ライフサイエンスコーパス: renal allograft

1 ctomy and received an orthotopic Dark Agouti renal allograft.

2 ffects of antibody on the endothelium of the renal allograft.

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

4 of tertiary lymphoid tissue within the human renal allograft.

5 titial and microvascular inflammation of the renal allograft.

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

7 asive technique for functional assessment of renal allografts.

8 de a path to using more ischemically damaged 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 se after both immune and nonimmune injury to renal allografts.

16 in grafts results in rejection of subsequent renal allografts.

17 c (75%) BM recipients developed tolerance to renal allografts.

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

19 ce of BKV replication in recipients of human renal allografts.

20 ion associated with long-term maintenance of renal allografts.

21 r transplantation may prevent loss of scarce renal allografts.

22 e the noninvasive detection of leukocytes in renal allografts.

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

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

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

26 ogether, these data suggest that spontaneous renal allograft acceptance evolves through a series of t

27 es have shown that this model of spontaneous renal allograft acceptance is associated with TGF-beta-d

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

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

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

31 om 33 patients who received ABO-incompatible renal allografts (after desensitization) were retrospect

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

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

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

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

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

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

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

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

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

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

42 both Foxp3+ T cells and IDO+ DCs in accepted renal allografts, and localization of both cell types wi

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

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

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

46 MHC-mismatched DBA/2 renal allografts are spontaneously accepted by C57BL/6 m

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

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

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

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

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

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

53 A total of 653 recipients of renal allografts between 1998 and 2005 had stress SPECT

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

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

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

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

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

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

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

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

62 Renal allograft biopsies performed after October 2003, r

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

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

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

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

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

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

69 All renal allograft biopsy samples with concomitant data on

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

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

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

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

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

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

76 ss of detectable TGF-beta immune regulation, renal allografts continue to function normally for >200

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

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

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

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

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

82 splant recipients, is a significant cause of renal allograft dysfunction and loss.

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

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

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

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

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

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

89 idence, progression, and severity of chronic renal allograft failure in patients with elevated serum

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

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

92 ferentiation of prerenal and intrinsic acute renal allograft failure.

93 induction therapy abolishes the disparity in renal allograft failure.

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

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

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

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

98 Moderate renal allograft fibrosis was reduced in treated patients

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

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

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

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

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

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

105 iniature swine received fully MHC-mismatched renal allografts from SLA(c/c) donors with 12 days of FK

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

107 No differences were observed in renal allograft function at 1 or 5 years between the rep

108 The renal allograft function by calculated creatinine cleara

109 Renal allograft function was assessed by serum creatinin

110 onged reductions in DSA levels, (3) improved renal allograft function, and (4) suppression of recurre

111 study, we correlated acute rejection rates, renal allograft function, and use of antibody induction

112 and messenger RNAs (mRNAs), and that AR, and renal allograft function, could be predicted with a high

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

114 Mouse renal allografts have a remarkable ability to promote ac

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

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

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

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

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

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

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

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

123 All posttransplant renal allograft indication biopsies performed in this co

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

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

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

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

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

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

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

131 These data indicate that the renal allograft is required for the indefinite maintenan

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

133 The 5-yr survival rate of renal allografts is significantly lower for grafts from

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

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

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

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

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

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

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

141 noninvasive, independent predictor for late renal allograft loss.

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

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

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

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

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

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

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

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

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

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

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

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

154 echnologies to better understand and predict renal allograft outcome.

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

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

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

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

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

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

161 Renal allograft pathology showed the same pattern of tub

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

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

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

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

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

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

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

169 is a retrospective analysis of all cadaveric renal allografts procured locally by our center over a 3

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

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

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

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

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

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

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

177 with posttransplant cardiac risk among 1102 renal allograft recipients at a single center in 1991 to

178 thymocyte globulin (rATG) is largely used in renal allograft recipients at risk for delayed graft fun

179 L-based therapy was efficacious in high-risk renal allograft recipients in the first year after trans

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

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

182 In renal allograft recipients presenting with graft dysfunc

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

184 with tacrolimus monotherapy has allowed many renal allograft recipients to be maintained on spaced we

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

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

187 Of 279 renal allograft recipients transplanted between March 20

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

189 ependent risk factors for BKV replication in renal allograft recipients treated with tacrolimus and m

190 Renal allograft recipients were included if he or she ha

191 One hundred twenty renal allograft recipients were studied prospectively at

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

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

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

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

196 eed to be verified in larger numbers of HIV+ renal allograft recipients with longer follow-up.

197 ned the outcomes of eight adult HIV+ primary renal allograft recipients with median 15 (range 8-47) m

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

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

200 Fifteen renal allograft recipients with therapy-naive HCV genoty

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

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

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

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

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

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

207 yclosporine (CsA) were compared in high-risk renal allograft recipients.

208 n, a situation commonly encountered in human renal allograft recipients.

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

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

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

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

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

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

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

216 - and CD86-specific fusion protein, prevents renal allograft rejection and alloantibody formation in

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

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

219 Focal PTC C4d staining in acute renal allograft rejection has not been studied extensive

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

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

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

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

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

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

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

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

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

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

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

231 to identify plasma proteins associated with renal allograft rejection.

232 -17A has also been implicated in cardiac and renal allograft rejection.

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

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

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

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

237 been reported in chronic pyelonephritis and renal allograft rejection; this suggests interstitial in

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

239 ut evidence exists that rATG infusion before renal allograft reperfusion improves early graft functio

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

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

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

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

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

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

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

247 ve rejection, yet provides similar long-term renal allograft survival and function.

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

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

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

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

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

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

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

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

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

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

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

259 Shorter renal allograft survival is reproducibly observed after

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

261 with isolated pancreas rejection have worse renal allograft survival than patients reported as havin

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

263 Renal allograft survival was also similar in the two gro

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

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

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

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

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

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

270 combination with cyclosporin A had prolonged renal allograft survival.

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

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

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

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

275 allospecific T cell responses and prolonged 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 tors (CNIs) have failed to improve long-term renal allograft survival.

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

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

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

283 lower risk for scarring in ABO-incompatible renal allografts; the generalizability of these results

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

285 ssue from biopsy or nephrectomy specimens of renal allografts, TL1A mRNA and protein were expressed i

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

287 To induce mixed chimerism and renal allograft tolerance in cynomolgus monkeys, cycloph

288 men for the induction of mixed chimerism and renal allograft tolerance in cynomolgus monkeys.

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

290 r CD154 blockade induced mixed chimerism and renal allograft tolerance, with significantly less morbi

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

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

293 SLA(a/d) renal allografts transplanted into tolerant recipients w

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

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

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

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

298 Renal allografts were subjected to 30 minutes of warm is

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

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