ライフサイエンスコーパス: graft loss

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

2 ociated with antibody-mediated rejection and graft loss.

3 ontribute to antibody-mediated rejection and graft loss.

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

5 was independently associated with subsequent graft loss.

6 opment and correlate with late rejection and graft loss.

7 of CARV isolation on progression to CLAD and graft loss.

8 ad a dose-dependent effect on both death and graft loss.

9 , and 25.0% of living recipients experienced graft loss.

10 tributions from the lower rates of death and graft loss.

11 ectively, and 22.1% of survivors experienced graft loss.

12 diator of chronic AMR, a major cause of late graft loss.

13 onents of this regimen exhibited significant graft loss.

14 ed mismatches on all-cause or death-censored graft loss.

15 s in SOT, to graft vasculopathy and often to graft loss.

16 sure to, CNI and either chronic rejection or graft loss.

17 mia time, delayed graft function, and 1-year graft loss.

18 = 0.006) were associated with death-censored graft loss.

19 stratification of patients at high risk for graft loss.

20 ion (MDR) can lead to rejection and possibly graft loss.

21 option for patients with primary intestinal graft loss.

22 models were constructed for 1-year post-HTx graft loss.

23 ical ABMR have distinct effects on long-term graft loss.

24 t increased risk of posttransplant death and graft loss.

25 66.7% sensitivity and 89.7% specificity for graft loss.

26 ffective therapy for select recipients after graft loss.

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

28 trahepatic cholangiopathy, which may lead to graft loss.

29 ndently associated with an increased risk of graft loss.

30 (IFTA) on 24-month biopsy and death-censored graft loss.

31 e and associated with increased incidence of graft loss.

32 mpatible allografts are at increased risk of graft loss.

33 ndently associated with an increased risk of graft loss.

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

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

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

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

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

39 have significantly increased rates of early graft loss.

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

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

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

43 vity and therapeutic intervention to prevent graft loss.

44 experience disproportionately high rates of graft loss.

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

46 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

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

48 and AA (n = 445), with AA experiencing more graft losses (18.2% vs 12.1%, P = 0.0351).

49 articipation increased the risk of all-cause graft loss 2.29-fold and the risk of all-cause mortality

50 reased risk per 10 units; P=0.004), and with graft loss (6% increased risk per 10 units; P<0.001), bu

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

52 ently associated with a 3.5-fold increase in graft loss (95% confidence interval, 2.1 to 5.7) along w

53 affected risk for posttransplant mortality, graft loss, acute graft rejection, chronic rejection, ca

54 more likely than whites to experience 5-year graft loss (adjusted hazard ratio [aHR], 1.39; 95% confi

55 lemtuzumab had the highest relative risk for graft loss (adjusted hazard ratio, 1.19; 95% confidence

56 ality was seen in ABMR patients experiencing graft loss after ABMR treatment (P = 0.004).

57 and chronic antibody-mediated rejection and graft loss after all solid organ transplantation.

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

59 Over this period, 5-year graft loss after DDKT improved from 51.4% to 30.6% for b

60 nsplant opioid exposure level with death and graft loss after deceased donor transplantation were als

61 s and from 37.3% to 25.0% for whites; 5-year graft loss after LDKT improved from 37.4% to 22.2% for b

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

63 nephropathy remains the main cause of renal graft loss after living-donor renal transplantation.

64 neumonia increased the risk of both CLAD and graft loss after lung transplantation.

65 thrombosis is the most common cause of early graft loss after renal transplantation.

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

67 (aHR, 1.11; 95% CI, 0.52-2.35; P = 0.79) and graft loss (aHR, 0.89; 95% CI, 0.42-1.88; P = 0.77) were

68 1.38-1.83, respectively) and death-censored graft loss (aHR, 1.41; 95% CI, 1.24-1.60 and aHR, 1.38;

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

70 < 0.001), and a 1.70-fold increased risk for graft loss (aHR, 1.70; 95% CI, 1.31-2.20; P < 0.001).

71 aHR, 2.24; 95% CI, 1.43-3.53; P < 0.001) and graft loss (aHR, 2.07; 95% CI, 1.33-3.22; P = 0.001) com

72 bstantially increased risk of death-censored graft loss (aHR, 5.24; 95% CI, 1.97-13.98, P = 0.001).

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

74 Cox regression models, we compared all-cause graft loss among 63,910 black and 145,482 white adults w

75 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

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

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

78 otentially remediable, risk factor for renal graft loss and all-cause mortality in RTR.

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

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

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

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

83 sion of liver disease, frequently leading to graft loss and early death.

84 n both groups, 86 and 57 were upregulated in graft loss and functioning allograft groups, respectivel

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

86 tibodies were compared between patients with graft loss and matched controls with functioning grafts.

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

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

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

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

91 ansplantation (baseline) and their impact on graft loss and mortality for up to 10 years (follow-up).

92 transplant vasculopathy is a major cause of graft loss and mortality in solid organ transplant recip

93 erm patient outcomes, decreasing the odds of graft loss and mortality over 10 years.

