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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
10 nduces tubular and endothelial damage in the renal graft and leads to delayed graft function (DGF) an
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
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
22 BACKGROUND DATA: Delayed function of the renal graft (DGF), which can result from hypotension and
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
32 CMV infection (risk ratio [RR] 2.5; P<0.02), renal graft failure (RR 2.41; P=0.05), pancreas graft fa
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
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
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
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
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
67 was assessed in intravascular leukocytes of renal grafts, in graft tissue and in recipient blood pla
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
72 (BKV) nephropathy remains the main cause of renal graft loss after living-donor renal transplantatio
74 011, we estimated overall and death-censored renal graft loss hazard ratios in patients diagnosed wit
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
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.
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.
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
100 720 is a sphingosine analog that can prevent renal graft rejections and suppress a variety of autoimm
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
109 t of graft donors or of recipients prolonged renal graft survival following IRI in both Lewis-to-Lewi
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
115 ched and sensitized patients, rejection-free renal graft survival of KALT group was inferior to the C
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
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
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