ライフサイエンスコーパス: renal allograft

1 ing antibody-mediated rejection (AMR) of the renal allograft.

2 of tertiary lymphoid tissue within the human renal allograft.

3 titial and microvascular inflammation of the renal allograft.

4 s the leading cause of long-term loss of the renal allograft.

5 ctomy and received an orthotopic Dark Agouti renal allograft.

6 diagnose T cell-mediated rejection (TCMR) of renal allografts.

7 is feasible and meaningful to predict DGF in renal allografts.

8 asive technique for functional assessment of renal allografts.

9 the efficacy of treatments for acute AMR in renal allografts.

10 rative, prospective study for deceased donor renal allografts.

11 vasive means of diagnosing fibrosis in human renal allografts.

12 rrent membranous glomerulonephritis (MGN) in renal allografts.

13 ntibody to complete MHC-mismatched heart and renal allografts.

14 shown to be unrelated to early TID in adult renal allografts.

15 o) all patients remain well with functioning renal allografts.

16 -2-associated X protein and caspase-3 in the renal allografts.

17 de a path to using more ischemically damaged renal allografts.

18 hted MRI, enables detection of leukocytes in renal allografts.

19 r transplantation may prevent loss of scarce renal allografts.

20 e the noninvasive detection of leukocytes in renal allografts.

21 ed with sirolimus, 7 (70%) had a functioning renal allograft 144 months after transplantation versus

22 rospective study, sera from 70 recipients of renal allografts (40 controls, 30 IFTA) were studied.

23 This chimerism was not sufficient to prolong renal allograft acceptance: the BMT/renal mean survival

24 Whether removal of the failed renal allograft affects survival while receiving long-te

25 ked by low urine output and may pose risk to renal allografts after RTx.

26 aplan-Meier survival curves were plotted for renal allograft and patient survival.

27 to induce tolerance to a concurrently placed renal allograft and that the presence of this chimerism

28 has been de-emphasized in the allocation of renal allografts and further discounting is planned in t

29 may result in antibody-mediated rejection of renal allografts and introduce a physiologically relevan

30 in 11 of 13 recipients of previously placed renal allografts and long-term survival without immunosu

31 long-term beneficial effect on CMV-infected renal allografts and suggest a potential role for NK cel

32 DCD renal allografts compared to the non-DCD renal allografts and the effects of increased immunosupp

33 was to investigate the expression of CD55 in renal allografts and to correlate it with the expression

34 re increased in association with acute VR of renal allografts and to evaluate the impact of LG3 on va

35 sent longitudinal imaging of immune cells in renal allografts and tumor development in the colon.

36 four had CKD stage 1-4, five had received a renal allograft, and three were dialysis-dependent at st

37 has a protective effect on PTC C4d negative renal allografts, and the pattern of PTC CD55 expression

38 with prior gastrointestinal bypass surgery, renal allografts are also at risk of oxalate nephropathy

39 ribing the efficacy of treatments for AMR in renal allografts are of low or very low quality.

40 Noninvasive methods to diagnose rejection of renal allografts are unavailable.

41 ubular capillary C4d staining from long-term renal allografts are unknown.

42 ecipients in this study lost their islet and renal allografts as a result of cellular and humoral rej

43 ution and intensity of CXCR4 upregulation in renal allografts as determined by SUVs on PET and diffus

44 ft activation of cellular gene expression in renal allografts at 2 days posttransplant.

45 bjective and complete assessment of procured renal allografts at pretransplantation time.

