ABO-incompatible Transplant Recipients Research Articles

Clinical characteristics and risk factors for late-onset pneumocystis jirovecii pneumonia in kidney transplantation recipients.

Pneumocystis jirovecii pneumonia (PJP) is a common and troublesome complication of kidney transplantation. In the era of prophylaxis, the peak incidence of PJP after kidney transplantation and specific characteristics of late-onset PJP have always been debated. We performed a retrospective study by analysing the data of post-transplantation pneumonia in adult kidney transplantation recipients between March 2014 and December 2021 in The Affiliated First Hospital of University of Science and Technology of China (USTC). A total of 361 patients were included and divided into early-onset PJP, late-onset PJP and non-PJP groups. The characteristics of each group and related risk factors for the late-onset patients were investigated. Some patients developed PJP 9 months later with a second higher occurrence between month 10 and 15 after transplantation. Compared with non-PJP, ABO-incompatible and cytomegalovirus (CMV) viremia were significantly associated with late onset of PJP in multivariate analysis. The use of tacrolimus, CMV viremia, elevated CD8(+) T cell percent and hypoalbuminemia were risk factors for late PJP. Receiver operating characteristic curve analysis demonstrated that a combination of those factors could increase the sensitivity of prediction remarkably, with an area under the curve of 0.82, a sensitivity of 80% and a specificity of 83%. PJP could occur months after kidney transplantation. ABO-incompatible transplant recipients are at high risk of PJP. In the later stages of transplantation, CMV viremia, T lymphocyte subsets percentage and serum albumin levels should be monitored in patients using tacrolimus.

The First ABO Incompatible Kidney Transplantation without Splenectomy in India - A Review at 12 Years.

The First ABO Incompatible Kidney Transplantation without Splenectomy in India - A Review at 12 Years.

Significance of revised criteria for chronic active T cell-mediated rejection in the 2017 Banff classification: Surveillance by 1-year protocol biopsies for kidney transplantation.

Diagnostic criteria for chronic active T cell-mediated rejection (CA-TCMR) were revised in the Banff 2017 consensus, but it is unknown whether the new criteria predict graft prognosis of kidney transplantation. We enrolled 406 kidney allograft recipients who underwent a 1-year protocol biopsy (PB) and investigated the diagnostic significance of Banff 2017. Interobserver reproducibility of the 3 diagnosticians showed a substantial agreement rate of 0.68 in Fleiss's kappa coefficient. Thirty-three patients (8%) were classified as CA-TCMR according to Banff 2017, and 6 were previously diagnosed as normal, 12 as acute TCMR, 10 with borderline changes, and 5 as CA-TCMR according to Banff 2015 criteria. Determinant factors of CA-TCMR were cyclosporine use (vs tacrolimus), previous acute rejection, and BK polyomavirus-associated nephropathy. In survival analysis, the new diagnosis of CA-TCMR predicted a composite graft endpoint defined as doubling serum creatinine or death-censored graft loss (log-rank test, P<.001). In multivariate analysis, CA-TCMR was associated with the second highest risk of the composite endpoint (hazard ratio: 5.42; 95% confidence interval, 2.02-14.61; P<.001 vs normal) behind antibody-mediated rejection. In conclusion, diagnosis of CA-TCMR in Banff 2017 may facilitate detecting an unfavorable prognosis of kidney allograft recipients who undergo a 1-year PB.

ABO Incompatible Heart Transplantation in Pediatric Recipients with High Isohemagglutinin Titers in the U.S.: A Multi-Institutional Analysis

