ライフサイエンスコーパス: kidney allograft

1 primary JCPyV infection originating from the kidney allograft.

2 es in patients with acute dysfunction of the kidney allograft.

3 slet cell clusters xenograft together with a kidney allograft.

4 nine levels, but not with viral loads in the kidney allograft.

5 ted to 100% recipient without rejection of a kidney allograft.

6 ymptoms, without any appreciable harm to the kidney allograft.

7 tion for patients with T1DM bearing a stable kidney allograft.

8 o identify active JCPyV infection within the kidney allograft.

9 mmunologic and graft survival benefit to the kidney allograft.

10 the recipient previously made tolerant to a kidney allograft.

11 ion even in unsensitized recipients of first kidney allograft.

12 ess of the priority of the candidate for the kidney allograft.

13 redictive of acute cellular rejection in the kidney allograft.

14 ng evaluation of a poorly functioning second kidney allograft.

15 raft dysfunction (CGD), and graft failure of kidney allografts.

16 nd prognostic of acute cellular rejection in kidney allografts.

17 ith higher levels of beta-catenin protein in kidney allografts.

18 tient outcomes in HIV-infected recipients of kidney allografts.

19 raft dysfunction (CGD), and graft failure of kidney allografts.

20 in blood-derived MDSC from rat recipients of kidney allografts.

21 -human primate recipients of life-supporting kidney allografts.

22 g a lowered risk for acute rejection (AR) of kidney allografts.

23 n continued immunosuppression for functional kidney allografts.

24 flammation may improve long-term survival of kidney allografts.

25 pithelial-to-mesenchymal transition (EMT) in kidney allografts.

26 e an increased demand on a limited supply of kidney allografts.

27 cicularis) were transplanted with mismatched kidney allografts.

28 antigens might play a role in the failure of kidney allografts.

29 ompared HTK or UW for cold static storage of kidney allografts.

30 -1 antisense oligo extended the survivals of kidney allografts.

31 and all other groups received both heart and kidney allografts.

32 ions in recipients of simultaneous heart and kidney allografts.

33 theless they constitute a valuable source of kidney allografts.

34 ed into Lewis rat recipients of Brown Norway kidney allografts.

35 reduced the expression of ICAM-1 protein in kidney allografts.

36 10 has been observed in patients tolerant to kidney allografts.

37 ved in animals already tolerant of heart and kidney allografts.

38 s capable of inducing tolerance of heart and kidney allografts.

39 reatment algorithms for specific diseases of kidney allografts.

40 ant, 25.5% after irreversible rejection of a kidney allograft, 17.1% after a heart transplant, and 43

41 the expression of TGFbeta mRNA and abrogated kidney allograft acceptance.

42 l renal graft function, leading to long-term kidney allograft acceptance.

43 In conclusion, HIV-1 can infect kidney allografts after transplantation despite undetect

44 reas allograft (aHR, 0.99; CI, 0.86-1.37) or kidney allograft (aHR, 0.98; CI, 0.84-1.15) failure.

45 95% confidence interval (CI], 1.04-1.79] and kidney allograft (aHR, 1.36; CI, 1.02-1.82) failure over

46 the transplantation of MHC class I-disparate kidney allografts all became tolerant to the donor kidne

47 e-hundred and five pediatric recipients of a kidney allograft, all treated with a corticosteroid-free

48 Thymectomized animals receiving a kidney allograft alone or receiving separate thymic and

49 Recipients received 1) a kidney allograft alone, 2) a composite allogeneic thymok

50 duces durable and robust immune tolerance to kidney allografts, although incomplete tolerance to dono

51 We examined kidney allograft and patient survival by indication of s

52 rmine best practices associated with optimal kidney allograft and patient survival.

