ライフサイエンスコーパス: kidney allograft

1 ion even in unsensitized recipients of first kidney allograft.

2 redictive of acute cellular rejection in the kidney allograft.

3 ng evaluation of a poorly functioning second kidney allograft.

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

5 slet cell clusters xenograft together with a kidney allograft.

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

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

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

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

10 mmunologic and graft survival benefit to the kidney allograft.

11 ansplant may have a protective effect on the kidney allograft.

12 tudy, we describe the first case of KIN in a kidney allograft.

13 ment is crucial for MSC recruitment into the kidney allograft.

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

15 primary JCPyV infection originating from the kidney allograft.

16 o identify active JCPyV infection within the kidney allograft.

17 10 has been observed in patients tolerant to kidney allografts.

18 nd donor selection for HCV viremic liver and kidney allografts.

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

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

21 reatment algorithms for specific diseases of kidney allografts.

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

23 nd prognostic of acute cellular rejection in kidney allografts.

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

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

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

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

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

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

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

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

32 and donor selection of HCV viremic liver and kidney allografts.

33 cicularis) were transplanted with mismatched kidney allografts.

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

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

36 -1 antisense oligo extended the survivals of kidney allografts.

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

38 ions in recipients of simultaneous heart and kidney allografts.

39 ombination, correlating with survival of the kidney allografts.

40 n continued immunosuppression for functional kidney allografts.

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

42 Liver allograft (93.3% vs 93.1%, P = .29), kidney allograft (93.3% vs 93.1%, P = .91), and patient

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

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

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

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

47 95% confidence interval (CI], 1.04-1.79] and kidney allograft (aHR, 1.36; CI, 1.02-1.82) failure over

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

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

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

51 (SPK) improves quality-of-life and prolongs kidney allograft and patient survival in type-1 diabetic

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

53 s locus was associated with rejection of the kidney allograft and with production of anti-LIMS1 IgG2

54 nd alloimmune response in mice recipients of kidney allografts and syngeneic MSCs given on day 0 or o

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

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

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

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 ffects of prolonged cold-ischemia storage on kidney allografts are poorly understood.

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

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

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

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

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

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

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

69 l chow exhibited dysbiosis after receiving a kidney allograft but not an isograft, despite the avoida

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

71 DBA/2J kidney allografts, but not heart allografts, are spontan

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

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

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

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

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

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

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

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

80 ential relevance of this to heart, lung, and kidney allograft dysfunction.

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

82 eventing ischaemia-reperfusion injury in the kidney allograft (EMPIRIKAL) trial (ISRCTN49958194).

83 nding of donor-specific antibodies (DSAs) to kidney allograft endothelial cells that does not activat

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

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

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

87 recipients had significantly higher risk of kidney allograft failure (DD-KA: aHR (1.53) 2.20(3.17) ;

88 2) and decreased length of stay (P = 0.001), kidney allograft failure (P = 0.012), and dialysis durat

89 .02) and decreased length of stay (p=0.001), kidney allograft failure (p=0.012), and dialysis duratio

90 Associations of transplant type with kidney allograft failure and death (multivariable-adjust

91 Posttransplant diarrhea is associated with kidney allograft failure and death, but its etiology rem

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

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

94 Kidney allograft failure is a serious condition as it im

95 Kidney allograft failure is a serious condition, as it i

96 SA) on antibody-mediated rejection (AMR) and kidney allograft failure is well established.

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

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

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

100 ze the available literature on the causes of kidney allograft failure, both early and late, both noni

101 ze the available literature on the causes of kidney allograft failure, both early and late, both noni

102 thy (BKPyVAN) constitutes a serious cause of kidney allograft failure, but large-scale data in pediat

103 ipients increases delayed graft function and kidney allograft failure.

104 association with histology of AMR (AMRh) and kidney allograft failure.

105 redictor of alloantibody sensitization after kidney allograft failure.

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

107 ipients increases delayed graft function and kidney allograft failure.

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

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

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

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

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

113 ntive and therapeutic strategies that target kidney allograft fibrogenesis.

