ライフサイエンスコーパス: renal graft

1 ike replacement drug, and with a functioning renal graft).

2 relate with the ischemic time imposed on the renal graft.

3 ness of this classification algorithm on 166 renal grafts.

4 eservation injury and is poorly tolerated by renal grafts.

5 Delayed graft function occurred in 31% of renal grafts.

6 hat CARNs can reconstitute prostate ducts in renal grafts.

7 cute rejection.In patients with a functional renal graft 1 year after transplantation, PTDM was assoc

8 Forty-eight renal grafts (65.8%), thirteen livers (61.9%), and one p

9 nduces tubular and endothelial damage in the renal graft and leads to delayed graft function (DGF) an

10 lantation has a negative impact on long-term renal graft and patient survival.

11 issue recombinants were grown as subcapsular renal grafts and treated from the time of grafting with

12 oimmunized transplant patients with a failed renal graft; and second to understand the correlation be

13 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

14 This study shows that FTIR-based analysis of renal graft biopsy specimens is a reproducible and relia

15 In the independent set of 74 renal graft biopsy specimens, the EndMT markers for the

16 ivo could enhance the marginal donor pool of renal grafts by preventing graft loss due to ischemia.

17 ine genes in mononuclear cells purified from renal grafts confirmed the initial observations made on

18 severe ischemia-reperfusion injury (IRI) to renal grafts, contributing to delayed graft function (DG

19 wed markedly prolonged survival of the naive renal grafts (day 28, >150 and >150 days).

20 BACKGROUND DATA: Delayed function of the renal graft (DGF), which can result from hypotension and

21 erm tolerant in recipients bearing long-term renal grafts did not break tolerance.

22 otein 47 strongly, whereas those from normal renal grafts did not.

23 predicted late (up to 4 years after biopsy) renal graft dysfunction and proteinuria.

24 iopsies are the gold standard for evaluating renal graft dysfunction.

25 first time that Xe confers renoprotection on renal grafts ex vivo and is likely to stabilize cellular

26 could be rescued by three different methods: renal grafting, explant culture in the presence of andro

27 e protein (P=0.036) and after adjustment for renal graft failure (P=0.001).

28 CMV infection (risk ratio [RR] 2.5; P<0.02), renal graft failure (RR 2.41; P=0.05), pancreas graft fa

29 However, CRS failed to prevent renal graft failure after 48 hr of cold storage (14% sur

30 ids--seem to be more efficient in preventing renal graft failure than nondepleting agents (basilixima

31 dney disease increases the risk of death and renal graft failure, yet patients with hepatitis C and c

32 ation and factors contributing to subsequent renal graft failure.

33 nce of BKPyV reactivation in recipients of a renal graft from a donor carrying the MICA A5.1 mutant,

34 ined procurement of hepatic, pancreatic, and renal grafts from a controlled NHBD with right replaced

35 n changes and preserved significantly better renal graft function after transplantation.

36 iew the evidence relating acute rejection to renal graft function and graft survival.

37 CMV) activation is associated with decreased renal graft function and survival.

38 Deleterious effects on renal graft function are described for hypothermic prese

39 ss skin grafts by day 25, without changes in renal graft function or antidonor in vitro responses.

40 cold preservation frequently causes delayed renal graft function resulting from tubular epithelial i

41 SPLK recipients had lower rates of delayed renal graft function than SPK recipients.

42 Renal graft function was assessed by plasma creatinine l

43 All patients recovered renal graft function within 8 weeks posttransplant.

44 as also associated with a steeper decline in renal graft function, a higher risk of acute rejections

45 ell as subsequent restoration of near-normal renal graft function, leading to long-term kidney allogr

46 Renal graft function, structure, and survival are not di

47 kidney disease (PKD) had excellent long-term renal graft function, they had an increased incidence of

48 30 SPLK transplants, 29 (97%) had immediate renal graft function, whereas 79% of SPK kidneys had imm

49 To date all patients have stable renal graft function.

50 tcome of RTRs without detrimental effects on renal graft function.

51 pool, and improved short-term and long-term renal graft function.

52 Liver allograft provided renal graft immunoprotection if both organs are transpla

53 ufficient for respecification to prostate in renal grafts in vivo.

54 was assessed in intravascular leukocytes of renal grafts, in graft tissue and in recipient blood pla

55 endent pathogenic role for MICA in long-term renal graft injury and question the interest of posttran

56 Immune tolerance to MHC class II identical renal grafts is achievable in miniature swine following

57 Renal graft ischemic injuries that occur before and afte

58 (BKV) nephropathy remains the main cause of renal graft loss after living-donor renal transplantatio

59 ent, potentially remediable, risk factor for renal graft loss and all-cause mortality in RTR.

