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• W2028105877 abstract "Related Article, p. 1061 In the past decade, our increasing success at preventing acute renal allograft rejection has resulted in rejection rates of less than 20% and 1-year graft survivals of more than 90%.1Halloran P Mathew T Tomlanovich S Groth C Hooftman L Barker C Mycophenolate mofetil in renal allograft recipients: A pooled efficacy analysis of three randomized, double-blind, clinical studies in prevention of rejection.Transplantation. 1997; 63 (The International Mycophenolate Mofetil Renal Transplant Study Groups): 39-47Crossref PubMed Scopus (536) Google Scholar, 2Kahan BD Efficacy of sirolimus compared with azathioprine for reduction of acute renal allograft rejection: A randomised multicentre study.Lancet. 2000; 356 (The Rapamune US Study Group): 194-202Abstract Full Text Full Text PDF PubMed Scopus (860) Google Scholar This success has led us to focus on the improvement in long-term allograft survival, the prevention of diseases previously accounting for a relatively small percentage of graft loss, and the adjustment of immunosuppression to the individual need. Currently, all patients are treated with broad-spectrum immunosuppression with their myriad side effects. Yet, we know that some patients may discontinue or substantially lower immunosuppression without suffering any ill effects. The description of polymorphisms in many of the key immunoregulatory molecules involved in the rejection process has offered a possible explanation for the individual variation in susceptibility to rejection and differences in allograft survival independent of the many known contributory factors. Several interesting observations have been made that would suggest that genetic variability influencing allograft survival reaches beyond that of the major histocompatibility complex (MHC) molecules.3Akalin E Murphy B Gene polymorphisms and transplantation.Curr Opin Immunol. 2001; 13: 572-576Crossref PubMed Scopus (75) Google Scholar The influences of polymorphisms in cytokines, cytokine receptors, chemokines, adhesion molecules, and costimulatory molecules are among some of those studied in relation to outcomes in transplantation. However, results have differed with the organ transplanted and between investigators. For example, the −308 G/A polymorphism in the tumor necrosis factor-α (TNF-α) promoter and the −1082 G/A polymorphism in the interleukin-10 (IL-10) promoter, both with known functional differences in production, have been studied in kidney, kidney pancreas, cardiac, and liver transplant recipients. The combination of a high production of TNF-α with low IL-10 production was associated with acute rejection in heart transplant patients, whereas high producers of both TNF-α and IL-10 were associated with acute rejection in renal transplant patients.4Sankaran D Asderakis A Ashraf S Roberts ISD Short CD Dyer PA Sinnott PJ Hutshinson IV Cytokine gene plymorphisms predict acute graft rejection following renal transplantation.Kidney Int. 1999; 56: 281-288Crossref PubMed Scopus (274) Google Scholar, 5Turner D Grant SCD Yonan N Sheldon S Dyer PA Sinnott PJ Hutchinson IV Cytokine gene polymorphisms and heart transplant rejection.Transplantation. 1997; 64: 776-779Crossref PubMed Scopus (236) Google Scholar An increased rate of rejection was seen with high TNF-α production in liver and kidney/pancreas transplant recipients, but no effect was seen with IL-10.6Bathgate AJ Pravica V Perrey C Therapondos G Plevris JN Hayes PC Hutchinson IV The effect of polymorphisms in tumor necrosis factor-α, interleukin-10, and transforming growth factor-β1 genes in acute hepatic allograft rejection.Transplantation. 2000; 69: 1514-1517Crossref PubMed Scopus (96) Google Scholar, 7Pelletier R Pravica V Perrey C Xia D Ferguson RM Hutchinson IV Orosz C Evidence for a genetic predispostion towards acute rejection after kidney and simultaneous kidney-pancreas transplantation.Transplantation. 2000; 70: 674-680Crossref PubMed Scopus (91) Google Scholar Other groups have failed to demonstrate any association between TNF-α, IL-10, and acute rejection.8Marshall SE McLaren AJ Haldar NA Bunce M Morris PJ Welsh KI The impact of recipient cytokine genotype on acute rejection after renal transplantation.Transplantation. 2000; 70: 1485-1491Crossref PubMed Scopus (78) Google Scholar, 9Poli F Boschiero L Giannoni F Tonini M Scalamogna M Ancona G Sirchia G Tumour necrosis factor-alpha gene polymorphism: Implications in kidney transplantation.Cytokine. 