46 to identify a gene set capable of predicting renal allografts at risk of progressive injury due to fi

47 Seven of 33 renal allograft biopsies (12 AR and 21 normal) were prof

48 f intrarenal PV replication in corresponding renal allograft biopsies (manual counts and automated mo

49 independent microarray data-sets from human renal allograft biopsies (n = 101) from patients on majo

50 The study included 168 posttransplant renal allograft biopsies (T cell-mediated rejection [TCM

51 cted whole-genome expression profiles of the renal allograft biopsies at 3 months and correlated resu

52 y the expression and localization of US28 in renal allograft biopsies by immunohistochemistry and det

53 For comparison, renal allograft biopsies from a matched control group an

54 ified distinctly deregulated miRNAs in human renal allograft biopsies from patients undergoing acute

55 e rt-PCR were performed on RNA from protocol renal allograft biopsies in three groups: (1) +XM/TG+ bi

56 All for-cause renal allograft biopsies performed in 2007-2014 at the E

57 Finally, in renal allograft biopsies showing chronic rejection, casp

58 and chemokine receptor transcripts in human renal allograft biopsies, correlating transcript levels

59 More than 200 renal allograft biopsies, performed for allograft dysfun

60 prove helpful to distinguish APN from AR in renal allograft biopsies.

61 dings were correlated with clinical data and renal allograft biopsies.

62 strong predictor of acute rejection in human renal allograft biopsies.

63 baseline, at the time of protocol-specified renal-allograft biopsies (3, 12, and 24 months after tra

64 All renal allograft biopsy samples with concomitant data on

65 se results show that the presence of TRIs in renal allograft biopsy specimens associates with poor al

66 ohistochemical stainings for calprotectin in renal allograft biopsy specimens confirmed the serologic

67 antification of fibrosis and inflammation in renal allograft biopsy specimens.

68 ammation are the main histologic features of renal allograft biopsy specimens.

69 data (1991-2004) to identify BS cases among renal allograft candidates and recipients.

70 nhibitor bortezomib on DSA-PCs in sensitized renal allograft candidates and to assess if DSA-PC deple

71 in a group of 90 patients with a functioning renal allograft compared with 40 patients who rejected (

72 , we investigated the AR and function of DCD renal allografts compared to the non-DCD renal allograft

73 MCMV infection exacerbates late renal allograft damage and is associated with NK and mye

74 In particular, how disease recurrence in the renal allograft defines graft outcome is largely unknown

75 h is a well-known prognostic marker in other renal allograft diseases.

76 reduce ischemia-reperfusion injury (IRI) of renal allografts donated after cardiac death (DCD) in a

77 atients are difficult to match with suitable renal allograft donors and may benefit from xenotranspla

78 BK virus nephropathy (BKVN) may cause renal allograft dysfunction and failure.

79 In contrast, fms-I substantially inhibited renal allograft dysfunction and structural damage with a

80 free patients, including those with moderate renal allograft dysfunction, have the benefit of improve

81 virus-associated nephropathy (BKVAN) causes renal allograft dysfunction.

82 nogen is produced in the liver, and solitary renal allografts fail within 1 to 7 years with recurrent

83 enteric conversion; 11 patients experienced renal allograft failure (10 underwent a repeat kidney tr

84 Identification of risk factors for renal allograft failure after an episode of acute antibo

85 ant and returned to long-term dialysis after renal allograft failure between January 1994 and Decembe

86 sk of death or the combined risk of death or renal allograft failure were 0.7 (95% CI, 0.1-3.8) and 0

87 ar relationship between the cause of primary renal allograft failure, hemoglobin A1c (HbA1c) or fasti

88 induction therapy abolishes the disparity in renal allograft failure.

89 ferentiation of prerenal and intrinsic acute renal allograft failure.

90 There were six renal allograft failures in the nonsensitized group but

91 e candidate biomarker and predictor of human renal allograft fibrogenesis deserves further study.

92 tion between urinary CTGF (CTGFu) levels and renal allograft fibrosis during the first 2 years after

93 Its involvement in renal allograft fibrosis was recently demonstrated in a

94 Moderate renal allograft fibrosis was reduced in treated patients

95 n, which occurs in normal kidneys, including renal allografts, forming distinct alpha345(IV) and alph

96 CMV seronegative recipients (R-) receiving a renal allograft from a CMV seropositive donor (D+) have

97 Recipients receiving a renal allograft from NOD-treated donors had a significan

98 disparity remains between graft survival of renal allografts from deceased donors and from living do

99 It remains controversial whether renal allografts from donation after circulatory death (

100 application of ApoE(133-149) seem to protect renal allografts from fatal acute rejection.

