducing the expression of a DGF-associated gene signature.
17 ng (UNOS) database revealed that sex affects DGF outcomes in humans.
18 f 0.75 and 0.77, respectively, and also AKI (DGF + SGF) from IGF with area under the curves of 0.76 a
19 etransplant recipient immune marker for AKI (DGF + SGF), independent from donor and organ procurement
20                           Prediction of AKI (DGF + SGF) from IGF remained significant in multivariate
21                    On multivariate analysis, DGF [hazard ratio (HR), 165.7; 95% confidence interval (
22 dently associated with recovery from AKI and DGF.
23 sociation between center characteristics and DGF incidence after adjusting for known patient risk fac
24 rmined associations between risk factors and DGF using Poisson multivariate regression and between DG
25 ained significantly different between IF and DGF in DCD grafts (P < 0.01), but not in DBD grafts.
26            Clinical trial design for IRI and DGF were also discussed.
27 was used to test association of the KDRI and DGF with graft survival.
28 sk of DCGF associated with early events (AR, DGF, baseline serum Cr >2.0 mg/dL) to that associated wi
29  Poisson multivariate regression and between DGF and graft failure and mortality using Cox proportion
30  years (16.2% increase; P<0.001) and between DGF and mortality at both 1 year (7.1% increase; P<0.001
31  study is to examine the association between DGF and graft loss in pediatric and adolescent deceased
32 egistry, we examined the association between DGF, graft and patient outcomes between 1994 and 2012 us
33                     The associations between DGF status, overall and death-censored graft loss (DCGL)
34     The Remuzzi score did not differ between DGF and no DGF, P = 0.13.
35  miRNAs were significantly different between DGF and IF kidney grafts (P < 0.05) but, after correctio
36 ls were also significantly different between DGF and IGF kidneys at 4 hr (49.099 vs. 59.513 mM, P = 0
37 leucine were significantly different between DGF and IGF kidneys at 45 min (0.002 vs. 0.013 mM, P = 0
38 e was a direct dose-dependent effect between DGF duration and DCGL, with acute rejection explaining l
39        On average, 8% of the effects between DGF duration and DCGL were explained by acute rejection.
40 laining less than 10% of the effects between DGF duration and DCGL.
41  rejection was a causal intermediate between DGF and DCGL.
42 tors that lies in the causal pathway between DGF duration and allograft loss is essential.
43 nce suggesting a causal relationship between DGF and death-censored graft failure at both 1 year (13.
44                                         Both DGF definitions were associated with lower adjusted 12-m
45 ing that the effect is partially mediated by DGF.
46 generalizability and validity of the current DGF definition.
47  developed DGF and the other did not develop DGF using data from the Australia and New Zealand Dialys
48 idney transplant recipients, 27.0% developed DGF, with a range across centers of 3.2% to 63.3%.
49               Two patients (11.8%) developed DGF.
50 ysis was undertaken where 1 kidney developed DGF and the other did not develop DGF using data from th
51       Overall, 23 (33.8%) patients developed DGF.
52  Recipients at our institution who developed DGF had longer LOS (OR, 1.71; 95% CI, 1.50-1.95), sugges
53 as significantly lower in kidneys developing DGF -0.43 +/- 1.78 versus no DGF 0.91 +/- 2.17, P = 0.01
54 e creatinine or the likelihood of developing DGF.
55  significantly higher in patients developing DGF (n=18).
56 idney (SLK) transplant recipients developing DGF.
57 2 (22%) experiencing DGF requiring dialysis (DGF-D) in the first 72 hours after transplant.
58 age, Treg suppressive function discriminated DGF from immediate graft function recipients in multinom
59 ransplantation, one patient (5%) experienced DGF, and no patients experienced NODAT.
60           Of these, 1823 (24.6%) experienced DGF and 2553 (33.9%) experienced allograft loss.
61 t 3 years in recipients who have experienced DGF were 0.98 (95% CI, 0.96-1.01) and 1.70 (95% CI, 0.36
62  and DCGL in recipients who have experienced DGF-D was 2.08 (95% confidence interval [95% CI], 1.39-3
63 ared with recipients who did not experienced DGF-D, the adjusted hazard ratios for overall graft loss
64 nd 2014, 1497 (19.5%) recipients experienced DGF requiring dialysis.
