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1 ike replacement drug, and with a functioning renal graft).
2 relate with the ischemic time imposed on the renal graft.
3 cal trials of genetically engineered porcine renal grafts.
4 ness of this classification algorithm on 166 renal grafts.
5 eservation injury and is poorly tolerated by renal grafts.
6    Delayed graft function occurred in 31% of renal grafts.
7 hat CARNs can reconstitute prostate ducts in renal grafts.
8 cute rejection.In patients with a functional renal graft 1 year after transplantation, PTDM was assoc
9                                  Forty-eight renal grafts (65.8%), thirteen livers (61.9%), and one p
10 nduces tubular and endothelial damage in the renal graft and leads to delayed graft function (DGF) an
11 lantation has a negative impact on long-term renal graft and patient survival.
12 issue recombinants were grown as subcapsular renal grafts and treated from the time of grafting with
13 oimmunized transplant patients with a failed renal graft; and second to understand the correlation be
14 um Cr at discharge and at last follow-up for renal grafts are 4.3+/-0.5 and 1.9+/-0.3 mg/dl, respecti
15 This study shows that FTIR-based analysis of renal graft biopsy specimens is a reproducible and relia
16                 In the independent set of 74 renal graft biopsy specimens, the EndMT markers for the
17 ivo could enhance the marginal donor pool of renal grafts by preventing graft loss due to ischemia.
18  option for donation after circulatory death renal grafts compared with conventional hypothermic meth
19 ine genes in mononuclear cells purified from renal grafts confirmed the initial observations made on
20  severe ischemia-reperfusion injury (IRI) to renal grafts, contributing to delayed graft function (DG
21 wed markedly prolonged survival of the naive renal grafts (day 28, >150 and >150 days).
22     BACKGROUND DATA: Delayed function of the renal graft (DGF), which can result from hypotension and
23 erm tolerant in recipients bearing long-term renal grafts did not break tolerance.
24 otein 47 strongly, whereas those from normal renal grafts did not.
25  predicted late (up to 4 years after biopsy) renal graft dysfunction and proteinuria.
26                                              Renal graft dysfunction was seen in 11 of 25 (44%) cases
27       Among the 351 survivors, 19% sustained renal graft dysfunction, and there were 13 (4%) graft lo
28 iopsies are the gold standard for evaluating renal graft dysfunction.
29 first time that Xe confers renoprotection on renal grafts ex vivo and is likely to stabilize cellular
30 could be rescued by three different methods: renal grafting, explant culture in the presence of andro
31 e protein (P=0.036) and after adjustment for renal graft failure (P=0.001).
32 CMV infection (risk ratio [RR] 2.5; P<0.02), renal graft failure (RR 2.41; P=0.05), pancreas graft fa
33               However, CRS failed to prevent renal graft failure after 48 hr of cold storage (14% sur
34 ids--seem to be more efficient in preventing renal graft failure than nondepleting agents (basilixima
35 ransplant Recipients who were relisted after renal graft failure with new, unacceptable antigens corr
36 dney disease increases the risk of death and renal graft failure, yet patients with hepatitis C and c
37 ation and factors contributing to subsequent renal graft failure.
38       The increased utilization of high-risk renal grafts for transplantation requires optimization o
39                We previously showed accepted renal grafts form aggregates containing various immune c
40 nce of BKPyV reactivation in recipients of a renal graft from a donor carrying the MICA A5.1 mutant,
41 5(+) sorted cells from accepted and rejected renal grafts from 1-week to 6-months posttransplant.
42 ined procurement of hepatic, pancreatic, and renal grafts from a controlled NHBD with right replaced
43 n changes and preserved significantly better renal graft function after transplantation.
44 iew the evidence relating acute rejection to renal graft function and graft survival.
45 CMV) activation is associated with decreased renal graft function and survival.
46                       Deleterious effects on renal graft function are described for hypothermic prese
47  mitochondria, and achieve an improved early renal graft function compared with standard HMP or oxyge
48 ss skin grafts by day 25, without changes in renal graft function or antidonor in vitro responses.
49  cold preservation frequently causes delayed renal graft function resulting from tubular epithelial i
50   SPLK recipients had lower rates of delayed renal graft function than SPK recipients.
51                                              Renal graft function was assessed by plasma creatinine l
52     In a mouse kidney transplantation model, renal graft function was improved by more than 50% with
53                       All patients recovered renal graft function within 8 weeks posttransplant.
54                 Our data clearly show stable renal graft function without long-term immunosuppression
55 as also associated with a steeper decline in renal graft function, a higher risk of acute rejections
56 ell as subsequent restoration of near-normal renal graft function, leading to long-term kidney allogr
57                                              Renal graft function, structure, and survival are not di
58 kidney disease (PKD) had excellent long-term renal graft function, they had an increased incidence of
59  30 SPLK transplants, 29 (97%) had immediate renal graft function, whereas 79% of SPK kidneys had imm
60  pool, and improved short-term and long-term renal graft function.
61             To date all patients have stable renal graft function.
62 ansplant, which may result in improved early renal graft function.
63 tcome of RTRs without detrimental effects on renal graft function.
64                     Liver allograft provided renal graft immunoprotection if both organs are transpla
65    The spectrum of renal lesions observed on renal grafts in this context remains to be determined.
66 ufficient for respecification to prostate in renal grafts in vivo.
67  was assessed in intravascular leukocytes of renal grafts, in graft tissue and in recipient blood pla
68 nation with the recipient hepatic artery for renal graft inflow.