53 Four groups of rhesus monkeys received kidney allografts and immunosuppression.

54 nd seemed to be associated with rejection of kidney allografts and with coronary artery disease in he

55 nced staining for THSD7A was observed in the kidney allograft, and detectable anti-THSD7A antibodies

56 cating acute cellular rejection in the human kidney allograft, and that the combined metabolite and m

57 rcent of the cases occurred in patients with kidney allografts, and the remaining patients had liver,

58 r atrophy (IF/TA) contributes to the loss of kidney allografts, and treatment or preventive options a

59 A subclasses identify distinct phenotypes of kidney allograft antibody-mediated injury.

60 tiate the basis for acute dysfunction of the kidney allograft are preferable to invasive allograft bi

61 CR- cells found in long-term surviving mouse kidney allografts are alpha/beta-T cells that have downr

62 simultaneous transplants, heart, liver, and kidney allografts are themselves protected and protect t

63 ACI (RT1a) recipients rejected Lewis (RT1l) kidney allografts at a mean survival time of 8.5+/-1.1 d

64 Rat recipients acutely rejected kidney allografts at a mean survival time of 8.8 +/- 0.7

65 s recipients treated with CsA alone rejected kidney allografts at a median survival time of 8.5 days

66 We enrolled patients who received kidney allografts at two transplantation centers in Pari

67 opathies may account for about 40% of failed kidney allografts beyond the first year of engraftment,

68 MiRNA expression profiles of 8 human kidney allograft biopsies (4 IFTA and 4 normal biopsies,

69 s were collected from 27 patients undergoing kidney allograft biopsies for renal dysfunction after tr

70 Paraffin-fixed kidney allograft biopsies from 40 patients with COT (n=4

71 tween 1991 and 2009 who underwent a baseline kidney allograft biopsy at transplantation were included

72 1 days before induced tolerance to heart and kidney allografts but did not prolong skin graft surviva

73 y, severe RLN is uncommon in recipients of a kidney allograft, but black recipients, female recipient

74 i of renal proximal tubules of injured human kidney allografts, but not in those of stable allografts

75 test for determining HIV-1 infection of the kidney allograft by measuring HIV-1 DNA and RNA levels i

76 these surface TCR- cells were isolated from kidney allografts by flow cytometry and cultured in the

77 now report an attempt to induce tolerance to kidney allografts by transplanting donor thymic grafts s

78 cited in patients rejecting ABO-incompatible kidney allografts, can interact with the alpha-gal epito

79 In contrast, kidney allografts delayed for 40 days after pretreatment

80 nd the impaired ability to accumulate in the kidney allografts despite an otherwise MyD88-sufficient

81 Six months after transplantation, kidney allografts displayed histologic and functional fe

82 recipients with donors and identification of kidney allograft donor-recipient pairs at high risk for

83 epsilon-(gamma-glutamyl) lysine, in 23 human kidney allografts during the early posttransplantation p

84 pathy associated with BK polyomavirus causes kidney allograft dysfunction and failure.

85 irus nephropathy (PVAN) is a common cause of kidney allograft dysfunction and loss.

86 common (57%) in patients with new onset late kidney allograft dysfunction.

87 The remaining four rejected their kidney allografts either chronically or acutely.

88 are polymorphic proteins expressed on donor kidney allograft endothelium and are critical targets fo

89 All chimeric animals accepted donor-matched kidney allografts, even one without cyclosporine.

90 Eight of nine kidney allografts eventually failed, but all patients re

91 ed outcomes in 300 consecutive patients with kidney allograft failure and survival of more than 30 da

92 The relationship between cost and kidney allograft failure has not been fully investigated

93 The reasons for kidney allograft failure subsequent to pancreas after ki

94 Maintenance immunosuppression after kidney allograft failure was associated with a greater i

95 Maintenance immunosuppression after kidney allograft failure was associated with a greater i

96 Associations of D-BMI with pancreas and kidney allograft failure were assessed by multivariate C

97 iated rejection (ABMR) is a leading cause of kidney allograft failure.

98 redictor of alloantibody sensitization after kidney allograft failure.

99 ivariate analyses for the primary outcome of kidney allograft failure.

100 histologic lesions, and a risk predictor of kidney allograft failure.

101 mortality (3.7% vs 3.8%; P = 0.788), 1-year kidney allograft failure/rejection (16.7% vs 16.8%; P =

102 dataset for mortality, rehospitalization and kidney allograft failure/rejection for weekend (defined

103 acity of anti-HLA antibodies plays a role in kidney-allograft failure.

