ライフサイエンスコーパス: DSA

1 DSA characteristics were collected and related to the pr

2 DSA positivity in subTCMR was associated with histologic

3 DSA were detected in 81 patients (18.8%).

4 DSA+ = TSA+ patients had increased risk of allograft fai

5 DSA-level heterogeneity in DDLT rates was greater than p

6 DSA-M were detected in 9 of 20 (45%) patients and for 10

7 DSA-negative patients who developed dnDSA had the highes

8 DSA-positive AMR patients exhibited greater reactivity t

9 DSAs were monitored at transplant and at 1, 3, 6, 12, 24

10 In G1, we identified at least 1 DSA in 44 patients with test 1, and in 39 patients with

11 to 4 groups: DSA+/+ (n = 31), DSA+/- (n=19), DSA-/+ (n=10), and DSA-/- (n = 30).

12 In 17 patients (28 DSA) with posttransplant analyses, persisting DSA posttr

13 were divided into 4 groups: DSA+/+ (n = 31), DSA+/- (n=19), DSA-/+ (n=10), and DSA-/- (n = 30).

14 Plasma SAB analysis revealed 35 DSA in 20 patients pretransplant.

15 CDD had a modest positive correlation with 4 DSA factors: median match MELD, proportion of white deat

16 CDD had a modest positive correlation with 4 DSA factors: median match model for end-stage liver dise

17 of AMR (70%) compared with the DSA+/+ (45%), DSA+/- (11%), and DSA-/- (10%) patients (P < 0.0001).

18 elisted for "too sick" at 127 centers, in 53 DSAs, over 16 years.

19 ed suppression of 3 of 3, 4 of 6, and 8 of 8 DSA (cases 1-3) was achieved.

20 0-year graft survivals, respectively, for 8% DSA-positive transplants.

21 to October 2016, 90 HS patients (PRA > 80%, DSA+ = 50 versus DSA- = 40) received kidney transplantat

22 y 86 transplant patients (46 who developed a DSA post transfusion and 40 who remained DSA negative) w

23 ansplant donor is more likely to result in a DSA and TSA of shared antibody specificities.

24 n delisting MELD for "too sick" score across DSA and time.

25 DD donors/all deceased donors (%DCDD) across DSAs.

26 eased donors, the %DCDD varied widely across DSAs, with a median of 15.1% (interquartile range [9.3%,

27 eased donors, the %DCDD varied widely across DSAs, with a median of 15.1% (IQR [9.3%, 20.9%]; range 0

28 and used the deletion-substitution-addition (DSA) variable selection algorithm to build a final multi

29 es using the Deletion/Substitution/Addition (DSA) algorithm.

30 8 blockade as a superior strategy to address DSA via the sparing of CTLA-4 and more potent targeting

31 All DSA positive patients with cirrhosis of the graft showed

32 f patients with donor specific alloantibody (DSA) at the time of transplantation and identify new fac

33 ther the condition of missing self amplifies DSA-dependent NK cell activation to worsen chronic AMR.

34 In nonsupervised analysis, DSA positive subTCMR mostly clustered together with cTCM

35 Here, we analyzed DSA detected in the serum (sDSA) using single antigen be

36 (n = 31), DSA+/- (n=19), DSA-/+ (n=10), and DSA-/- (n = 30).

37 red with the DSA+/+ (45%), DSA+/- (11%), and DSA-/- (10%) patients (P < 0.0001).

38 F occurred in 137 of 375 patients (37%), and DSA were present in 85 of 375 patients (23%).

39 milar: Molecular and histologic activity and DSA were not important compared with injury.

40 In the absence of AMRh and DSA, anti-ARHGDIB antibodies were not clearly associated

41 e of the biopsy, Banff i, ci and ct, C4d and DSA.

42 inhibition of Tfh cell, germinal center, and DSA responses in vivo and better control of B cell respo

43 radiological information analyzed the CT and DSA in consensus.

44 However, the combined impact of DGF and DSA has not been studied in detail.

45 If possible, the combined risks of DGF and DSA should be avoided.

46 also found similar outcomes between DSA- and DSA+ patients when only including those who would have m

47 s and cytokines, germinal centers (GCs), and DSA formation in an RTx model in rats.

48 phenotypes with respect to histological and DSA responses.

49 amined associations between center-level and DSA-level characteristics and the adjusted probability o

50 Survival in DSA-negative and DSA-positive molecular ABMR was similar.

51 marker-based supervised methods semi-NMF and DSA.