2000; 12: 1778-1783Crossref PubMed Scopus (55) Google Scholar An increased susceptibility to acute rejection was found in association with a polymorphism in the costimulatory molecule CTLA-4 in liver and renal transplant recipients.10Slavcheva E, Efsevia A, Qingsheng J, Huong T, Bodian C, Knight R, Milford E, Schiano T, Tomer Y, Murphy B: CTLA-4 gene polymorphisms and susceptibility to acute allograft rejection. Transplantation (in press)Google Scholar A functional role for polymorphisms has also been implicated in the chronic rejection process. Polymorphisms in both interferon-γ (IFN-γ) and transforming growth factor-β (TGF-β) have been associated with allograft fibrosis in lung transplant recipients.11Awad MR El-Gamel A Hasleton P Turner DM Sinnott PJ Hutchinson IV Genotypic variation in the transforming growth factor-β1 gene.Transplantation. 1998; 66: 1014-1020Crossref PubMed Scopus (611) Google Scholar, 12Awad M Pravica V Perrey C El Gamel A Yonan N Sinnott PJ Hutchinson IV CA repeat allele polymoprhism in the first intron of the human interferon-γ gene is associated with lung allograft fibrosis.Hum Immunol. 1999; 60: 343-346Crossref PubMed Scopus (114) Google Scholar Two polymorphism in the adhesion molecule intercellular cell adhesion moledule-1 (ICAM-1) have been associated with increased chronic renal allograft dysfunction,13McLaren AJ Marshall SE Haldar NA Mullighan CG Fuggle SV Morris PJ Welsh KI Adhesion molecule polymorphism in chronic renal allograft failure.Kidney Int. 1999; 55: 1977-1982Crossref PubMed Scopus (94) Google Scholar while one of these polymorphism in ICAM-1 was found to have a protective effect with regard to chronic rejection in cardiac transplant recipients.14Borozdenkova S Smith J Marshall S Yacoub M Rose M Identification of ICAM-1 polymorphism that is associated with protection from transplant associated vasculopathy after cardiac transplantation.Hum Immunol. 2001; 62: 247-255Crossref PubMed Scopus (50) Google Scholar These data are just some of the increasing evidence that there is some validity to the hypothesis that polymorphisms in immunoregulatory molecules contribute to the heterogeneity in outcomes after transplantation. But, as with any complex genetic trait, it is the sum of many genotypes in the context of differing environmental or external influences, such as immunosuppressive protocols, that will determine the ultimate disease phenotype or pattern. The studies discussed above and others provide evidence for potential organ-specific effects, with differences between patient population and immunosuppressive protocols possibly accounting for the different outcomes between studies. Indeed, it is not just genetic variation in immunoregulatory molecules that may influence the outcome of transplant recipients. Barocci et al15Barocci S Ginevri F Valente U Torre F Gusmano R Nocera A Correlation between angiotensin-converting enzyme gene insertion/deletion polymorphism and kidney graft long-term outcome in pediatric recipients: A single-center analysis.Transplantation. 1999; 67: 534-538Crossref PubMed Scopus (40) Google Scholar have shown that the DD genotype of the ACE gene was associated with a shorter graft survival in 142 pediatric renal transplant patients, which may indicate a role for this genotype in the progression of non-antigenic injury leading to chronic allograft failure. In this issue of the Journal, Fischereder et al16Fischereder M Schneeberger H Lohse P Krämer BK Schlöndorff D Land W Increased rate of renal transplant failure in patients with the G20210A mutation of the prothrombin gene.Am J Kidney Dis. 2001; 38: 1061-1064Abstract Full Text Full Text PDF PubMed Scopus (38) Google Scholar retrospectively examine the outcomes of renal transplant recipients with respect to a known polymorphism in the prothrombin gene. The G20210A mutation in the 3′ untranslated region of the prothrombin gene occurs in 1% to 2% of the population and results in increased circulating levels of prothrombin with an associated increased risk of venous thrombosis and possible arterial thromboembolic phenomenon. In this study, 270 patients with a total of 311 transplants were geneotyped for the mutation and graft outcomes were analyzed. Nine patients accounting for 12 transplants were heterozygous for the mutant. Three of these transplants were lost to thrombotic events and 2 were lost to chronic rejection. Allograft survival was decreased in patients heterozygous for the mutant, with a mean graft survival of 65.9 as compared with 149 months for those homozygous for the wild-type 20210. Data delineating the cause of graft loss in the other recipients are not provided. Fischereder et al16Fischereder M Schneeberger H Lohse P Krämer BK Schlöndorff D Land W Increased rate of renal transplant failure in patients with the G20210A mutation of the prothrombin gene.Am J Kidney Dis. 2001; 38: 1061-1064Abstract Full Text Full Text PDF PubMed Scopus (38) Google Scholar demonstrate that G20210A is associated with a 2.95-fold increased risk for allograft loss. Oh et al17Oh J Schaefer F Veldmann A Nowak G Nowak-Gottl U Tonshoff B Kreuz W Heterozygous prothrombin gene mutation: A new risk factor for early renal allograft thrombosis.Transplantation. 