UNOS has liberalized the criteria for ABO incompatible (ABOi) heart transplant (HT) for patients less than two years of age. However, to date, the impact of high isohemagglutinin titers on graft survival has not been studied. Pediatric recipients (age <2) listed for heart transplantation in the UNOS database from 2008-2018 were reviewed. We compared graft survival between ABO-compatible (ABOc) and ABOi recipients and also between ABOi recipients transplanted with low (<;1:16) and high isohemagglutinin titers (>;1:16). Of 1687 HT performed in patients less than 2 years of age, 209 (13%) received ABOi transplants. (Figure 1) Majority of recipients listed for ABOi transplants had blood group O (67.5%). 18/209 (8.6%) recipients had high titers pre-transplant. Compared to ABOc recipients, ABOi recipients had similar distribution of age, gender, ethnicity, and were on similar cardiac support (inotropes, ventilator, ECMO, VAD) (p >; 0.05 for all). The wait-list times were also similar between both groups (64.2±50.8 vs 63.5±45.4 days, p >; 0.05). In patients less than 2 years, compared to ABOc transplants, ABOi transplants had similar 1-year (12.8 vs. 11%; P=0.39) and overall graft failure (21.1 vs. 19.9%; P=0.68). Compared to those with low-titers, patients transplanted with high isohemagglutinin titers, had similar 1-year (5.6% vs 12.6%; P=0.70) and overall graft failure (16.7% vs 18.2%; P=0.99) (Figure 1). Overall, utilization of ABOi transplantation is low in the relevant age group with most common recipients being blood group O. The use of ABOi transplant does not involve patient selection bias and has not affected the wait time. ABOi transplant recipients have graft survival similar to ABOc recipients. Most importantly, strength of anti-A or B titers do not impact graft survival in ABOi recipients.

Outcomes and complications following ABO-incompatible kidney transplantation performed after desensitization by semi-selective immunoadsorption - a retrospective study.

Because of the current organ shortage, ABO-incompatible (ABOi) transplantations have been increasingly performed in recent years. The results seem comparable to those of compatible transplantations, but there have also been reports of increased side effects possibly because of the desensitization therapy. To address an increase in severe infectious complications, we compared the outcomes of 48 ABOi transplant recipients to outcomes of 96 matched ABO-compatible (ABOc) controls transplanted at Heidelberg University Hospital from August 2005 to April 2018. Over a follow-up period of 8years, ABOi transplant recipients had comparable graft and patient survival as well as graft function compared with ABOc patients. T-cell-mediated and antibody-mediated rejections were not different between groups. In ABOi transplant recipients, urosepsis (22.9% vs. 8.5%; P=0.019) and pneumonia with opportunistic pathogens (8.3% vs. 1.0%, P=0.025) appeared more frequently. As a consequence, a significantly higher number of deaths from infection have been observed after ABOi transplantations (6.3% vs. 0%, P=0.010). High-titer recipients (isoagglutinin titer of ≥1:256) showed a higher incidence of BK virus replication and postoperative bleeding complications. ABO-incompatible transplantations can be performed with results that are not different from results after ABOc transplantations. However, an increased rate of serious infectious complications must be taken into account.

Repeat A2 Into B Kidney Transplantation After Failed Prior A2 Into B Transplant: A Case Report

Kidneys from donors with blood type A2 can be successfully transplanted into blood type B and O recipients without the need for desensitization if the recipient's starting anti-A hemagglutinin titer is within an acceptable range. National kidney allocation policy now offers priority for eligible B recipients to receive A2 or A2B deceased donor kidneys, and therefore, the frequency with which A2 or A2B to B transplants will occur is expected to increase. The precise mechanisms by which antibody-mediated rejection is averted in these cases despite the presence of both circulating anti-A antibody and expression of the A2 antigen on the graft endothelium are not known. Whether this process mirrors proposed mechanisms of accommodation, which can occur in recipients of ABO incompatible transplants, is also not known. Repeated exposure to mismatched antigens after retransplantation could elicit memory responses resulting in antibody rebound and accelerated antibody-mediated rejection. Whether this would occur in the setting of repeated A2 donor exposure was uncertain. Here we report the case of a patient with history of a prior A2 to B transplant which failed owing to nonimmunologic reasons; the patient successfully underwent a repeat A2 to B transplant. Neither rebound in anti-A2 antibody nor clinical evidence of antibody-mediated rejection were observed after the transplant. Current kidney allocation will likely enable more such transplants in the future, and this may provide a unique patient population in whom the molecular mechanisms of incompatible graft accommodation may be investigated.

Pregnancy and the kidney transplant recipient.

The current article reviews the available literature on the incidence, complications, outcomes, and management of pregnancies in kidney transplant recipients. Pregnancy can be a reasonable option for women with a kidney transplant. More than 4700 successful pregnancies have been reported after kidney transplantation. New data have emerged regarding the risk of allograft dysfunction following pregnancy. There is a lack of consensus on the optimal time for conception, immunosuppressive targets, the safety of allograft biopsy, and infection surveillance. Successful pregnancies have recently been reported in ABO-incompatible transplant recipients and recipients of combined heart-kidney transplants. The ideal contraceptive method, timing of conception, immunosuppressant protocol, infection surveillance, and the method of delivery should be individualized depending on the patient's age and medical conditions.