52 imilar in DSA-positive (DSApos)-patients and DSA-negative (DSAneg)-patients (40% versus 36%; P = 0.45

53 graft survival between the DSA-positive and DSA-negative groups.

54 28 or 56 days to allow chronic rejection and DSA formation.

55 tion-controlled 3D multilayer structures and DSA processes for sub-10 nm line-spacing patterns.

56 Leukocytes, B-cell subsets, and DSA were measured using flow cytometry; expression of cy

57 ound Spinal digital subtraction angiography (DSA) exposes patients and operators to substantial amoun

58 hy (CTA) or digital subtraction angiography (DSA) from 207 patients with BTAs and a control group of

59 With Digital Subtraction Angiography (DSA) perfusion analysis, we are able to identify hypoper

60 Digital subtraction angiography (DSA) tubogram revealed rupture and separation of the PEG

61 hy (CTA) or digital subtraction angiography (DSA) were evaluated.

62 pretransplant donor-specific HLA antibodies (DSA) and its association with occurrence of antibody-med

63 relevance of donor-specific HLA antibodies (DSA) detection by Luminex single-antigen (LSA) flow bead

64 mpact of donor-specific anti-HLA antibodies (DSA) on antibody-mediated rejection (AMR) and kidney all

65 ecific memory B cell-derived HLA antibodies (DSA-M) in renal allograft recipients with pretransplant

66 pretransplant donor-specific HLA-antibodies (DSA) are both regarded as risk factors for rejection and

67 The importance of donor-specific antibodies (DSA) after liver transplantation (LT) for graft and pati

68 w-level preformed donor-specific antibodies (DSA) against an RMM on transplant outcomes.

69 Donor-specific antibodies (DSA) against HLA and non-HLA antigens in the glomeruli a

70 he development of donor-specific antibodies (DSA) and antibody-mediated rejection (AMR) posttransplan

71 relationship with donor-specific antibodies (DSA) and histological phenotype.

72 s associated with donor-specific antibodies (DSA) and poorer outcomes after renal transplantation (RT

73 ture PC producing donor-specific antibodies (DSA) and reduced DSA, when administered after primary an

74 Donor-specific antibodies (DSA) are putatively associated with a worse prognosis fo

75 he development of donor-specific antibodies (DSA) directed against mismatched donor human leukocyte a

76 Donor-specific antibodies (DSA) play a major role in antibody-mediated rejection (A

77 ses in high-titer donor-specific antibodies (DSA) that are most often generated as anamnestic respons

78 ncidence of these donor-specific antibodies (DSA), but its mechanism is suboptimal for the inhibition

79 ainst 3, 6, and 8 donor-specific antibodies (DSA), including those that were historically C1q+ bindin

80 stically with HLA donor-specific antibodies (DSA).

81 formation of donor-specific HLA antibodies (DSAs) and transplant outcomes, we conducted a cohort stu

82 De novo donor-specific antibodies (DSAs) are associated with antibody-mediated rejection (A

83 o predict de novo donor-specific antibodies (DSAs) during the first year of transplant and explored h

84 Donor-specific antibodies (DSAs) have a strong negative correlation with long-term

85 lls and preformed donor-specific antibodies (DSAs) have all been implicated in accelerated allograft

86 Binding of donor-specific antibodies (DSAs) to kidney allograft endothelial cells that does no

87 contributing to donor-specific HLA antibody (DSA) development after lung transplantation have not bee

88 The impact of donor-specific HLA antibody (DSA) following liver transplantation remains controversi

89 ct of resulting donor-specific HLA antibody (DSA) positivity on long-term kidney graft survival in 32

90 elopment of de novo donor-specific antibody (DSA) after kidney transplantation.

91 ical analysis, and donor- specific antibody (DSA) characterization with their current strengths and l

92 Reduction in donor-specific antibody (DSA) has been associated with improved renal allograft s

93 out outcomes of HLA donor-specific antibody (DSA) negative (DSA-) microvascular inflammation (MVI).

94 tion of deleterious donor-specific antibody (DSA) responses remain poorly understood.

95 al AMR based on the donor-specific antibody (DSA) testing may result in better outcomes.

96 se in patients with donor-specific antibody (DSA).

97 ime posttransplant, donor-specific antibody [DSA]) and molecular and histologic features reflecting i

98 policy eliminated the donation service area (DSA) as the first geographic tier of allocation.

