Disease relevance of Graft Survival

• Glomerulonephritis patients transplanted with cadaver kidneys had a significantly higher one-year graft survival when immunosuppressed with cyclosporin rather than standard therapy (80% versus 59%, p less than 10(-5] [1].
• Neither patient nor graft survival was significantly affected by the presence of either GBV-C RNA or anti-E2 antibody before OLT [2].
• Metallothionein protects islets from hypoxia and extends islet graft survival by scavenging most kinds of reactive oxygen species [3].
• Diltiazem given both to donor grafts and to recipients produced a significant reduction in the rate of delayed graft function but failed to improve one-year graft survival [4].
• Daily treatment with losartan but not lacidipine resulted in a significant decrease in the amount of proteinuria, preserved glomerular and tubulointerstitial structure, and improved graft survival compared with corresponding parameters in control untreated rats [5].

High impact information on Graft Survival

• Kidney-transplant data from the United Network for Organ Sharing Renal Transplant Registry were used to calculate graft-survival rates with Kaplan-Meier analysis [6].
• With national kidney sharing, the projected 10-year rate of graft survival for transplants in which there were no HLA-A, B, or DR mismatches was 66 percent, as compared with 39 percent for transplants with more than two HLA-A, B, or DR mismatches [7].
• We analyzed the effect of matching for HLA-B and HLA-DR antigens on graft survival in patients treated with cyclosporine [8].
• We conclude that the two cyclosporine regimens result in comparable patient and graft survival, but that changing to azathioprine and prednisolone at three months improves graft function [9].
• Here we examined the effects of caspase inhibition by Ac-YVAD-cmk on cell death immediately after donor tissue preparation and on long-term graft survival [10].

Chemical compound and disease context of Graft Survival

• The spontaneous risk for viral recurrence after transplantation is high but has been effectively decreased in hepatitis B infected recipients with the use of HBIG and lamivudine with dramatic improvements in patient and graft survivals [11].
• Although the data are incomplete, the use of cyclosporine may not confer the advantage of improving graft survival in patients with systemic sclerosis as compared with SLE patients [12].
• No significant differences between groups existed for serum creatinine levels, presence of significant proteinuria, or 1- and 5-year graft survival [13].
• CONCLUSION: Aspirin reduced the rate of early graft thrombosis of renal transplants in this series but did not improve renal function or graft survival [14].
• Motor function, graft survival and gliosis in rats with 6-OHDA lesions and foetal ventral mesencephalic grafts chronically treated with L-dopa and carbidopa [15].

Biological context of Graft Survival

• We determined if the implantation of murine MSCs engineered to release erythropoietin (Epo) would be feasible in major histocompatibility complex (MHC)-mismatched allogeneic mice without immunosuppression, and we monitored hematocrit (Hct) as a reporter of MSC graft survival [16].
• Furthermore, depletion of IGRP206-214-specific CD8+ T cells by peptide administration delayed islet graft survival, suggesting IGRP206-214-specific CD8+ T cells play a role early in islet graft rejection but are displaced with time by other specificities, perhaps by epitope spread [17].
• While the combination of anti-CD154 antibody with blockade of the CD28 pathway reduced donor antibody production, graft survival was not significantly improved over that achieved with anti-CD154 antibody alone [18].
• METHODS: Data from two multicenter, randomized, placebo-controlled trials were evaluated with regard to graft survival, patient survival, incidence of malignancies (including lymphoma), renal function (serum creatinine and glomerular filtration rate [GFR]), and current maintenance immunosuppressive regimen [19].
• Effect of major histocompatibility complex expression on murine intestinal graft survival [20].

Anatomical context of Graft Survival

• P-selectin-null hearts transplanted into wild-type recipients demonstrated a marked (13-fold) reduction in graft neutrophil infiltration and increased graft survival compared with wild-type hearts transplanted into wild-type recipients [21].
• Recipient lymphocyte sensitivity to methylprednisolone affects cadaver kidney graft survival [22].
• Repetitive intraperitoneal injection of Enbrel, a TNF receptor blocker, significantly decreased hepatocyte 8-OHdG levels and the frequency of deleted mtDNA while greatly extending graft survival time [23].
• Disruption of CD154-CD40 signaling in recipients at the T cell side (CD154-deficient) but not at the APC side (CD40-deficient) abrogated accelerated (<2 days) rejection and resulted in long-term (>100 days) graft survival [24].
• Addition of a single treatment with cyclosporin A after pretransplant immunization via the portal vein led to indefinite graft survival in over 70% of recipients [25].

Associations of Graft Survival with chemical compounds

• Perfusion of the donor animal before thyroidotomy and the addition of fetal calf serum to the culture medium did not have a significant effect on graft survival, but the percentage of grafts lacking generalized infiltration was slightly increased by the addition of hydrocortisone to the culture medium [26].
• Treatment of these recipients with as little as 1.5 mg/kg cyclophosphamide for 14 d induces prolonged graft survival [27].
• Aminoguanidine treatment prolonged graft survival, improved graft contractile function, and significantly reduced the histologic grade of rejection [28].
• In the absence of cyclosporin A (CsA), there was no difference in graft survival time between CX(3)CR1(-/-) and CX(3)CR1(+/+) recipient mice [29].
• Two additional in vivo parameters of cellular immunologic reactivity were examined in streptozotocin-induced diabetes: delayed footpad swelling was essentially eliminated; skin graft survival across the H-2 area was significantly prolonged from 10.2 days in the controls to 14.4 days in moderately diabetic A/J mice [30].

Gene context of Graft Survival

• Decreased graft survival in IL-10 -/- recipients was associated with increases in iNOS and IFN-gamma-driven responses [31].
• In wild-type and IL-4 -/- recipients immunosuppressed with a 30-d course of anti-CD4 and anti-CD8, graft survival was > 87 d [31].
• Treatment of the recipients with donor splenocytes and a single dose of anti-CD40L mAb induces long-term graft survival (> 100 days) in all animals [32].
• A clinical relevance of these findings is suggested by the observation that matching for HLA-B antigens is of greater importance for kidney graft survival than matching for HLA-A [33].
• Mismatching for HLA-B and DR antigens was also found to correlate with transplant survival in highly sensitized patients and in patients transplanted since 1981, the "cyclosporine era." Recipients who were HLA-DR1 positive were found to have the highest graft survival compared to recipients negative for this antigen [34].

Analytical, diagnostic and therapeutic context of Graft Survival

• During the transplantation hospitalization period, cyclosporine was associated with significantly better graft survival (88.7% vs 71.0%) and lower (standardized) costs ($37,174 vs $52,983) [35].
• Finally, administration of CTLA4-Ig to CD28/CTLA4(-/-) cardiac allograft recipients significantly prolongs graft survival [36].
• Systemic lupus erythematosus after renal transplantation: patient and graft survival and disease activity. The Dutch Working Party on Systemic Lupus Erythematosus [37].
• Transient macrophage inhibition, particularly in hepatic Kupffer cells, is associated with significant prolongation of graft survival after intraportal islet allotransplantation (ITx) in rats: 7.2 days in the control group versus 11.9 days in the GdCl3 group (P < 0.01) and 15.6 days in the Cl2MDP group (P < 0.0006), respectively [38].
• Cyclosporine (CsA), an immunosuppressive cyclic endecapeptide utilized to prolong graft survival in human organ transplant patients, affects PRL binding to MNC [39].

References