65 en 1990 and 2012, with 82 (22%) experiencing DGF requiring dialysis (DGF-D) in the first 72 hours aft
66 pecies-specific, cell-surface gene families (DGF-1 and PSA) with no apparent structural similarity ar
67 back loop is then a delayed global feedback (DGF) loop.
68 the importance of divergence with gene flow (DGF) in the generation of biological diversity.
69 -free miR-505-3p as prognostic biomarker for DGF.
70 and use of a creatinine-based definition for DGF.
71                             Risk factors for DGF in the hepatitis C virus (HCV)-negative recipient po
72 uality comprise significant risk factors for DGF.
73 d miR-505-3p as an independent predictor for DGF (odds ratio, 1.12; P = 0.028).
74 dels may aid in both risk quantification for DGF prevention clinical trials and personalized clinical
75                          The odds ratios for DGF compared with nonobese patients were 1.34 [95% confi
76  weight classes are at an increased risk for DGF after renal transplantation, although differences in
77 tion lack sensitivity in predicting risk for DGF.
78 sion, obese patients have increased risk for DGF.
79 omposite endpoint across all risk strata for DGF risk, whereas IL2-Ra was associated with increased a
80  association between delayed graft function (DGF) after kidney transplantation and worse long-term ou
81 r rapid detection of delayed graft function (DGF) after kidney transplantation are unreliable.
82                      Delayed graft function (DGF) after renal transplantation can be diagnosed accord
83 recipient obesity on delayed graft function (DGF) and graft survival after renal transplantation.
84 iles of kidneys with delayed graft function (DGF) and immediate graft function (IGF).
85 nown risk factor for delayed graft function (DGF) and its interaction with donor characteristics, the
86                      Delayed graft function (DGF) and pretransplant donor-specific HLA-antibodies (DS
87                      Delayed graft function (DGF) and slow graft function (SGF) are a continuous spec
88                      Delayed graft function (DGF) and slow graft function (SGF) are ischemia-reperfus
89 sulting increases in delayed graft function (DGF) and transplant-related costs (TRC).
90 usually manifests as delayed graft function (DGF) and, in severe cases, results in primary nonfunctio
91 recipients developed delayed graft function (DGF) between 2000 and 2010.
92                      Delayed graft function (DGF) caused by ischemia/reperfusion injury (I/RI) negati
93 vel risk factors for delayed graft function (DGF) have been well described.
94 sociation of PP with delayed graft function (DGF) in all (n=94,709) deceased donor kidney transplants
95 rococept in reducing delayed graft function (DGF) in deceased donor renal transplantation, we underto
96 perfusion injury and delayed graft function (DGF) in human kidney transplant recipients.
97 tion between sex and delayed graft function (DGF) in patients who received deceased donor renal trans
98                      Delayed graft function (DGF) in renal transplant is associated with reduced graf
99                      Delayed graft function (DGF) is a risk factor for acute rejection (AR) in renal
100                      Delayed graft function (DGF) is an established complication after donation after
101                      Delayed graft function (DGF) is associated with an increased risk of graft loss
102                      Delayed graft function (DGF) is associated with inferior posttransplant outcomes
103 rolonged duration of delayed graft function (DGF) may be associated with adverse allograft outcomes,
104               Kidney delayed graft function (DGF) rates were similar between the 2 groups (P = .11),
105 gan transplantation, delayed graft function (DGF) remains a major concern in deceased donor kidney tr
106  Index (KDRI) versus delayed graft function (DGF) to predict graft survival in the HIV (+) kidney tra
107  acute rejection and delayed graft function (DGF) using logistic regression, and length of stay (LOS)
108 acute rejection, and delayed graft function (DGF) using logistic regression, and length of stay (LOS)
109             Rates of delayed graft function (DGF) were significantly lower in organs preserved with H
110                      Delayed graft function (DGF), a common complication after transplantation of dec
111 ne of these outcomes-delayed graft function (DGF), acute rejection, graft or patient survival at 1 or
112 tion between CIT and delayed graft function (DGF), allograft survival, and patient survival for 1267
113 splantation (NODAT), delayed graft function (DGF), and graft failure.