99 social determinants and Donor Service Area (DSA) characteristics may be associated with determinatio

100 In November 2017, the donation service area (DSA) was removed as the primary unit of US donor lung al

101 racteristics within a donation service area (DSA).

102 oved AC and the existing Donor Service Area (DSA)/Region-based allocation schemes.

103 ationally and within donation service areas (DSAs), we conducted a registry study that included all U

104 of donors across the 58 donor service areas (DSAs).

105 tation (DDLT) across donation service areas (DSAs).

106 f donors across the 58 donor services areas (DSAs).

107 t loss well, both in DSA+ cohorts as well as DSA- patients.

108 A strong correlation between DSA and graft survival or function cannot be statistical

109 We also found similar outcomes between DSA- and DSA+ patients when only including those who wou

110 Complement-binding DSA per se were not significantly associated with allogr

111 graft failure in patients positive for both DSA and anti-ARHGDIB antibodies (aMFI >= 1000) versus pa

112 graft failure in patients positive for both DSA and anti-ARHGDIB antibodies (aMFI>=1000) versus pati

113 MFI>=1000) versus patients negative for both DSA and anti-ARHGDIB antibodies, compared to a 4.4-fold

114 I >= 1000) versus patients negative for both DSA and anti-ARHGDIB antibodies, compared with a 4.4-fol

115 nt models of childhood exposures selected by DSA indicated significant associations of NOX with FA [

116 nt models of pregnancy exposures selected by DSA, higher concentration of fine particles was associat

117 Forty-five patients (52%) had C1q DSA, and 42 (51%) had C3d DSA.

118 ents (52%) had C1q DSA, and 42 (51%) had C3d DSA.

119 d had sustained disappearance of circulating DSA for <=30 months.

120 n be diagnosed in the absence of circulating DSA.

121 ence intensity values of DSA with concurrent DSA-M (5877) were higher than those of DSA without DSA-M

122 ibe a unique donor-specific flow crossmatch (DSA-FXM) that distinguishes HLA class I or II donor-spec

123 inex single antigen bead (SAB) assay-defined DSA but negative complement-dependent cytotoxicity cross

124 ts (18%) than in patients without detectable DSA (9%, P = 0.027).

125 the 2 Luminex assays available for detecting DSA in the postkidney transplant setting.

126 d from those of patients who did not develop DSAs or ABMR.

127 Of 460 recipients, 205 (45%) developed DSA; the majority developed Class II DSA (n = 175, 85%),

128 = 175, 85%), and 145 of 205 (71%) developed DSA to HLA-DQ alleles.

129 Recipients who developed DSA had significantly lower quantities of peripheral CXC

130 candidates with the same MELD in 2 different DSAs were expected to have a 2.2-fold difference in DDLT

131 d) were biopsied after the detection of a dn DSA, 65.3 months (median) after kidney transplantation.

132 versus >8 ng/ml had increased risk of DR/DQ DSA at 1 year (HR 2.34, 95% CI 1.05-5.22, p = .04).

133 there was a graded increase in risk of DR/DQ DSA in intermediate (HR 15.39, 95% CI 2.01-118.09, p = .

134 ophore associated capillary electrophoresis (DSA-FACE) on a serum sample 1 week after LT.

135 18 allocated to 150-mile circles eliminating DSA/region boundaries.

136 SA responses to be prevented and established DSA responses to be reversed.

137 has not been elucidated when and in how far DSA are harmful for graft and patient survival.

138 Patients with complement-fixing DSAs identified by a positive C3d binding assay (n=73, 5

139 Following DSA removal, there was a 9-day decrease in median waitli

140 We demonstrate that perfusion analysis for DSA can be performed in real time.

141 Positivity criteria for DSA determination differ and interpretation should take

142 Positivity criteria for DSA was mean fluorescence intensity greater than 500 for

143 The area under the curve for DSA at 1 year was 0.84 and 0.82 for HLA-DR and HLA-DQ ep

144 ant recipients and examined risk factors for DSA development using Cox regression models.

145 olitis remained independent risk factors for DSA development.

146 e cutoff level and 1-year graft survival for DSA-positive transplants was found when using signal-to-

147 le subTCMR biopsies (n = 71) were tested for DSA with bead assays.

148 Patients were divided into 4 groups: DSA+/+ (n = 31), DSA+/- (n=19), DSA-/+ (n=10), and DSA-/

149 mean fluorescence intensity DSA (<3000) had DSA-M.