104 ntive and therapeutic strategies that target kidney allograft fibrogenesis.

105 Kidney allograft fibrosis results from a reactive proces

106 to decipher the mechanism and management of kidney allograft fibrosis.

107 ransplants, with a total of 994 558 years of kidney allograft follow-up time.

108 Reduced intensity conditioning preceded a kidney allograft, followed the next day by FCRx.

109 an existing liver allograft could protect a kidney allograft from immunologic injury due to histoinc

110 Included are 795 adults, recipients of kidney allografts from 2000 to 2006.

111 In contrast, kidney allografts from ACI rats were hyperacutely reject

112 tial inflammatory events that develop within kidney allografts from brain-dead donors could be normal

113 al of unmodified Lew recipients sustained by kidney allografts from brain-dead, normal anesthetized,

114 Blood group O piglets received kidney allografts from group A (AO-incompatible) or grou

115 ls (n=4); group 4 animals received heart and kidney allografts from lethally irradiated donors (n=7);

116 Ten (38.5%) received kidney allografts from pediatric donors (age < or = 18)

117 e with 20.0 mg per 2 ml of IP-9125 protected kidney allografts from rejection (37.5+/-7.5 days; P < 0

118 However, unlike kidney allografts, full tolerance to cardiac allografts

119 d with CMV disease, BK virus nephropathy, or kidney allograft function at 1 year.

120 Pancreas and kidney allograft function is routinely monitored with se

121 Long-term kidney allograft function remained stable in all patient

122 ent mixed chimerism, and the function of the kidney allograft has been normal for more than 28 months

123 liver, given that spontaneous acceptance of kidney allografts has been reported, although less commo

124 loped end-stage renal failure and received a kidney allograft in 1 of 6 Dutch university hospitals be

125 We found that HIV-1 infected the kidney allograft in 68% of these patients.

126 ic rejection ultimately leads to loss of the kidney allograft in most transplants.

127 All consecutive patients receiving a kidney allograft in our transplantation department over

128 r weight]) inhibits the rejection process of kidney allografts in a rat model was examined.

129 rmation on microvascular tissue perfusion in kidney allografts in more detail.

130 -Collins solution, prolonged the survival of kidney allografts in rats.

131 id and stable tolerance to class I-disparate kidney allografts in thymectomized recipients.

132 ng its potential as a biomarker of incipient kidney allograft injury.

133 i-human HLA antibodies and antibody-mediated kidney allograft injury.

134 chemia-reperfusion injury in cadaveric (CAD) kidney allografts is associated with tubular cell injury

135 histologic feature associated with a failing kidney allograft, is diagnosed using the invasive allogr

136 When given to recipients of kidney allografts, it resulted in indefinite graft survi

137 We used a murine orthotopic kidney allograft (KTx) model to analyze the impact of CD

138 Membranous nephropathy (MN) can recur in kidney allografts leading to graft dysfunction and failu

139 The adjusted 10-year mean kidney allograft lifespan was higher in Ki/SPK compared

140 Primary outcome was kidney allograft lifespan, defined as the time free from

141 uated the utility, defined as posttransplant kidney allograft lifespan, of this practice.

142 ure swine that were tolerant of heart and/or kidney allografts long term underwent transplantation of

143 associated with 1.63 times increased risk of kidney allograft loss (hazards ratio 1.63; 95% confidenc

144 variables assessed, factors associated with kidney allograft loss after PAK include impaired renal f

145 nephritis (GN) remains an important cause of kidney allograft loss and whether rapid discontinuation

146 In our analysis, post-PAK kidney allograft loss was strongly associated with glome

147 vels to the risk of death from any cause and kidney allograft loss were examined.

148 urrence of AAGN contributed independently to kidney allograft loss, emphasizing the importance of cli

149 The main outcome was kidney allograft loss.

150 y improve individual risk stratification for kidney allograft loss.

151 lar atrophy (TA) is the most common cause of kidney allograft loss.

152 dently associated with the risk of death and kidney allograft loss.

153 rization increases performance in predicting kidney allograft loss.

154 mediated rejection (AMR) is a major cause of kidney allograft loss.