101 n summary, HCMV-encoded US28 was detected in renal allografts from HCMV-positive donors independent o

102 Male BalbC recipients received renal allografts from male C57BL/6J donors.

103 ive diagnosis of BKVN and prognostication of renal allograft function after BKVN diagnosis are feasib

104 Renal allograft function was assessed by serum creatinin

105 ought to evaluate outcomes and predictors of renal allograft futility (RAF-patient death or need for

106 Mouse renal allografts have a remarkable ability to promote ac

107 the resistive index was not associated with renal-allograft histologic features.

108 To determine the value of renal allograft histology in predicting outcomes, we eva

109 hyroidism and may have beneficial effects on renal allograft histology.

110 ases IRI and subsequent tissue injury in DCD renal allografts in a large animal transplant model.

111 listing guidelines, SLKT potentially wastes renal allografts in both high-acuity liver recipients at

112 Long-term tolerance of class I disparate renal allografts in miniature swine can be induced by a

113 involved in tolerance of class I-mismatched renal allografts in miniature swine treated with 12 days

114 ajor histocompatibility complex-incompatible renal allografts in the first 3 months after transplanta

115 All posttransplant renal allograft indication biopsies performed in this co

116 s a potential candidate for the diagnosis of renal allograft inflammation.

117 rogression for patients with CKD and chronic renal allograft injury (CAI), but the underlying mechani

118 t with a Syk inhibitor significantly reduced renal allograft injury in a model of severe antibody-med

119 assay in urine samples from 84 patients with renal allograft injury, 29 patients with stable graft fu

120 e basis of this broadened concept of chronic renal allograft injury, we examine the challenges of cli

121 All causes of renal allograft injury, when severe and/or sustained, ca

122 d by intratubular neutrophil clusters in the renal allograft is a surrogate marker for urinary tract

123 y of patients returning to HD with a failing renal allograft is unknown.

124 Glomerular size in renal allografts is impacted by donor-recipient factors

125 The association between renal allograft loss and death and smoking as a time-dep

126 eased incidence of acute rejection and early renal allograft loss due to calcineurin inhibitors (CNIs

127 This report highlights the risk of renal allograft loss in patients with undiagnosed adenin

128 ve markers that identify patients at risk of renal allograft loss may stratify patients for more inte

129 In the tolerant group, no renal allograft loss was reported, whereas 3 were lost i

130 upporting the existence of several causes of renal allograft loss, the incidences of which peak at di

131 ified as a strong risk factor for subsequent renal allograft loss, the optimal cutoff for the fractio

132 Recipient death is a leading cause for renal allograft loss.

133 noninvasive, independent predictor for late renal allograft loss.

134 nephropathy (BKVN) is a significant cause of renal allograft loss.

135 rejection (cAMR) results in the majority of renal allograft losses.

136 Abnormal para-renal allograft masses should be biopsied to allow swift

137 ted damage to noninfected tissues: Rejecting renal allografts, melanomas clinically responding to ant

138 lant cohorts revealed higher levels of human renal allograft methylarginine-metabolizing enzyme gene

139 ) cause most antibody-mediated rejections of renal allografts, non-anti-HLA Abs have also been postul

140 o ESRD and prevent recurrence of LCDD in the renal allografts of those who subsequently receive a kid

141 be taken into account in prognostication of renal allograft outcome and could be implemented in trea

142 recipients has been associated with adverse renal allograft outcome and with a large gammadelta T-ce

143 coagulation cascades in the donor to improve renal allograft outcome in the recipient.

144 The relative impact on renal allograft outcome of specific histological diagnos

145 ssion, independent factors predicting poorer renal allograft outcome were older age at transplant (ha

146 y quality opens new possibilities to improve renal allograft outcome.

147 cute rejection is a risk factor for inferior renal allograft outcome.

148 rejection (AR) is a risk factor for inferior renal allograft outcome.