69 endent pathogenic role for MICA in long-term renal graft injury and question the interest of posttran
70   Immune tolerance to MHC class II identical renal grafts is achievable in miniature swine following
71                                              Renal graft ischemic injuries that occur before and afte
72  (BKV) nephropathy remains the main cause of renal graft loss after living-donor renal transplantatio
73 ent, potentially remediable, risk factor for renal graft loss and all-cause mortality in RTR.
74 011, we estimated overall and death-censored renal graft loss hazard ratios in patients diagnosed wit
75  nephropathy (BKVN) is an important cause of renal graft loss in recent years.
76 eased risk of overall but not death-censored renal graft loss in renal transplant recipients with PTD
77 sting of death, major cardiovascular events, renal graft loss or creatinine doubling, and survival fr
78               There was a lower incidence of renal graft loss resulting from chronic rejection among
79 ysis, SDMA was significantly associated with renal graft loss, all-cause death, and major cardiovascu
80 PTH) levels and major cardiovascular events, renal graft loss, and all-cause mortality by Cox Proport
81 s mellitus (PTDM) is associated with overall renal graft loss, but not death-censored graft loss.
82 th increased risk of all-cause mortality and renal graft loss.
83 ys after transplantation was associated with renal graft loss.
84 quartile, >1.38 mumol/L) was associated with renal graft loss; hazard ratio (HR), 5.51; 95% confidenc
85 , a higher risk of acute rejections and more renal grafts lost due to acute rejection.In patients wit
86 er host alloresponsiveness in an LBNF1-Lewis renal graft model by treatment with sPSGL in combination
87 l and blood glucose control in a subcapsular renal graft model in immuno-incompetent diabetic mice.
88                                              Renal grafts obtained from living donors (LD) typically
89                                        While renal grafts of Wnt5a(-/-) murine prostates revealed tha
90 oantibodies are known to be a risk factor in renal graft outcome.
91 g-donor kidney transplantation does not harm renal graft outcome.
92 class I chain-related A (MICA) antibodies on renal graft outcomes is unclear.
93 wo commercially available kits, on long-term renal graft outcomes.
94                   After autotransplantation, renal grafts preserved with NEVKP demonstrated lower ser
95 renal ischemia-reperfusion injury and confer renal graft protection.
96                                In total, 119 renal graft recipients experiencing a first biopsy-prove
97 e pharmacoepidemiological study, 718 de novo renal graft recipients treated with SRL in 65 centers in
98 TTB) is a serious opportunistic infection in renal graft recipients with a 30-70 fold higher incidenc
99 araffin-embedded tissue sections coming from renal graft recipients.
100 720 is a sphingosine analog that can prevent renal graft rejections and suppress a variety of autoimm
101                     However, the shortage of renal grafts remains a big challenge.
102                            PKD recipients of renal grafts should be watched closely early after trans
103                                Monitoring of renal graft status through peripheral blood (PB) rather
104 ass of biomarkers for frequent evaluation of renal graft status.
105  versus 13% reduction; P<0.05) and prolonged renal graft survival (28.0 days versus 5.2 days; P<0.01)
106 re was no difference in mortality (P>0.6) or renal graft survival (P>0.6) between the PKD-GI and PKD-
107 fferent in KPR and KR, but the correlates of renal graft survival are different in these two groups o
108                              In KPR, reduced renal graft survival did not correlate with AR (P=0.44),
109 t of graft donors or of recipients prolonged renal graft survival following IRI in both Lewis-to-Lewi
110 retransplant HD adversely affected pediatric renal graft survival in a linear manner.
111 controlled hypertension correlates with poor renal graft survival in African-Americans.
112 ere is a paucity of data regarding long-term renal graft survival in hepatitis C virus positive (HCV+
113 f donor/recipient size mismatch on long-term renal graft survival in pediatric patients undergoing li
114            One and three-year rejection-free renal graft survival of KALT and CLKT groups were differ
115 ched and sensitized patients, rejection-free renal graft survival of KALT group was inferior to the C
116                                              Renal graft survival rates after SPK have been less well
117                                  With 1 year renal graft survival rates of greater than 90% the best
118        The PKD patients had better long-term renal graft survival than the non-PKD patients (P=0.08).
119 ute and chronic rejection and rejection-free renal graft survival was compared between two groups.
120   Clinical, biopsy, and demographic data and renal graft survival were compared, and the association
121 have been implicated in decreasing long-term renal graft survival.
122 required to protect the graft and to prolong renal graft survival.
123        There are known racial disparities in renal graft survival.
124  antithrombotic therapy in the prevention of renal graft thrombosis are scarce.
125 days, the main cause for early graft loss is renal graft thrombosis because kidney transplant outcome
126  in combination with chemical inhibitors and renal grafting to clarify the role of Hh signaling in pr
127 derwent retransplantation after losing their renal grafts to BK virus-associated nephropathy (BKAN) a
128 s in 843 adult recipients of first cadaveric renal grafts, transplanted at a single institution and f
129 ws convincing results for treating malignant renal graft tumors and should be a useful treatment opti
130 ion of fibrosis and its functional impact on renal grafts, we compared 76 uDCD recipients with 86 rec
131                               A total of 893 renal grafts were lost during the study period, either d
132                                A total of 82 renal grafts were perfused with VSL, and 80 were perfuse
133                                    Lewis rat renal grafts were stored in Soltran preservative solutio
134                                          SPK renal grafts were transplanted with a shorter cold ische
135 rarely compromises kidney function except in renal grafts, where it causes a tubulointerstitial infla
136 ses ischemia-reperfusion injury (IRI) in the renal graft, which is considered to contribute to the oc
137  from the same donor (184 KPT/184 KT), i.e., renal grafts with the same pretransplant functional and

 
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