1999; 68: 575-578Crossref PubMed Scopus (42) Google Scholar previously published a case series in which 2 patients heterozygous for G20210A in the prothrombin gene, with a total of 3 renal transplants, experienced graft loss due to thrombosis perioperatively in all 3 allografts. One of the patients receiving hemodialysis had a significant history of arteriovenous graft thrombosis before transplantation. Several other studies lend further support to the importance of a genetic tendency toward thrombophilia on allograft survival.18Fischereder M Gohring P Schneeberger H Lohse P Von Appen K Samtleben W Schlondorff D Land W Early loss of renal transplants in patients with thrombophilia.Transplantation. 1998; 65: 936-939Crossref PubMed Scopus (64) Google Scholar, 19Wuthrich RP Cicvara-Muzar S Booy C Maly FE Heterozygosity for the factor V Leiden (G1691A) mutation predisposes renal transplant recipients to thrombotic complications and graft loss.Transplantation. 2001; 72: 549-550Crossref PubMed Scopus (43) Google Scholar In a cohort of 202 renal transplant patients, Wuthrich et al19Wuthrich RP Cicvara-Muzar S Booy C Maly FE Heterozygosity for the factor V Leiden (G1691A) mutation predisposes renal transplant recipients to thrombotic complications and graft loss.Transplantation. 2001; 72: 549-550Crossref PubMed Scopus (43) Google Scholar found that patients heterozygous for factor V mutant (factor V Leiden) were at higher risk of intraoperative perfusion difficulties, and 2 of 8 grafts were lost to vascular thrombosis in the early postoperative period. Fischereder et al16Fischereder M Schneeberger H Lohse P Krämer BK Schlöndorff D Land W Increased rate of renal transplant failure in patients with the G20210A mutation of the prothrombin gene.Am J Kidney Dis. 2001; 38: 1061-1064Abstract Full Text Full Text PDF PubMed Scopus (38) Google Scholar suggest that their initial results provide the basis to screen renal transplant recipients before transplantation. While their results are indeed suggestive of the clinical significance of the G20210A mutant, issues that must be considered are the validation of these results with a larger number of patients and the cost benefit ratio of screening all renal transplant candidates for a genetic mutation that occurs in 1% to 2% of the population. Greater benefit may be gained by focusing on patients with a known history of thrombotic events. However, in this initial study, Fischereder et al16Fischereder M Schneeberger H Lohse P Krämer BK Schlöndorff D Land W Increased rate of renal transplant failure in patients with the G20210A mutation of the prothrombin gene.Am J Kidney Dis. 2001; 38: 1061-1064Abstract Full Text Full Text PDF PubMed Scopus (38) Google Scholar have not provided us with information concerning the presence or absence of a prior history of thrombosis in the 9 patients with the G20210A mutant. Interestingly, patients with the G20210A mutant have a decreased graft survival, with a maximum of 101 months compared with 237 months for those patients homozygous for wild type. The contribution of platelet activation and thrombophilia to an increased incidence of both acute rejection and also decreased long-term allograft survival has been implied in previous studies.18Fischereder M Gohring P Schneeberger H Lohse P Von Appen K Samtleben W Schlondorff D Land W Early loss of renal transplants in patients with thrombophilia.Transplantation. 1998; 65: 936-939Crossref PubMed Scopus (64) Google Scholar, 19Wuthrich RP Cicvara-Muzar S Booy C Maly FE Heterozygosity for the factor V Leiden (G1691A) mutation predisposes renal transplant recipients to thrombotic complications and graft loss.Transplantation. 2001; 72: 549-550Crossref PubMed Scopus (43) Google Scholar, 20Salido E Martin B Barrios Y Linares JD Hernandez D Cobos M Checa MD Hortal L Fernandez A Garcia JJ Torres A The PlA2 polymorphism of the platelet glycoprotein IIIA gene as a risk factor for acute renal allograft rejection.J Am Soc Nephrol. 