150 Seven patients still had DSA with a mean MFI of 1298 +/- 930 at the last follow-u

151 intragraft DSA (gDSA) in 86 patients who had DSA and underwent a kidney biopsy for cause (n = 58) or

152 transplant (P = 0.090), and presence of HLA DSA (P = 0.003).

153 retrospective, cross-sectional study of HLA DSA and AT1R antibodies in 2 cohorts of pediatric liver

154 itudinally assess the clinical impact of HLA DSA and AT1R antibodies.

155 However, AT1R antibodies combined with HLA DSA in patients with active allograft dysfunction were a

156 outcomes and response to treatment with HLA DSA- MVI patients are similarly poor to those with DSA+

157 HLA-DSA-positive and HLA-DSA-negative biopsy specimens with

158 histology, those with ABMR histology and HLA-DSA had higher allograft failure risk (hazard ratio [HR]

159 HLA-DSA-positive and HLA-DSA-negative biopsy specimens with ABMR histology displa

160 anscriptional signature, irrespective of HLA-DSA status.

161 2017 criteria for ABMR, irrespective of HLA-DSA status.

162 h ABMR histology was not associated with HLA-DSA status but was caused by concomitant T cell-mediated

163 % CI], 3.04 to 17.20) than cases without HLA-DSA (HR, 2.33; 95% CI, 0.85 to 6.33), despite the absenc

164 ting donor-specific anti-HLA antibodies (HLA-DSAs) are often absent in serum of kidney allograft reci

165 olving ABMR histology without detectable HLA-DSAs represent a distinct clinical and molecular phenoty

166 of these (46.4%) lacked detectable serum HLA-DSAs.

167 We hypothesized DSA IgG subclass characteristics, compared to total DSA

168 , and their magnitude was predictive of IgG3 DSA generation, more severe allograft injury, and higher

169 A prominent IgG4 DSA profile was strongly correlated with greater HLA mis

170 Our data suggest that IgG4 DSA may serve as a useful biomarker to identify, among c

171 veloped DSA; the majority developed Class II DSA (n = 175, 85%), and 145 of 205 (71%) developed DSA t

172 Occurrence of HLA class II DSA after LT is associated with graft cirrhosis and may

173 thout class II DSA, those with IgG4 class II DSA MFI sum >2000 exhibited an odds ratio (OR) of 20.79

174 ifically, compared to those without class II DSA, those with IgG4 class II DSA MFI sum >2000 exhibite

175 (50%) subjects tested positive for class II DSA.

176 Immunodominant DSA reduction at 14 days differed significantly (early A

177 is of active sAMR were MFI of immunodominant DSA > 4000, MFI of the sum of DSA > 6300, age of the rec

178 is of active sAMR were MFI of immunodominant DSA >4000, MFI of the sum of DSA >6300, age of the recip

179 ariate analysis revealed that immunodominant DSA reduction > 50% at 14 days was associated with impro

180 ediatric candidates, compared to only 46% in DSA/Region-based allocation (P<0.001).

181 g histology predict graft loss well, both in DSA+ cohorts as well as DSA- patients.

182 metry breaking and superlattice formation in DSA of BCP.

183 ABMR is associated with slower increases in DSA, which may be high or low titer and transient or per

184 rrhosis occurred significantly more often in DSA positive patients (18%) than in patients without det

185 factors to improve graft loss prediction in DSA+ patients.

186 The incidence of DGF was similar in DSA-positive (DSApos)-patients and DSA-negative (DSAneg)

187 Survival in DSA-negative and DSA-positive molecular ABMR was similar

188 ormed well predicting 5-year outcome well in DSA+ patients (Mayo C statistic = 0.784 and Paris C stat

189 d due to illness, which was more apparent in DSAs with low pediatric transplant volumes; we advocate

190 with AMR and low mean fluorescence intensity DSA (<3000) had DSA-M.

191 assays combined with the study of intragraft DSA (gDSA) in 86 patients who had DSA and underwent a ki

192 gest that DSA MFI and presence of intragraft DSA might provide prognostic information during posttran

193 FF-treated rats, which was reflected by less DSA in certain IgG subclasses.

194 Desensitization therapy-mediated DSA reductions approached statistical significance (P =

195 C using a density and sound velocity meter (DSA 5000M).

196 In a multivariate Cox model, DSA with DGF was an independent predictor for graft (haz

197 HLA donor-specific antibody (DSA) negative (DSA-) microvascular inflammation (MVI).

198 e often DSA-M (6/12; 50%) than nonpersisting DSA (2/16; 13%).