114 e, the occurrence of delayed graft function (DGF), and long-term graft survival.
115 ury (IRI) leading to delayed graft function (DGF), defined by the United Network for Organ Sharing as
116                      Delayed graft function (DGF), graft failure, and patient death were ascertained
117      Recipients with delayed graft function (DGF), however, often have a suboptimal allograft milieu,
118  of whom experienced delayed graft function (DGF).
119 rfusion injuries and delayed graft function (DGF).
120 rgans with prolonged delayed graft function (DGF).
121 udy endpoint was the delayed graft function (DGF).
122 rmance in predicting delayed graft function (DGF=dialysis requirement during initial posttransplant w
123 e rejection [AR] and delayed graft function [DGF] before day 90) were recorded; serum creatinine (Cr)
124 plant [DDKT] without delayed graft function [DGF] hazard ratio: 24.634.447.9, P < 0.001; with DGF: 10
125 D DATA: Delayed function of the renal graft (DGF), which can result from hypotension and pressor use
126 level adjustments, only 41.8% of centers had DGF incidences consistent with the national median and 2
127 he definition of DGF accordingly may improve DGF's utility in clinical care and as a surrogate endpoi
128 ear if there are center-level differences in DGF and if measurable center characteristics can explain
129                 Significant heterogeneity in DGF incidences across centers, even after adjusting for
130 ter KTx (8-12 hr), MDA values were higher in DGF recipients (on average, +0.16 mumol/L) and increased
131 ion of CIT is associated with an increase in DGF rates and LOS, resulting in increased TRC.
132 e concentrations were significantly lower in DGF kidneys compared to those with IGF at both 45 min (7
133      Future predictive models should include DGF as a variable.
134 is a risk marker for complications including DGF, graft failure, and death.
135 ds of the composite endpoint with increasing DGF risk.
136 -;0.98; P = 0.001) were associated with less DGF.
137             In the linear probability model, DGF was associated with increased risk of both graft fai
138 -;1.10; P < 0.001) were associated with more DGF.
139 uzzi score did not differ between DGF and no DGF, P = 0.13.
140  The rate of DGF was 7.3% in group 1, but no DGF was seen in group 2 (P = 0.0600).
141 neys developing DGF -0.43 +/- 1.78 versus no DGF 0.91 +/- 2.17, P = 0.01.
142 ciated with improved kidney function with no DGF post-KT, and improved patient and graft survival.
143 7lo/-TNFR2+ Treg cell predicted DGF from non-DGF (IGF + SGF) with area under the curves of 0.75 and 0
144 first week posttransplant) compared with non-DGF (P = 0.002).
145  delayed graft function/primary nonfunction (DGF/PNF), estimated glomerular filtration rate (eGFR), a
146     After adjusting for LOS, neither CIT nor DGF were independently associated with increased TRC.
147          We characterized the association of DGF with the use of ESW versus continued steroid mainten
148 it is equally important to document cases of DGF in nature.
149  variability and improving the definition of DGF accordingly may improve DGF's utility in clinical ca
150 nt and Transplantation Network definition of DGF is based on dialysis in the first week, which is sub
151  10 definitions of DGF, and no definition of DGF was associated with impaired graft survival.
152 r filtration rate for 1 of 10 definitions of DGF, and no definition of DGF was associated with impair
153 utcome was comparable for all definitions of DGF.
154 fic, but of low sensitivity for detection of DGF.
155  For kidneys from DCD donors, development of DGF was only associated with poorer 1-year estimated glo
156 ement activation prevents the development of DGF.
157 The median (interquartile range) duration of DGF was 7 (9) days, with 25% requiring dialysis for 14 d
158 2 groups (P = .11), although the duration of DGF was longer for DCD SLK recipients (20 vs 4 days, P =
159 he association between threshold duration of DGF, acute rejection and long-term allograft loss remain
160  regression models to evaluate the effect of DGF on LOS and TRC.