155 ted rejection (ABMR) is the leading cause of kidney allograft loss.

156 Graft injury phenotype and the time to kidney-allograft loss were assessed.

157 ful in identifying patients at high risk for kidney-allograft loss.

158 Radiosensitive elements in kidney allograft may be responsible for tolerance induct

159 the renal tubular space, we reasoned that a kidney allograft may function as an in vivo flow cytomet

160 stication of acute cellular rejection in the kidney allograft may help realize the full benefits of k

161 itial fibrosis and tubular atrophy (IFTA) in kidney allografts may point toward pathologic mechanisms

162 2 days) resulted in a long-term survival of kidney allografts (mean survival time [MST] > 100.0 days

163 CES revealed a 49% reduction of kidney allograft microperfusion 2 hr after the intake of

164 tudy was to explore whether acute changes of kidney allograft microperfusion due to the administratio

165 In contrast, kidney allograft microperfusion was neither significantl

166 In a fully MHC mismatched mouse kidney allograft model, we describe the synthesis of an

167 histocompatibility complex-incompatible rat kidney allograft model.

168 n=3) or combined class I disparate heart and kidney allografts (n=3), followed in both cases by a 12-

169 isparate heart allografts (n=5) or heart and kidney allografts (n=4).

170 0, IL-12, IL-18, TNF-alpha, and IFN-gamma in kidney allografts on days 3, 5, and 7 after grafting, as

171 med to assess the effect of SSD on long-term kidney allograft outcome and to compare the immunization

172 long-term impact of tacrolimus treatment on kidney allograft outcome.

173 lant complications and patient, pancreas and kidney allograft outcomes were evaluated.

174 complement-binding DQ DSA negatively impacts kidney allograft outcomes.

175 act of recipient APOL1 gene distributions on kidney allograft outcomes.

176 t of reported isolated pancreas rejection on kidney allograft outcomes.

177 tion (LAR) has been associated with inferior kidney allograft outcomes.

178 recipients were sensitized and rejected the kidney allografts rapidly after transplantation.

179 evaluated in first cadaveric or living donor kidney allograft recipients (n = 144) transplanted at th

180 ctive, multicenter study among 106 pediatric kidney allograft recipients aged 11.4 +/- 5.9 years, we

181 in body mass index (BMI) is also observed in kidney allograft recipients and deceased organ donors.

182 rolonged survival times of non-human primate kidney allograft recipients both as monotherapy and most

183 ntly extended the median survival time of BN kidney allograft recipients from 9 to 36.5-77 days, and

184 Thirty-five kidney allograft recipients matched for age, gender, and

185 al parenchymal tissue perfusion of 32 stable kidney allograft recipients was evaluated with CES befor

186 ombination may provide particular benefit to kidney allograft recipients who develop delayed graft fu

187 We identified 351 kidney allograft recipients who had serum levels of 25-h

188 We reviewed the records of 1166 kidney allograft recipients who received their allograft

189 Included were 63 kidney allograft recipients with biopsy proven primary M

190 ombination may provide particular benefit to kidney allograft recipients with DGF.

191 Kidney allograft recipients with hypercalcemia and eleva

192 lower risk for posttransplant malignancy in kidney allograft recipients with negative pretransplant

193 Hispanic kidney allograft recipients without evidence of preexist

194 he incidence of acute rejection in heart and kidney allograft recipients, its role in lung transplant

195 However, in contrast to kidney allograft recipients, long-term heart allograft r

196 In HCV-infected kidney allograft recipients, the progression of fibrosis

197 graft-to-periphery CCL5 gradient in tolerant kidney allograft recipients, which controls recruitment

198 cells of the kidney, causing nephropathy in kidney allograft recipients, while JC virus (JCV) replic

199 (UTI) is a frequent, serious complication in kidney allograft recipients.

200 sera (n=256) from an historical cohort of 22 kidney allograft recipients.

201 nal biopsies, all from simultaneous pancreas-kidney allograft recipients.

202 ibody-mediated rejection (ABMR) therapies in kidney allograft recipients.

203 red the immunological responses of heart and kidney allograft recipients.