114 Kidney allograft fibrosis results from a reactive proces

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

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

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

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

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

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

121 Five pairs of human kidney allografts from donation after circulatory death

122 Kidney allografts from donors with persistent AKI are of

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

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

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

126 recipients enrolled in the Deterioration of Kidney Allograft Function (DeKAF) study were evaluated:

127 nflammation has been implicated in decreased kidney allograft function and survival, but the underlyi

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

129 Pancreas and kidney allograft function is routinely monitored with se

130 The procedure was safe and kidney allograft function remained stable after 3 years.

131 g the prospective Long-term Deterioration of Kidney Allograft Function study database, we sought to b

132 This reduced kidney allograft futility (death or continued need for h

133 This reduced kidney allograft futility (death or continued need for h

134 ecific antibodies are essential mediators of kidney allograft glomerular injury caused by prolonged c

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

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

137 female recipients of offspring living donor kidney allografts have inferior outcomes.

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

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

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

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

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

143 rience with the use of HCV viremic liver and kidney allografts in HCV-negative recipients is limited

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

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

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

147 MIgARD in the kidney allograft is associated with poor prognosis.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

162 ediated rejection (AMR) accounts for >50% of kidney allograft loss.

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

164 The main outcome was kidney allograft loss.

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

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

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

168 y improve individual risk stratification for kidney allograft loss.

169 rization increases performance in predicting kidney allograft loss.

170 ular atrophy (IFTA) is an important cause of kidney allograft loss; however, noninvasive markers to i

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

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

173 About half of late kidney allograft losses are attributed to death with fun

174 About half of late kidney allograft losses are attributed to death with fun

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

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

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

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

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

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

181 In contrast, kidney allograft microperfusion was neither significantl

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

183 0, IL-12, IL-18, TNF-alpha, and IFN-gamma in kidney allografts on days 3, 5, and 7 after grafting, as

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

185 Kidney allograft outcomes are good in APRT deficiency pa

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

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

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

189 centration-to-dose ratio (C/D ratio), affect kidney allograft outcomes.

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

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

192 perspectral images of distinct components of kidney allografts (parenchyma, ureter) were acquired 15

193 rted to be associated with AR, using a large kidney allograft recipient cohort of 2390 European Ameri

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

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

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

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

198 We enrolled 71 kidney allograft recipients for serial fecal specimen co

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

200 Identifying kidney allograft recipients who are predisposed to acute

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

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

203 dies (HLA-DSAs) are often absent in serum of kidney allograft recipients whose biopsy specimens demon

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

205 Kidney allograft recipients with hypercalcemia and eleva

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

207 Hispanic kidney allograft recipients without evidence of preexist

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

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

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

211 e nucleotide polymorphisms, and 2 cohorts of kidney allograft recipients-a discovery cohort and a con

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

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

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

215 immunosuppressive agents during treatment of kidney allograft recipients.

216 upregulated during operational tolerance in kidney allograft recipients.

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

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

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

220 and the role of MIR146A in the risk of AR in kidney allograft recipients.

221 on, appears to have predictive value also in kidney allograft recipients.

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

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

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

225 Kidney allograft rejection can occur in clinically stabl

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

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

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

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

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

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

232 Acute kidney allograft rejection was modestly attenuated in TL

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

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

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

236 phropathy, ureteral obstructive disease, and kidney allograft rejection.

237 med a two-stage genetic association study of kidney allograft rejection.

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

239 , we retrospectively studied 52 mRNAs in 256 kidney allograft samples taken from NHP kidney recipient

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

241 The continued kidney allograft shortage has generated interest in the

242 Kidney allograft status is currently characterized using

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

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

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

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

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

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

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

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

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

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

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

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

255 Kidney allograft survival rates at 3, 5, 7, and 10 years

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

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

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

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

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

261 The best kidney allograft survival was for patients who received

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

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

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

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

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

267 ronic rejection with antibiotics may improve kidney allograft survival.

268 , 3.9-8.1 years), we report 100% patient and kidney allograft survival.

269 ssociated with decreased patient, liver, and kidney allograft survivals (respective HR: 1.4 [1.1, 1.8

270 Five-year liver and kidney allograft survivals were 67% and 64% in the T-cel

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

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

273 spite improvements in short-term survival of kidney allografts, this progress was not matched in long

274 n model that subjected MHC-mismatched BALB/c kidney allografts to cold-ischemia storage for 0.5 or 6

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

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

277 s comprising the inflammatory infiltrates in kidney allografts undergoing acute and/or chronic reject

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

279 lloimmunity changes over time in patients on kidney allograft waiting lists, and an apparent lack of

280 The rate of BPAR of kidney allografts was low in both control (9.5%) and inv

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

282 -term immunosuppression-free survival of the kidney allograft were achieved in 7 of the 10 patients,

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

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

285 , native kidneys, and spontaneously accepted kidney allografts were analyzed using flow cytometry and

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

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

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

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

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

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

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

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

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

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