1999; 10: 2599-2605PubMed Google Scholar Although direct clinical data is lacking, the hypothesis is substantiated by experimental evidence that platelet aggregation and activation may lead to activation of endothelial cells and the subsequent expression of prothrombotic and proinflammatory mediators, thereby inducing endothelial injury and vascular disease.21Bustos M Saadi S Platt JL Platelet-mediated activation of endothelial cells: Implications for the pathogenesis of transplant rejection.Transplantation. 2001; 72: 509-515Crossref PubMed Scopus (42) Google Scholar With our growing understanding of the pathways involved in the rejection processes, an increasing number of candidate genes are being identified. Moreover, it now seems apparent that potential genes of interest extend beyond those directly involved in the immune response and may include genes involved in nonimmunological responses and drug metabolism.22Danesi R Mosca M Boggi U Mosca F Del Tacca M Genetics of drug response to immunosuppressive treatment and prospects for personalized therapy.Mol Med Today. 2000; 6: 475-482Abstract Full Text Full Text PDF PubMed Scopus (26) Google Scholar Indeed, there is evidence that genetic polymorphisms may influence the propensity of an individual to develop certain posttransplant complications such as lymphoproliferative disorders, bone loss, diabetes mellitus, and recurrence of the original disease.23Cesarman E Chadburn A Liu YF Migliazza A Dalla-Favera R Knowles DM BCL-6 gene mutations in posttransplantation lymphoproliferative disorders predict response to therapy and clinical outcome.Blood. 1998; 92: 2294-2302PubMed Google Scholar, 24Hay JE Vitamin D receptor polymorphism and posttransplantation bone loss.Liver Transpl. 2001; 7: 68-69Crossref PubMed Scopus (9) Google Scholar, 25Nam JH Lee HC Kim YH Cha BS Song YD Lim SK Kim KR Huh KB Identification of glucokinase mutation in subjects with post-renal transplantation diabetes mellitus.Diabetes Res Clin Pract. 2000; 50: 169-176Abstract Full Text Full Text PDF PubMed Scopus (8) Google Scholar, 26Zein NN Tumor necrosis factor gene promoter polymorphism and recurrent hepatitis C after liver transplantation: The missing link to pathogenesis or a casual association?.Liver Transpl. 2000; 6: 381-383Crossref PubMed Scopus (4) Google Scholar While new technologies now allow the typing of patients on a large-scale basis for multiple polymorphisms, thereby making genetic screening clinically feasible, this area of investigation is in its infancy. The studies to date are association studies and, therefore, do not differentiate effects of neighboring genes. More extensive genetic studies will be required to establish a definitive causal effect of a candidate gene from potential linkage disequilibrium with another gene. Hence, it is premature at present to use either recipient or donor genotyping to predict transplant outcomes or to alter therapy. Nonetheless, the initial studies provide the rationale to further investigate associations already identified and to extend the studies to other candidate genes. Greater success may initially be experienced with specific pathological entities such as the thrombotic events discussed in Fischereder et al16Fischereder M Schneeberger H Lohse P Krämer BK Schlöndorff D Land W Increased rate of renal transplant failure in patients with the G20210A mutation of the prothrombin gene.Am J Kidney Dis. 2001; 38: 1061-1064Abstract Full Text Full Text PDF PubMed Scopus (38) Google Scholar as opposed to the complex polygenic process of rejection. The identification of genetic determinants for the susceptibility to disease offers us the opportunity not only to tailor therapy to the individual need, but also to define mechanisms of pathogenesis and identify new therapeutic options. Increased rate of renal transplant failure in patients with the G20210A mutation of the prothrombin geneAmerican Journal of Kidney DiseasesVol. 38Issue 5PreviewIn patients with thrombophilia caused by reduced physiological anticoagulation, renal transplant failure occurs more frequently. Previous studies showed the importance of the protein C system, a physiological anticoagulatory pathway that inhibits thrombus formation. However, excess activation of the hemostatic system also may result in thrombosis. The G20210A mutation in the prothrombin gene is such a prothrombotic risk factor that results in increased thrombus formation because of elevated factor II levels in plasma. Full-Text PDF" @default.
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