149 erum iron as a critical protective factor in renal allograft outcome.

150 echnologies to better understand and predict renal allograft outcome.

151 The aim of this study was to determine renal allograft outcomes for pediatric recipients of a D

152 e U.S. Renal Data System was used to analyze renal allograft outcomes in patients with peripheral vas

153 he effect of HLA matching on deceased and LD renal allograft outcomes in pediatric recipients.

154 cute rejection (AR) is associated with worse renal allograft outcomes.

155 We report two cases of renal allograft oxalate nephropathy in patients with rem

156 The standardization of renal allograft pathology began in 1991 at the first Ban

157 Renal allograft pathology showed the same pattern of tub

158 B cells play an important role in renal allograft pathology, particularly in acute and chr

159 n summary, these data show that in long-term renal allografts, peritubular capillary staining for C4d

160 antibody production, which may be harmful to renal allografts, possibly explaining a mechanism underl

161 e preservation fluids most commonly used for renal allograft preservation in the UK are University of

162 Marshall's solution as a preferred fluid for renal allograft preservation.

163 old storage is the most prevalent method for renal allograft preservation.

164 as to compare the outcomes of deceased donor renal allografts preserved with these fluids using data

165 may provide additional information regarding renal allograft prognosis.

166 pression profiles using tissue from 53 human renal allograft protocol biopsies obtained both at impla

167 MEDLINE search of current literature on renal allograft RCC and selection of appropriate studies

168 A 76-year-old African male renal allograft recipient was admitted for acute visual

169 Prompted by the clinical course of a renal allograft recipient, who lost his graft because of

170 levels in a highly sensitized cohort of 244 renal allograft recipients (67 with preformed donor-spec

171 In a retrospective cohort study of renal allograft recipients (n=169), increased baseline l

172 We prospectively collected biopsies from renal allograft recipients (n=204) with stable renal fun

173 Single-organ renal allograft recipients (n=2217) who had MMF introduc

174 We included 1518 renal allograft recipients in this prospective, observat

175 was assessed in spot urine of 182 outpatient renal allograft recipients on maintenance immunosuppress

176 In renal allograft recipients presenting with graft dysfunc

177 from donor-specific antibody-positive (DSA+) renal allograft recipients prompted study of DSA+ liver

178 We examined 530 renal allograft recipients transplanted at our center an

179 te mofetil (MMF), and prednisone with BKN in renal allograft recipients transplanted between 1997 and

180 f CTLA4 immunoglobulin, both in vitro and in renal allograft recipients treated with CTLA4Ig, with or

181 Renal allograft recipients were included if he or she ha

182 We present cases of two renal allograft recipients who developed Strongyloides h

183 All 1,197 renal allograft recipients who were transplanted at a si

184 We obtained 21 urine specimens from 21 renal allograft recipients with graft dysfunction and bi

185 adjunctive human interferon-gamma therapy in renal allograft recipients with invasive fungal diseases

186 We present three pediatric and adolescent renal allograft recipients with multiple, recalcitrant v

187 ntibody-secreting cells in the blood of nine renal allograft recipients with normal kidney function b

188 ory B cell-derived HLA antibodies (DSA-M) in renal allograft recipients with pretransplant donor-spec

189 Fifteen renal allograft recipients with therapy-naive HCV genoty

190 neously secrete proinflammatory cytokines in renal allograft recipients with transplant glomerulopath

191 ion and reduced acute rejection in untreated renal allograft recipients without displaying adverse ef

192 In 189 consecutively transplanted primary renal allograft recipients, sera were collected sequenti

193 rformed a single-center cohort study in 1000 renal allograft recipients, transplanted between March 2

194 ol to establish the risk of MN recurrence in renal allograft recipients.

195 evelopment of CAN in a prospective cohort of renal allograft recipients.

196 ungal diseases are a major cause of death in renal allograft recipients.

197 ograft rejection from other causes of AKI in renal allograft recipients.

198 ure studies targeting tolerance induction in renal allograft recipients.

199 be validated using an independent cohort of renal allograft recipients.