204 ecular characteristics of PTLD in cynomolgus kidney allograft recipients.

205 a major cause of morbidity and mortality in kidney allograft recipients.

206 This report extends the study to pediatric kidney allograft recipients.

207 ase in a large cohort (n = 301) of pediatric kidney allograft recipients.

208 brosis/tubular atrophy = 59) from 168 unique kidney allograft recipients.

209 ctive to prevent AMR including in sensitized kidney allograft recipients.

210 immunosuppressive agents during treatment of kidney allograft recipients.

211 upregulated during operational tolerance in kidney allograft recipients.

212 Autopsy revealed no evidence of liver or kidney allograft rejection and evidence of chronic sickl

213 rived endothelial cell precursors (ECPs) and kidney allograft rejection and function.

214 Kidney allograft rejection can occur in clinically stabl

215 The role of NK cells in kidney allograft rejection has not been studied.

216 Although the features of chronic heart and kidney allograft rejection have been well characterized,

217 ive immunosuppressant in prevention of acute kidney allograft rejection in cynomolgus monkeys and syn

218 ly reduces functional and histologic chronic kidney allograft rejection in the rat.

219 essed the effect of complement inhibition on kidney allograft rejection phenotype and the clinical re

220 re associated with a specific histomolecular kidney allograft rejection phenotype that can be abrogat

221 st immune response toward the development of kidney allograft rejection remains unclear.

222 Here, we investigated the role of TLR4 in kidney allograft rejection using a fully major histocomp

223 Acute kidney allograft rejection was modestly attenuated in TL

224 Tolerance induction can prevent acute kidney allograft rejection without chronic immunosuppres

225 adapter protein is an important mediator of kidney allograft rejection, yet the precise role of MyD8

226 -mismatched, life-sustaining murine model of kidney allograft rejection.

227 osuppression, which can subsequently lead to kidney allograft rejection.

228 CR can be used as an aid in the diagnosis of kidney allograft rejection.

229 nd 9 survived for more than 100 days without kidney allograft rejection.

230 ulopathy (TG) is a histopathologic entity of kidney allografts related to anti-human leukocyte antige

231 elicited by incompatible A or B antigens on kidney allografts results in activation of anti-Gal B-ce

232 In conclusion, even though PVAN and TCMR kidney allografts share great similarities on gene pertu

233 The continued kidney allograft shortage has generated interest in the

234 Kidney allograft status is currently characterized using

235 nvestigate whether urine metabolites predict kidney allograft status, we determined levels of 749 met

236 ed in the serum of patients who had rejected kidney allografts, suggesting a potential role for these

237 Analysis of interval heart-kidney allografts suggests the need for partial antigeni

238 Px was not associated with kidney allograft survival (P = 0.16).

239 (BKV)-associated nephropathy is a threat to kidney allograft survival affecting up to 15% of renal t

240 unosuppression with sirolimus supports human kidney allograft survival and asked if this combination

241 a suggest that, in SPK recipients, long-term kidney allograft survival and function are not statistic

242 The implications of this policy for kidney allograft survival are not well understood.

243 Kidney allograft survival at 5 years was 83.6% for T1DM,

244 examined the effect of HLA compatibility on kidney allograft survival by studying all first adult ki

245 The association of HLA mismatching with kidney allograft survival has been well established.

246 cal rejection has long-term consequences for kidney allograft survival in an observational prospectiv

247 BM protocol is simple and produces long-term kidney allograft survival in NHP although additional tre

248 We evaluated the 15-year kidney allograft survival in patients with primary glome

249 We examined whether piceatannol prolongs kidney allograft survival in the stringent ACI-to-Lewis

250 h early episodes of acute rejection, reduces kidney allograft survival over time.