Borderline rejection in ABO-incompatible kidney transplantation.

The clinical results of ABO-incompatible (ABOi) and ABO-compatible (ABOc) kidney transplantation (KT) are similar. Protocol kidney biopsies (PKB) of ABOi transplant recipients show positivity for C4d without evidence of antibody-mediated rejection (ABMR), but little is known about the histologic progression. We evaluated histologic parameters in PKB at 12months and also compared clinical outcome at 1year. This is a prospective observational study conducted between 2009 and 2013. We performed 146/30 ABOc/ABOi consecutive living-donor KT with PKB as well as additional indication biopsies. In the ABOi group, the desensitization protocol consisted of rituximab, plasma exchange or immunoadsorption, and immunoglobulins. In indication biopsies during the first year, T-cell-mediated rejection Banff ≥immunoadsorption was 8.2% vs 6.7% (P=.561) and ABMR 4.8% vs 13.3% (P=.095). At 1year, PKB (ABOc/ABOi) showed differences in borderline rejection lesions (6.8% vs 23.3% [P=.012]) and in C4d positivity in the ABOi group (P=.001). Interstitial fibrosis and tubular atrophy (IFTA) lesions (ABOc/ABOi) were 68.4% vs 63.2% (P=.348). Transplant glomerulopathy was 0.7% vs 3.3% (P=.373) at 1year. Our PKB ABOi series shows at 1year more borderline lesions independent of ABO titers, HLA incompatibility, and the presence of antidonor antibody, but do not show more IFTA nor transplant glomerulopathy. No clinical differences were observed between ABOi and ABO transplants.

Development of B-cell memory in early childhood and the impact on antigen-specific tolerance after heart transplantation

Young children show better survival after heart transplant compared with older individuals and can receive heart transplants safely from ABO-incompatible donors. Children develop immunologic tolerance to donor ABH antigens reflected in persistent absence of specific antibodies. We hypothesized that immature T-independent B-cell response and lack of B-cell memory play a crucial role in tolerance of ABH antigens after ABOi transplants. We determined phenotypes of splenic lymphocytes from adults and children and peripheral blood from ABO-incompatible or ABO-compatible heart transplant recipients and control subjects by flow cytometry. In vitro immune response to T-independent stimulation, erythrocytes, and ABH antigens was assessed using proliferation assays. A predominant role for CD27(+) B cells in T-independent activation was demonstrated; these cells were significantly less frequent in infants than older subjects. Only IgM(+)CD27(+) B cells proliferated in response to non-self erythrocytes. In blood, IgM(+) and switched IgM(-) memory B cells were rare in infants, increasing to near-adult levels in children 5 years old. IgM(+)CD27(+) B cells were significantly fewer in ABO-incompatible transplant recipients than in ABO-compatible recipients. CD27(+) cells play a key role in T-independent B-cell activation. Response to ABH antigens is mediated by IgM(+)CD27(+) B cells, and donor ABO-specific tolerance after ABO-incompatible transplantation in children is facilitated by low prevalence of these cells. The pattern of B-cell memory development is altered after ABO-incompatible transplant. Memory B cells may be quantified to assess eligibility for ABO-incompatible transplant and represent a potential therapeutic target to extend the benefits of the immature immune system to older age groups.

Kidney transplantation in highly sensitized patients.

Desensitization, a term loosely referring to a collection of antibody reduction and B-cell depletional therapies aimed at improving rates of transplantation in highly HLA and ABO-incompatible transplant recipients, has seen significant growth in the last decade. Advancements relate to an increasing unmet medical need for FDA-approved therapies, advancements in antibody detection methodologies and improved renal pathological assessments of antibody-mediated rejection (ABMR). Data reviewed include collective summaries of experience with high-dose intravenous immunoglobulin (IVIG), B-cell depletion with rituximab and the use of plasma exchange with low-dose IVIG. Consensus suggests that these protocols are the most commonly used while experiences with other agents (i.e. bortezomib) are evolving. Controversy exists as to the extent of resources required, expense and outcomes of desensitization protocols. Here we review and synthesize data from evolving protocols and summarize developments of novel biologics aimed at modification of B-cells, antibodies and complement activation which will likely improve desensitization and treatment of ABMR.