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

95 ining whether social participation predicted graft loss and mortality were performed.

96 s of RAS blockade with a lower risk of total graft loss and mortality were stronger with more severe

97 readmission is independently associated with graft loss and mortality.

98 I was an independent predictor of pancreatic graft loss and patient death in the short term (P<0.001)

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

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

101 ngly associated with cerebrovascular events, graft loss and progression of kidney failure and mortali

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

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

104 fic rates of advanced fibrosis, HCV-specific graft loss and response of antiviral therapy were examin

105 investigate the association between time to graft loss and the explanatory variables.

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

107 oves recognition of patients at high risk of graft loss and to assess the ability of adult filling-pr

108 nosuppressed patients, but they also mediate graft loss and tolerance resistance.

109 nsights into the mechanisms behind long-term graft loss and with it the opportunity to target these p

110 At follow-up, information on all-cause graft-loss and mortality was noted.

111 Sixty-six patients (17%) had death-censored graft loss, and 116 (30%) patients died.

112 evels and major cardiovascular events, renal graft loss, and all-cause mortality by Cox Proportional

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

114 diverse as diagnosing rejection, predicting graft loss, and determining who can safely be removed fr

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

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

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

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

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

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

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

122 Overall, 4 patients demonstrated graft loss as a consequence of chronic rejection.

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

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

125 udies considered morbidities; the depression-graft loss association suggests that linkages with morbi

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

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

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

129 Graft loss at 6 months post-transplant was significantly

130 Graft loss at 6 months posttransplantation was higher in

131 Graft loss because of hepatitis C virus recurrence is a

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

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

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

135 ABMR was strongly associated with increased graft loss, but TCMR was not.

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

137 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

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 ibody status could improve predictability of graft loss by 5 years.

141 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%

142 d 6 month before the last follow-up visit or graft loss by single-antigen beads.

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

144 gy, and the renal pathology of patients with graft loss caused by CRS between 2006 and 2011 at our ce

145 We identified seven cases of graft loss caused by CRS, six cases of CRS type II, and

146 lant IgA-aB2GPI-ab have a high risk of early graft loss caused by thrombosis and a high risk of delay

147 The proportion of death-censored graft losses caused by CRS was 4.6% (7/152 patients).

148 q + DSAs have a higher risk of rejection and graft loss compared to C1q-DSA.

149 nsplant glomerulopathy showed higher risk of graft loss compared with patients without rejection.

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

151 ions, including cardiovascular morbidity and graft loss, contribute to reduced graft and patient surv

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

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

154 ent and contribute to further death-censored graft loss (DCGL).

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

156 ury remains the leading cause of late kidney graft loss despite improvements in immunosuppressive dru

157 ical significance (only 22% of patients with graft loss developed de novo DSA).

158 cteristics for ABMR patients with or without graft loss did not differ.

159 Risk factors for 1-year post-HTx graft loss differ on the basis of pre-HTx cardiac diagno

160 chronic rejection (14% vs 5%; P = 0.21) and graft loss due to AR (18% vs 7%; P = 0.14) were numerica

161 immunosuppressive (IS) drugs and to prevent graft loss due to rejection or drug toxicity.

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

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

164 Early graft loss (EGL) after kidney transplantation is a catas

165 tion identified patients at greater risk for graft loss even in children with mild angiographic vascu

166 Hg identifies children at increased risk of graft loss even in the presence of only mild angiographi

167 ufficient to detect patients at high risk of graft loss even with mild angiographic disease.

168 specially if C1q binding, is associated with graft loss, even if the antibodies are not specific for

169 t SSD is a major contributing factor of late graft loss following ATG induction and that anti-Neu5Gc

170 In adjusted analyses, the hazards ratio for graft loss for Indigenous compared with non-Indigenous r

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

172 easingly recognized as a major cause of late graft loss, for which we have few effective therapies.

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 Early graft loss from renal vein thrombosis occurred in two si

177 >/=8; proportion, >85%) in both groups were graft loss, graft function, chronic rejection, acute rej

178 sist after transplantation was higher in the graft loss group (10% vs 1%, P = 0.034).

179 was significantly associated with long-term graft loss (>10 years, P = 0.02).

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

181 fidence interval 0.9-1.9) or post-transplant graft loss (hazard ratio 1.3, 95% confidence interval 0.

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

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

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

185 .13-1.88; P < 0.001), but not death-censored graft loss (hazard ratio, 1.25; 95% confidence interval,

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

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

188 30; 95% CI, 1.07 to 1.58) and death-censored graft loss (HR, 1.41; 95% CI, 1.12 to 1.78).

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

190 ient death (HR, 1.65; 95% CI, 1.01-2.71) and graft loss (HR, 1.75; 95% CI, 1.06-2.88).

191 however, significantly increase the risk of graft loss (HR, 2.78; P < 0.01).