60 011, we estimated overall and death-censored renal graft loss hazard ratios in patients diagnosed wit

61 nephropathy (BKVN) is an important cause of renal graft loss in recent years.

62 eased risk of overall but not death-censored renal graft loss in renal transplant recipients with PTD

63 sting of death, major cardiovascular events, renal graft loss or creatinine doubling, and survival fr

64 There was a lower incidence of renal graft loss resulting from chronic rejection among

65 ysis, SDMA was significantly associated with renal graft loss, all-cause death, and major cardiovascu

66 PTH) levels and major cardiovascular events, renal graft loss, and all-cause mortality by Cox Proport

67 s mellitus (PTDM) is associated with overall renal graft loss, but not death-censored graft loss.

68 th increased risk of all-cause mortality and renal graft loss.

69 ys after transplantation was associated with renal graft loss.

70 quartile, >1.38 mumol/L) was associated with renal graft loss; hazard ratio (HR), 5.51; 95% confidenc

71 , a higher risk of acute rejections and more renal grafts lost due to acute rejection.In patients wit

72 er host alloresponsiveness in an LBNF1-Lewis renal graft model by treatment with sPSGL in combination

73 l and blood glucose control in a subcapsular renal graft model in immuno-incompetent diabetic mice.

74 While renal grafts of Wnt5a(-/-) murine prostates revealed tha

75 oantibodies are known to be a risk factor in renal graft outcome.

76 g-donor kidney transplantation does not harm renal graft outcome.

77 class I chain-related A (MICA) antibodies on renal graft outcomes is unclear.

78 wo commercially available kits, on long-term renal graft outcomes.

79 After autotransplantation, renal grafts preserved with NEVKP demonstrated lower ser

80 renal ischemia-reperfusion injury and confer renal graft protection.

81 In total, 119 renal graft recipients experiencing a first biopsy-prove

82 e pharmacoepidemiological study, 718 de novo renal graft recipients treated with SRL in 65 centers in

83 TTB) is a serious opportunistic infection in renal graft recipients with a 30-70 fold higher incidenc

84 720 is a sphingosine analog that can prevent renal graft rejections and suppress a variety of autoimm

85 However, the shortage of renal grafts remains a big challenge.

86 PKD recipients of renal grafts should be watched closely early after trans

87 Monitoring of renal graft status through peripheral blood (PB) rather

88 ass of biomarkers for frequent evaluation of renal graft status.

89 re was no difference in mortality (P>0.6) or renal graft survival (P>0.6) between the PKD-GI and PKD-

90 fferent in KPR and KR, but the correlates of renal graft survival are different in these two groups o

91 In KPR, reduced renal graft survival did not correlate with AR (P=0.44),

92 t of graft donors or of recipients prolonged renal graft survival following IRI in both Lewis-to-Lewi

93 retransplant HD adversely affected pediatric renal graft survival in a linear manner.

94 controlled hypertension correlates with poor renal graft survival in African-Americans.

95 ere is a paucity of data regarding long-term renal graft survival in hepatitis C virus positive (HCV+

96 f donor/recipient size mismatch on long-term renal graft survival in pediatric patients undergoing li

97 One and three-year rejection-free renal graft survival of KALT and CLKT groups were differ

98 ched and sensitized patients, rejection-free renal graft survival of KALT group was inferior to the C

99 Renal graft survival rates after SPK have been less well

100 With 1 year renal graft survival rates of greater than 90% the best

101 The PKD patients had better long-term renal graft survival than the non-PKD patients (P=0.08).

102 ute and chronic rejection and rejection-free renal graft survival was compared between two groups.

103 Clinical, biopsy, and demographic data and renal graft survival were compared, and the association

104 have been implicated in decreasing long-term renal graft survival.

105 required to protect the graft and to prolong renal graft survival.

106 There are known racial disparities in renal graft survival.

107 in combination with chemical inhibitors and renal grafting to clarify the role of Hh signaling in pr

108 derwent retransplantation after losing their renal grafts to BK virus-associated nephropathy (BKAN) a

109 s in 843 adult recipients of first cadaveric renal grafts, transplanted at a single institution and f

110 ion of fibrosis and its functional impact on renal grafts, we compared 76 uDCD recipients with 86 rec

111 A total of 893 renal grafts were lost during the study period, either d

112 A total of 82 renal grafts were perfused with VSL, and 80 were perfuse

113 Lewis rat renal grafts were stored in Soltran preservative solutio

114 SPK renal grafts were transplanted with a shorter cold ische

115 rarely compromises kidney function except in renal grafts, where it causes a tubulointerstitial infla

116 ses ischemia-reperfusion injury (IRI) in the renal graft, which is considered to contribute to the oc

117 from the same donor (184 KPT/184 KT), i.e., renal grafts with the same pretransplant functional and