200 We obtained 114 urine specimens from 114 renal allograft recipients: 48 from 48 recipients with f

201 ngle-center, prospective study involving 321 renal-allograft recipients, we measured the resistive in

202 ntaneously accepted fully MHC-mismatched A/J renal allografts, recipients containing donor-reactive m

203 f Rituximab for the treatment of CD20+ acute renal allograft rejection (AR) demonstrated transient de

204 ly, CD19 mAb treatment significantly reduced renal allograft rejection and abrogated allograft-specif

205 association between these IMPDH variants and renal allograft rejection and graft survival.

206 cular profiling in the setting of diagnosing renal allograft rejection and how this will improve tran

207 Current diagnostic methods of renal allograft rejection are neither sensitive nor spec

208 lls) were the critical effector mechanism of renal allograft rejection induced by memory CD4 T cells.

209 IFNgamma neutralization did not prevent the renal allograft rejection induced by memory helper T cel

210 CD4 and CD8 T cells also did not prevent the renal allograft rejection induced by memory helper T cel

211 opsy discordance rate, our data suggest that renal allograft rejection is a poor surrogate for pancre

212 Renal allograft rejection is more frequent under belatac

213 ributes to the immune responses that promote renal allograft rejection is unknown.

214 In this study, a murine acute renal allograft rejection model was used to investigate

215 orphism rs1050501 affected susceptibility to renal allograft rejection or loss and transplant recipie

216 le publicly and from our Genomics of Chronic Renal Allograft Rejection study.

217 ept exert different effects on mechanisms of renal allograft rejection, particularly at the level of

218 mismatched, life-sustaining, murine model of renal allograft rejection.

219 in cellular and humoral mechanisms of acute renal allograft rejection.

220 le of molecular analysis in the diagnosis of renal allograft rejection.

221 of a c-fms kinase inhibitor (fms-I) in acute renal allograft rejection.

222 ) is a hallmark of antibody-mediated chronic renal allograft rejection.

223 to identify plasma proteins associated with renal allograft rejection.

224 -17A has also been implicated in cardiac and renal allograft rejection.

225 , and this is associated with acute cellular renal allograft rejection.

226 a full adaptive immune response and mediates renal allograft rejection.

227 cy and reduced side effects in patients with renal allograft rejection.

228 has defined roles in the pathophysiology of renal allograft rejection.

229 There were significantly more renal allograft rejections in the sensitized group (5 vs

230 A total of 1124 renal-allograft resistive-index measurements were includ

231 These results suggest that the DCD renal allograft seems to be more vulnerable to AR; enhan

232 eloma responses and induce tolerance for the renal allograft, seven patients (median age: 48 years [r

233 Proteinuria is routinely measured to assess renal allograft status, but the diagnostic and prognosti

234 on patterns may serve as biomarkers of human renal allograft status.

235 al-transplantation centers for assessment of renal-allograft status, although the value of the resist

236 tory responses and endothelial activation in renal allografts suggest that intragraft enrichment of T

237 bly predict long-term immunosuppression-free renal allograft survival (P < 0.0001).

238 body (DSA) has been associated with improved renal allograft survival after antibody-mediated rejecti

239 notypes will develop CKD or manifest shorter renal allograft survival after transplantation.

240 try data (1995-2008) was performed comparing renal allograft survival among KAH recipients with patie

241 neys is associated with improved patient and renal allograft survival and decreased hospital length o

242 mines the effect of repeat HLA mismatches on renal allograft survival and function in all renal after

243 receiving a DCD kidney transplant have good renal allograft survival at 3-year follow-up, comparable

244 here was no significant difference in 3-year renal allograft survival between the DCD and DBD groups

245 Progress in long-term renal allograft survival continues to lag behind the pro

246 blood monocytes in vitamin D3 and IL-10, on renal allograft survival in a clinically relevant rhesus

247 LA antibodies (DSA) is associated with worse renal allograft survival in adult patients.

248 (DCD) kidney transplantation has acceptable renal allograft survival in adults but there are few dat

249 t of presensitization on patient and overall renal allograft survival in CLK.