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

193 ls and graft biopsy can be used to determine graft loss, identifying early predictors of graft functi

194 nfection, biopsy-proven graft rejection, and graft loss in 1,414 patients receiving heart (n=97), kid

195 Second graft loss in 30 days or less was not associated with in

196 characteristics, longitudinal MMF doses, and graft loss in 525 kidney transplantation recipients.

197 was not associated with an increased risk of graft loss in a competing risk model.

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

199 ted with a lower risk of acute rejection and graft loss in AA kidney transplant recipients, whereas n

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

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

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

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

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

205 risks of posttransplant death and all-cause graft loss in live donor recipients with the highest qua

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

207 cause was identified as the single cause of graft loss in only 6.9% of the cases.

208 Modeling effectively stratifies the risk of graft loss in patients with cardiomyopathy and may be an

209 fs, there was a significantly higher rate of graft loss in patients with de novo non-DSA.

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

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

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

213 Recurrence led to graft loss in seven patients (88%) within a median of 11

214 ne cell activation and subsequent associated graft loss in syngeneic recipients.

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

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

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

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

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

220 urvival, demonstrating that very early first graft loss is not associated with poor second transplant

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

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

223 Significant multivariate predictors of graft loss/mortality were male gender (HR 2.40, P = 0.00

224 for their association with >1-year combined graft loss/mortality, late rejection, cancer, or infecti

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

226 Neither patient or graft loss nor vascular rejection, nor hemolysis, was en

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

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

229 se outcomes categorized as partial and total graft loss occurred in four (6.90%) and three (5.17%) pa

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

231 C1q-binding de novo DSA are associated with graft loss occurring quickly after their appearance.

232 r-specific antibody is associated with early graft loss of cell transplants and reduced long-term sur

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

234 t CMV, biopsy-proven acute rejection (BPAR), graft loss, opportunistic infections (OI), new-onset dia

235 n or rates of biopsy-proven acute rejection, graft loss, opportunistic infections, or new-onset diabe

236 composite efficacy failure endpoint (tBPAR, graft loss or death) occurred in 11.5% of EVR+Reduced TA

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

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

239 sociated with fewer episodes of CMV relapse, graft loss, or death.

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

241 No deaths, graft losses, or episodes of rejection occurred.

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

243 reased the risk of mortality (P = 0.005) and graft loss (P = 0.018).

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

245 C4d versus C4d ABMR did not predict graft loss (P = 0.086).

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

247 gher risk of death and an 85% higher risk of graft loss (P<0.001) compared with low/normal values.

248 ing DSA was associated with a higher risk of graft loss (P<0.001).

249 -ab was an independent risk factor for early graft loss (P=0.04) and delayed graft function (P=0.04).

250 match increased the hazard of death-censored graft loss, particularly in patients with detectable pan

251 tinine ratio 2.81 (1.20-6.00) compared to no graft loss patients 1.16 (0.15-2.53), (P < 0.01), and a

252 eukins and their receptors and granulysin in graft loss patients compared to patients with a function

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

254 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

255 ients in the United States, including higher graft loss rates among recipients treated with alemtuzum

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

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

258 ime, yet increased rejection and immunologic graft loss rates remain associated with pancreas retrans

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

260 ologic risk factor correlated with long-term graft loss regardless of the timing of ACR.

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 Depression increased death-censored graft loss risk (RR, 1.65; 95% CI, 1.21-2.26, 3 studies)

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

265 The risks of graft loss (RR, 0.77; 95% CI, 0.29-2.09; I, 31%) and pat

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

267 C1q positivity, whereas 43% of patients with graft loss showed C1q-positive antibodies, although not

268 intensity of 500 or higher was higher in the graft loss than in the nonrejector group (76% vs 40%, P

269 To demonstrate acute graft loss, the animals were injected with streptozotoci

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

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 atients have lost their graft, and the early graft loss was associated with lower dose of ATG during

274 Graft loss was associated with older age at first transp

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

276 Death-censored graft loss was higher with late versus early AMR (P = 0.

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 A 43% reduction in the risk of death or graft loss was observed for both the more-intensive and

280 sity remained unchanged in groups II and III.Graft loss was observed in 80% and 20% of patients from

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

282 Risk of kidney graft loss was over 1.5-fold higher among group II SLK r

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

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

285 ed and undamaged organs (p = 0.28); however, graft loss was significantly more frequent in pancreata

286 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 =

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

288 The most frequent cause of graft loss was thrombosis of the vessels, which was obse

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

290 atients, odds of patient mortality and liver graft loss were about 1.2-fold and twofold higher in the

291 iomyopathy, disease-specific risk models for graft loss were developed with the use pre-HTx recipient

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

293 ween mannose-binding lectin or Ficolin-1 and graft loss were found.

294 Risk factors for graft loss were identified in patients with cardiomyopat

295 Data on death-censored graft loss were obtained from the Norwegian Renal Regist

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

297 However, 5 of 11 (45.4%) graft losses were due to recurrent MN.

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

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

300 d rejection (AMR) is a major cause of kidney graft loss, yet assessment of individual risk at diagnos