251 del identified three risk strata with 6-year kidney allograft survival rates of 6.0% (high-risk group

252 ion (AR) and delayed graft function (DGF) on kidney allograft survival remain controversial, and the

253 The effect of recipient obesity on kidney allograft survival remains enigmatic.

254 ching leads to nephron underdosing and worse kidney allograft survival remains poorly defined, partic

255 ump of 2.5, 5, 10, or 20 mg/kg BIMO extended kidney allograft survival to 11.5 +/- 2.2 d (P < 0.03),

256 on to CsA showed significant prolongation of kidney allograft survival to 71 days (n=3; P<0.04) or 63

257 among M and NM patients, respectively, while kidney allograft survival was 88% in M and 92% in NM gro

258 One-year patient, pancreas, and kidney allograft survival were 95%, 93%, and 90%, respec

259 suppressive activity by prolonging heart and kidney allograft survival, displaying synergy in the imm

260 ed with CsA significantly enhanced heart and kidney allograft survival, even at doses of CsA ineffect

261 c composite prognostic ABMR score to predict kidney allograft survival, integrating the disease chara

262 To improve long-term kidney allograft survival, management paradigms should p

263 ronic rejection with antibiotics may improve kidney allograft survival.

264 , 3.9-8.1 years), we report 100% patient and kidney allograft survival.

265 duced by 50-75% the CsA dose needed for 100% kidney allograft survival.

266 determine the impact of HLA compatibility on kidney allograft survival.

267 of human leucocyte antigen (HLA) matching in kidney allograft survival.

268 d, have less chances of actually receiving a kidney allograft, than younger counterparts.

269 In mouse kidney allografts that survive to 3 wk after transplanta

270 Cynomolgus monkeys were transplanted with kidney allografts that were incompatible in mixed lympho

271 of full immunosuppression for a functioning kidney allograft, the need for Px for symptoms and radio

272 bearing combined class I disparate heart and kidney allografts, the nonthymectomized recipients accep

273 mg/kg/day IP-9125 prolonged the survival of kidney allografts to 39.2+/-16.4 days; 5.0 mg/kg/day, to

274 ponse gene 88 (MyD88) induced donor-specific kidney allograft tolerance.

275 A total of 133 recipients of kidney allograft transplantations recruited in the Unite

276 lupus nephritis (RLN) among recipients of a kidney allograft vary among single-center reports.

277 espite VCA rejection, tolerance of heart and kidney allografts was maintained.

278 average of 3.1 yr, 21 episodes of AMR of the kidney allograft were identified.

279 One-year survival rates for recipient and kidney allografts were 100% and 98% for living donors, 9

280 Donor-matched kidney allografts were also accepted without additional

281 Kidney allografts were harvested at days 2, 7, and 56 an

282 -up of 6.1 yr, 154 participants died and 260 kidney allografts were lost.

283 d twenty-three recipients of first cadaveric kidney allografts were randomized to receive tacrolimus

284 d twenty-three recipients of first cadaveric kidney allografts were randomized to receive tacrolimus+

285 Brown Norway (BN) rat heart or kidney allografts were transplanted into the abdomen of

286 omolgus monkey recipients of life-supporting kidney allografts were treated orally with STN alone or

287 Recipients of first cadaveric kidney allografts were treated with tacrolimus+mycopheno

288 ended survival of MHC/non-MHC mismatched rat kidney allografts, whereas a 90-day therapy induced tran

289 ase and recipient of a zero-antigen mismatch kidney allograft which developed worsening proteinuria o

290 mpared with kidneys without ARF, receiving a kidney allograft with ARF was not associated with increa

291 osis who was a recipient of a living related kidney allograft with diminished but stable graft functi

292 Among 6850 recipients of a kidney allograft with systemic lupus erythematosus, 167

293 unknown whether KIM-1 expression changes in kidney allografts with delayed graft function (DGF), whi

294 t both minimally invasive procedures yielded kidney allografts with excellent early function and a mi

295 We examined this question in the human kidney allografts with interstitial fibrosis and tubular

296 ts (n=5); group 2 animals received heart and kidney allografts with no other manipulation (n=4); grou

297 formed protocol biopsies in 25 recipients of kidney allografts with progressive allograft dysfunction

298 hesis, we treated tolerant rat recipients of kidney allografts with recombinant rat CCL5 to restore n

299 ical expression of PI-9 has been observed in kidney allografts with subclinical rejection, suggesting

300 We reviewed our experience rescuing kidney allografts with this severe AMR phenotype by usin