161                 Furthermore, in the event of DGF, elevated donor urinary YKL-40 concentration associa
162              However, the combined impact of DGF and DSA has not been studied in detail.
163 ion suggests that the differential impact of DGF between DBD and DCD grafts relates to donor-type spe
164          We aimed to determine the impact of DGF duration on allograft outcomes and to assess whether
165                                The impact of DGF on DBD and DCD graft survival was evaluated in 6635
166 observation implies a differential impact of DGF on DBD and DCD graft survival.
167  (DCD) kidney transplants, but the impact of DGF on graft outcomes is uncertain.
168         This study shows an absent impact of DGF on long-term graft survival in DCD kidneys.
169                             The incidence of DGF (29.3% versus 29.2%, P = 0.9), acute rejection (11.2
170                             The incidence of DGF (29.3% vs. 29.2%, p=0.9), acute rejection (11.2% vs.
171 cetylcysteine (NAC) reduces the incidence of DGF in adult human kidney transplant recipients.
172         Despite a 3-fold higher incidence of DGF in DCD grafts, large studies show equivalent long-te
173                             The incidence of DGF varied widely depending on the definition used (DBD;
174                             The incidence of DGF was similar between donors pretreated with or withou
175                             The incidence of DGF was similar in DSA-positive (DSApos)-patients and DS
176 tics and is able to predict the incidence of DGF.
177 Tx might be an early prognostic indicator of DGF, and levels on day 7 might represent a useful predic
178 5 uRE or lesser in PB with the occurrence of DGF, with OR of 120 and positive and negative predictive
179 rs or longer experienced an increased odd of DGF compared with those with total ischemic time less th
180 T was associated with a 5% increased odds of DGF (adjusted odds ratio: 1.05, 95% confidence interval
181  by donor type and CIT, the adjusted odds of DGF were lower with PP across all CIT in SCD transplants
182               Within each group, the odds of DGF with and without PP was determined after adjusting f
183 lay significant roles in the pathogenesis of DGF.
184   The utility of clusterin for prediction of DGF (hemodialysis within 7 days of transplantation) was
185 e-1 only modestly improved the prediction of DGF, whereas NGAL, serum creatinine, and the creatinine
186 nhanced the clinical model for prediction of DGF.
187  of 80.8% (p < 0.0001) for the prediction of DGF.
188 rs in graft preservation fluid predictive of DGF after kidney transplantation.
189 1, and NGAL concentration were predictive of DGF.
190  independent pretransplantation predictor of DGF and SGF.
191 nly CI and CV were independent predictors of DGF (P<0.01).
192 y and suppressive function are predictors of DGF and SGF after kidney transplantation.
193 al creatinine were independent predictors of DGF.
194 nsplant recipients; however, the presence of DGF continues to have a negative impact on the graft sur
195 s a promising strategy for the prevention of DGF after transplantation.
196 al decision-making may improve prevention of DGF and may represent an opportunity to improve posttran
197 y differences in the metabolomic profiles of DGF and IGF kidneys that might have a predictive role in
198 termine the association between quartiles of DGF duration, acute rejection at 6 months and death-cens
199  organs having a significantly lower rate of DGF (odds ratio 0.65, 95% confidence interval 0.53-0.80,
200 CIT was associated with an increased rate of DGF (odds ratio [OR], 1.41; 95% confidence interval [CI]
201                                  The rate of DGF was 7.3% in group 1, but no DGF was seen in group 2
202 group, there was a significant lower rate of DGF, BPAR, and infections requiring readmission.A cost a
203 ents, post-LSG recipients had lower rates of DGF (5% vs 20%) and renal dysfunction-related readmissio
204                           Incidence rates of DGF were 25.1% and 26.3% for the development and validat
205 had significantly (P < 0.05) higher rates of DGF, 32% versus 19%; hypotension, 14% versus 4%; acute m
206 ciated with 2.5-fold increase in the risk of DGF (P=0.04).