199 munized group, one patient developed de novo DSA (A24-MFI 970; biopsy for cause did not show biopsy-p

200 Whether monitoring of de novo DSA (dnDSA) paired with systematic kidney biopsy should

201 DSA, an RMM was not associated with de novo DSA development, rejection, or allograft loss.

202 r, without a safe threshold at which de novo DSA did not occur.

203 alleles could also help to minimize de novo DSA formation and potentially improve transplant outcome

204 n HLA-DQ confer substantial risk for de novo DSA formation, graft rejection, and graft failure after

205 and monitored for the development of de novo DSA in kidney transplant recipients during the first-yea

206 No patient developed a de novo DSA in the DSA-positive group.

207 ody-verified eplet mismatch load and de novo DSA occurrence and graft failure, mainly explained by DQ

208 of AMBR requires the anamnestic and de novo DSA responses to be prevented and established DSA respon

209 Frequency of de novo DSA was 63% (27/44).

210 y-three recipients (24.2%) developed de novo DSA within 1-year posttransplant.

211 f circulating de novo DSA, number of de novo DSA, and C1q binding activity when compared to other phe

212 ted with the presence of circulating de novo DSA, number of de novo DSA, and C1q binding activity whe

213 ided with the presence and number of de novo DSA.

214 the incidence and clinical impact of de novo DSAs (dnDSAs) and compared with dnDSA- patients.

215 De novo DSAs occurred in 43 (4.6%) patients.

216 h protocol biopsy and development of de-novo DSAs.

217 plain the histology of AMR in the absence of DSA.

218 Assessment of DSA-M might be a novel tool to supplement serum HLA anti

219 ad the aim to investigate the association of DSA with complications after LT.

220 entify recipients at risk for development of DSA.

221 The identification of DSA positive subclinical rejection might help to define

222 better understanding of the immunobiology of DSA production is necessary and also the development of

223 The use of the sum of the intensity of DSA improved the sensitivity and specificity of the 2 te

224 A, consisting of perioperative management of DSA (polyvalent immunoglobulins +/- perioperative plasma

225 to be better defined, the high prevalence of DSA and the correlation with acute rejection highlight t

226 Our objective was to determine the risk of DSA development associated with the isolation of Pseudom

227 iratory specimens would increase the risk of DSA development.

228 tis are associated with an increased risk of DSA development.

229 ion are associated with an increased risk of DSA development.

230 ositive Pseudomonas cultures and the risk of DSA development.

231 Signal-to-noise ratios (SNRs) of DSA and kinetic image pairs were compared.

232 immunodominant DSA > 4000, MFI of the sum of DSA > 6300, age of the recipient < 45 y, and the absence

233 immunodominant DSA >4000, MFI of the sum of DSA >6300, age of the recipient <45 years old, and the a

234 rrent DSA-M (5877) were higher than those of DSA without DSA-M (1476), 3 of 6 patients with AMR and l

235 median mean fluorescence intensity values of DSA with concurrent DSA-M (5877) were higher than those

236 nd activated B cells paralleled emergence of DSAs in blood, and their magnitude was predictive of IgG

237 In contrast, persistent low levels of DSAs do not seem to impair graft outcome in these recipi

238 persisting DSA posttransplant had more often DSA-M (6/12; 50%) than nonpersisting DSA (2/16; 13%).

239 uantitative thresholds and analysis based on DSA perfusion may assist with real-time dosage estimatio

240 0.0001) increased risk in patients with only DSA, and a 4.1-fold (95% CI, 1.4-11.7; P = 0.009) increa

241 0.0001) increased risk in patients with only DSA, and a 4.1-fold (95%CI,1.4-11.7;p=0.009) increased r

242 smatches (FXM) using traditional FXM and our DSA-FXM method from 94 patients (enriched for auto+/allo

243 Overall, DSA elimination was associated with increased posttransp

244 l actors interact is unclear, but peripheral DSA may be a marker of immune cellular activity in the s

245 SA) with posttransplant analyses, persisting DSA posttransplant had more often DSA-M (6/12; 50%) than

246 LOS increased from 17 to 19 days in the post-DSA era (P = .01).

247 At last follow-up, preexisting DSA had decreased or stabilized.

248 Persistence of preexisting DSAs or development of dnDSA after transplant is associa

249 cal risk only in the presence of a preformed DSA in patients undergoing retransplantation.