250 ression may be used as a potential marker of renal allograft survival in patients with no evidence of

251 ited to the new 478 DDKTs replicated shorter renal allograft survival in recipients of APOL1 2-renal-

252 with or without alefacept reliably prolonged renal allograft survival in rhesus monkeys.

253 ctive CD8+ Tmem is associated with prolonged renal allograft survival induced by DCreg infusion in CT

254 Shorter renal allograft survival is reproducibly observed after

255 transplantation hyperglycemia with long-term renal allograft survival is unknown.

256 Three-year renal allograft survival was 95.2% in the DCD group, 87.

257 Renal allograft survival was also similar in the two gro

258 Five-year renal allograft survival was superior for children recei

259 Five-year renal allograft survival was superior for children recei

260 Patient and renal allograft survival were 100%.

261 ions between donor age and APOL1 genotype on renal allograft survival were nonsignificant.

262 f 19 months, there was 100% (death-censored) renal allograft survival with estimated glomerular filtr

263 g risk analysis revealed that APOL1 impacted renal allograft survival, but not recipient survival.

264 tors (CNIs) have failed to improve long-term renal allograft survival.

265 ward that, ultimately, may improve long-term renal allograft survival.

266 t the hypothesis that ApoE(133-149) promotes renal allograft survival.

267 g might serve as a tool to improve long-term renal allograft survival.

268 combination with cyclosporin A had prolonged renal allograft survival.

269 transgenic mice increases skin, cardiac, and renal allograft survival.

270 impermanent, T cell-poor, mixed-chimerism on renal allograft survival.

271 ty may offer opportunities to optimize ideal renal allograft survival.

272 histologic AMR reversal influences long-term renal allograft survival.

273 targets Granzyme B pathway to prolong human renal allograft survival.

274 allospecific T cell responses and prolonged renal allograft survival.

275 D) transplants, analyzing 3-year patient and renal allograft survival.

276 mediated rejection (AMR) is a major risk for renal allograft survival.

277 ransplant recipients and results in improved renal allograft survival.

278 onor age have independent adverse effects on renal allograft survival.

279 ed by tubulointerstitial inflammation in the renal allograft, these conditions are treated with oppos

280 Renal allograft thrombosis is the most frequent and deva

281 lation remains the main treatment to prevent renal allograft thrombosis, although new preventive stra

282 d for murine skin allograft tolerance (TOL), renal allograft TOL has been achieved after induction of

283 nrichment of Treg is a critical mechanism of renal allograft TOL induced by transient mixed chimerism

284 el/duration of chimerism required for stable renal allograft TOL, we retrospectively analyzed these p

285 Renal allograft tolerance (TOL) has been successfully in

286 long-term follow-up data show that sustained renal allograft tolerance and prolonged antimyeloma resp

287 ted with clinical and phenotypic parameters, renal allograft tolerance was strongly associated with a

288 onic hepatitis C virus (HCV) infection after renal allograft transplantation has been an obstacle bec

289 or sufficient for TLR4 underwent heterotopic renal allograft transplantation, with an additional grou

290 ic study was performed in 12 recipients of a renal allograft using a combination of tacrolimus and MM

291 eptors are implicated in the pathogenesis of renal allograft vascular rejection and in progressive va

292 red graft survival at 5 years for the second renal allograft was 90.6% for the BK group and 83.9% for

293 Survival of renal allografts was better in diffuse PTC CD55 staining

294 Using human renal allografts we found increased expression of 6-O-su

295 Renal allografts were subjected to 30 minutes of warm is

296 Predicting which renal allografts will fail and the likely cause of failu

297 Prograde flushing (PF) of living donor renal allografts with preservation solution via the rena

298 , we compared local immunologic responses in renal allografts with those in T-cell-mediated rejection

299 ropathy (PVN) is a common viral infection of renal allografts, with biopsy-proven incidence of approx

300 and prevention of immunologic injury to the renal allograft, yet there remains no consensus on how b