207 er clinical variables to predict the risk of DGF after kidney transplantation.
208  fluid are associated with increased risk of DGF after kidney transplantation.
209                    Additionally, the risk of DGF and graft failure was assessed.
210         Strategies aim to reduce the risk of DGF could potentially improve graft survival in DCD kidn
211 oncentration associated with reduced risk of DGF in both recipients of AKI donor kidneys (adjusted re
212      PP is associated with a reduced risk of DGF irrespective of donor type and CIT.
213 ependently associated with a greater risk of DGF irrespective of storage method, but this effect was
214 etion induction when the anticipated risk of DGF is increased.
215 ey recipients based on pretransplant risk of DGF using a validated model.
216 e composite endpoint with increasing risk of DGF, especially at the higher risk spectrum of DGF.
217 PP modifies the impact of CIT on the risk of DGF, it does not eliminate its association with DGF, sug
218 ury were associated with the highest risk of DGF.
219 e was independently associated with risks of DGF (adjusted odds ratio, 1.78; 95% confidence interval
220           If possible, the combined risks of DGF and DSA should be avoided.
221   In this study, we investigate the roles of DGF in the genesis and stability of spatiotemporal excit
222 F, especially at the higher risk spectrum of DGF.
223  to describe the relationship between CIT on DGF and length of stay (LOS).
224 cumulated over the last dozen or so years on DGF in the chipmunk (Tamias) radiation with new data tha
225 s defined as immediate good function (IF) or DGF.
226  the creatinine reduction ratio also predict DGF within 12 hr of reperfusion.
227 a lower expression of Netrin-1 might predict DGF development (training area under the receiver operat
228 ve HSI is feasible and meaningful to predict DGF in renal allografts.
229                         The power to predict DGF of the combination of high BAX/BCL2 expression in PI
230 ld personalized prognostic models to predict DGF.
231        Day 1 MDA levels accurately predicted DGF (AUC-ROC=0.90), with a performance higher than SCr (
232 r of CD4+CD127lo/-TNFR2+ Treg cell predicted DGF from non-DGF (IGF + SGF) with area under the curves
233 nine reduction ratio independently predicted DGF.
234  a significant independent factor predicting DGF; P = 0.015, Wald = 5.95, odds ratio = 0.72, 95% conf
235                      The RTCA score predicts DGF and is a valid option to be applied in renal transpl
236  complement-blockade in BD donors to prevent DGF and improve graft survival.
237 or testing interventions aimed at preventing DGF within this high-risk patient subgroup.
238             The delayed graft function rate (DGF), defined as the requirement for dialysis within the
239 was not associated with donor AKI, recipient DGF, or 12-month allograft function.
240 ined independently associated with recipient DGF for donors without AKI (relative risk, 1.31; 95% con
241  C5a concentrations associate with recipient DGF, providing a foundation for testing interventions ai
242 deceased donor kidney transplant recipients (DGF, n = 18; SGF, n = 34; immediate graft function [IGF]
243 F, suggesting the optimal strategy to reduce DGF is to minimize CIT and utilize PP in all deceased do
244 ntial impact was not caused by a more severe DGF phenotype in DBD grafts.
245                    Regardless of HCV status, DGF is associated with inferior posttransplant outcomes.
246 as an instrument to test the hypothesis that DGF causes death-censored graft failure and mortality at
247                    This study has shown that DGF, encompassing a spectrum of renal dysfunction after
248 IV (+) cohort was significantly worse in the DGF (+) group than the DGF (-) group (logrank P<0.01).
249 ficantly worse in the DGF (+) group than the DGF (-) group (logrank P<0.01).
250                                     When the DGF is negative, only concordant P2 patterns exist.
251                                     When the DGF is positive, both concordant and discordant P2 patte
252 P < .001) and significantly shorter times to DGF resolution (average: 6.1 vs 7.4 days, P = .003) than
253 ept is a safe and feasible approach to treat DGF in deceased donor kidney transplantation.