250 ients were crossmatch negative and preformed DSA were detected by single antigen beads alone.

251 In the absence of preformed DSA, an RMM was not associated with de novo DSA developm

252 alysis revealed that patients with preformed DSA against an RMM were independently at risk of antibod

253 Next, we determined pretransplant DSA using various MFI cutoffs, signal-to-background rati

254 Overall, pretransplant DSA/DSA-Mpos allograft recipients showed a higher incide

255 into antibody-secreting cells that produced DSAs.

256 donor-specific antibodies (DSA) and reduced DSA, when administered after primary and secondary DSA r

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

258 d a DSA post transfusion and 40 who remained DSA negative) were HLA typed.

259 0.0001) compared to recipients who remained DSA-negative over the first-year posttransplant.

260 Changing a candidate's DSA would have had a greater impact on the candidate's L

261 hen administered after primary and secondary DSA responses had been established.

262 This more severe DSA+ associated graft injury in subTCMR was converged wi

263 determine whether ASG removal during spinal DSA in adults reduces radiation dose while maintaining d

264 tive study included adults undergoing spinal DSA between January and December 2016.

265 Although Gulf State DSAs have lower expected donation rates, these differenc

266 On unadjusted analyses, Gulf State DSAs were associated with 3.52 fewer expected kidney don

267 and uninsurance were higher among Gulf State DSAs.

268 to have provided higher quality images than DSA in 69.0% (2462 of 3570) of the comparisons.

269 The lawsuit claimed that DSA borders are arbitrary and that allocation should be

270 Our data suggest that DSA mean fluorescence intensity and presence of gDSA mig

271 Our data suggest that DSA MFI and presence of intragraft DSA might provide pro

272 The data suggest that DSA reduction may be associated with improved DCGS in bo

273 The DSA- group had higher MVI scores but lower C4d scores.

274 by comparing the graft survival between the DSA-positive and DSA-negative groups.

275 No patient developed a de novo DSA in the DSA-positive group.

276 ific antibody 36.2% of the time based on the DSA-FXM.

277 ps had significantly worse outcomes than the DSA+-negative controls without AMR.

278 We demonstrate that the DSA-FXM is able to define categorically distinct and cli

279 = .0025) and AMR (P = .02) compared with the DSA+ != TSA+ patients.

280 est incidence of AMR (70%) compared with the DSA+/+ (45%), DSA+/- (11%), and DSA-/- (10%) patients (P

281 These DSA elicit cycles of injury and repair that manifest as

282 rative plasmapheresis sessions, according to DSA level, as well as induction therapy) and systematic

283 eater reactivity to autoantigens compared to DSA-negative (P < .0001) and AMR patients with DSA and P

284 s confirmed that addition of missing self to DSA-induced NK cell activation increased endothelial dam

285 allocated to 150-mile circles in addition to DSAs/regions, and the policy selected 12/18 allocated to

286 subclass characteristics, compared to total DSA IgG, might correlate with specific histopathological

287 ss expression of TCMR-associated transcript, DSA positivity in subTCMR was associated with an upregul

288 nosis and treatment of subclinical AMR using DSA monitoring may improve outcomes after kidney transpl

289 90 HS patients (PRA > 80%, DSA+ = 50 versus DSA- = 40) received kidney transplantation after DES wit

290 mostly clustered together with cTCMR, while DSA negative subTCMR clustered together with NHR.

291 at antibodies to non-HLA are associated with DSA-positive AMR although their specific role in mediati

292 A-negative (P < .0001) and AMR patients with DSA and PRA > 10% were identified as the subgroup with s

293 dies has an additive effect in patients with DSA on the risk of graft failure via AMRh.

294 nsplant risk stratification in patients with DSA.

295 VI patients are similarly poor to those with DSA+ MVI patients, supporting a critical role for MVI in

296 were 54 patients without DSAs; of those with DSAs, ABMR emerged in 20 patients, but not in 31 patient

297 Within DSAs, we observed a median 2.3-fold variation between ce

298 (5877) were higher than those of DSA without DSA-M (1476), 3 of 6 patients with AMR and low mean fluo

299 There were 54 patients without DSAs; of those with DSAs, ABMR emerged in 20 patients, b

300 patient survival compared with those without DSAs after transplant.