254                                Although UNOS-DGF does not adequately predict 12-month function on its
255 ased-donor kidney recipients to compare UNOS-DGF to a definition that combines impaired creatinine re
256        In 560 recipients, 215 (38%) had UNOS-DGF, 330 (59%) met the combined definition, 14 (3%) died
257  Sharing as dialysis in the first week (UNOS-DGF), associates with poor kidney transplant outcomes.
258 licating comparison between studies that use DGF as an endpoint.
259                         Primary endpoint was DGF defined by the need for at least one dialysis sessio
260                                         When DGF is absent, concordant and discordant P2 patterns occ
261 t use of lymphocyte-depletion induction when DGF is anticipated.
262                                        While DGF severely impacted 10-year graft survival in DBD graf
263  hazard ratio: 24.634.447.9, P < 0.001; with DGF: 10.815.221.4, P < 0.001; live donor kidney transpla
264 T without DGF: 14.120.830.7, P < 0.001; with DGF: 9.0312.818.0, P < 0.001; LDKT: 9.0018.241.3, P < 0.
265 s analyzed; 19(73%) with IGF and 7(27%) with DGF.
266                  Obesity was associated with DGF (relative risk, 1.41; 95% confidence interval, 1.26-
267 a means of identifying genes associated with DGF development.
268 atinine is not significantly associated with DGF in pediatric renal transplant recipients.
269 sion ratio greater than 2.29 associated with DGF with an odds ratio of 2.00.
270 mass index (p = 0.0017) were associated with DGF.
271 however, urinary C5a was not associated with DGF.
272 ed that there was a greater association with DGF in male recipients than in female recipients.
273 , it does not eliminate its association with DGF, suggesting the optimal strategy to reduce DGF is to
274 rom DD, BCL2 levels were lower in cases with DGF, whereas no differences were observed concerning CAS
275        In a multivariate Cox model, DSA with DGF was an independent predictor for graft (hazard ratio
276               Recipients of DCD kidneys with DGF experienced a higher incidence of overall and death-
277                                 Kidneys with DGF furthermore displayed significant lower StO2 (p = 0.
278 t association of high miR-505-3p levels with DGF was confirmed in an independent validation cohort us
279  graft survival was significantly lower with DGF (64% versus 79%; P = 0.01).
280 cantly more frequent in DSApos-patients with DGF (5/34; 15%) compared to DSApos-patients without DGF
281 antly longer (18.6 +/- 1.6) in patients with DGF (p < 0.01).
282               Moreover, DSApos-patients with DGF had a higher 1-year incidence of subclinical rejecti
283 kers and may allow triaging of patients with DGF within 4 hr of transplantation.
284 Donor C5a was higher for the recipients with DGF (defined as dialysis in the first week posttransplan
285 rs), a greater proportion of recipients with DGF had experienced overall graft loss and death-censore
286                              Recipients with DGF had lower odds of ESW (aOR=(0.60)0.67(0.75)).
287 ll graft loss at 3 years for recipients with DGF was 4.31 (95% confidence interval [95% CI], 1.13-16.
288                        Among recipients with DGF, ESW was associated with a similar increase in rejec
289 es use ESW inconsistently in recipients with DGF.
290 ), but only with harms among recipients with DGF.
291 lead to worse KT outcomes in recipients with DGF.
292 ltivariable logistic and Cox regression with DGF-ESW interaction terms.
293 ality was substantially higher (DDKT without DGF: 14.120.830.7, P < 0.001; with DGF: 9.0312.818.0, P
294 34; 15%) compared to DSApos-patients without DGF (2/51; 4%), and DSAneg-patients with/without DGF (3/
295             Compared with recipients without DGF, the adjusted hazard ratio for overall graft loss at
296 spectively, compared with recipients without DGF.
297  loss at 3 years compared with those without DGF (14% vs 4%, P = 0.04 and 11% vs 0%, P < 0.01, respec
298 sored graft loss compared with those without DGF.
299 (2/51; 4%), and DSAneg-patients with/without DGF (3/103; 3% and 4/187; 2%, respectively) (P = 0.005).
300 raft survival was not different with/without DGF (81% versus 83%; P = 0.48).

 
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