Successful Pediatric ABO-Incompatible Kidney Transplantation without Pretransplant Plasmapheresis: Report of a Case

Immunologic responses of infants and younger children differ from those of adults. Therefore, application of different pretransplant strategies for antibody depletion in younger ABO-incompatible transplant recipients is appropriate. A 12-month-old male infant with end stage renal disease after acute tubular necrosis was scheduled to undergo kidney transplantation from an ABO-incompatible living donor. He did not undergo pretransplant plasmapheresis, as the titer of the anti-ABO antibody was less than 1:4. After kidney transplantation, posttransplant renal function and anti-ABO titers were stable until posttransplant 2 years.

Blockade of invariant TCR-CD1d interaction specifically inhibits antibody production against blood group A carbohydrates

AbstractPreviously, we detected B cells expressing receptors for blood group A carbohydrates in the CD11b+CD5+ B-1a subpopulation in mice, similar to that in blood group O or B in humans. In the present study, we demonstrate that CD1d-restricted natural killer T (NKT) cells are required to produce anti-A antibodies (Abs), probably through collaboration with B-1a cells. After immunization of wild-type (WT) mice with human blood group A red blood cells (A-RBCs), interleukin (IL)-5 exclusively and transiently increased and the anti-A Abs were elevated in sera. However, these reactions were not observed in CD1d−/− mice, which lack NKT cells. Administration of anti-mouse CD1d blocking monoclonal Abs (mAb) prior to immunization abolished IL-5 production by NKT cells and anti-A Ab production in WT mice. Administration of anti-IL-5 neutralizing mAb also diminished anti-A Ab production in WT mice, suggesting that IL-5 secreted from NKT cells critically regulates anti-A Ab production by B-1a cells. In nonobese diabetic/severe combined immunodeficient (NOD/SCID/γcnull) mice, into which peripheral blood mononuclear cells from type O human volunteers were engrafted, administration of anti-human CD1d mAb prior to A-RBC immunization completely inhibited anti-A Ab production. Thus, anti-CD1d treatment might constitute a novel approach that could help in evading Ab-mediated rejection in ABO-incompatible transplant recipients.

Hepatic Artery Reconstruction in Living Donor Liver Transplantation: Running Suture Under Surgical Loupes by Cardiovascular Surgeons in 180 Recipients

ObjectivesThe aim of our study was to retrospectively investigate the outcomes of hepatic artery (HA) reconstruction by cardiovascular surgeons in adult-to-adult living donor liver transplantation (A-A LDLT). MethodsFrom April 2007 to April 2011, 187 recipients underwent A-A LDLT. After excluding seven ABO-incompatible transplant recipients, we reviewed the courses of 180 patients including 125 men and 55 women of mean age 52.5 ± 9.2 years (range = 23–71). One hundred seventy-seven patients received right-lobe grafts with inclusion of middle hepatic vein (MHV); two, right-lobe grafts without MHV; and one, left-lobe graft. A continuous, single-stitch, running suture with the parachute technique was used for HA reconstruction. The anastomosis was performed by cardiovascular surgeons employing surgical loupes with 4.5× magnification. ResultsThe mean time for an arterial reconstruction was 10.7 ± 4.0 minutes (median = 10, range = 4–30). Hepatic arterial thrombosis (HAT) was encountered in 3 (1.66%) patients. One HAT that developed on postoperative day 1 was successfully rescued by the intra-arterial infusion of urokinase. Another patient required reoperation due to a redundant kinked HA. A third HAT patient underwent successful retransplantation with a cadaveric graft on postoperative day 6. In our series, no delayed HAT was detected and no recipient deaths were related to HAT. ConclusionHA reconstruction with a running suture under surgical loupes is a feasible technique in A-A LDLT. A speedy reconstruction can be performed by an experienced cardiovascular surgeon with a low incidence of HAT.

Decrease of blood type antigenicity over the long-term after ABO-incompatible kidney transplantation

Background Few studies have investigated the changes in the antigenicities of the transplanted organs after transplantation. Methods We examined, by immunohistochemical assay, the changes in expression of the blood-type antigens on the transplanted kidneys over the long-term after ABO-incompatible kidney transplantation with A- or B-antigen incompatibility (blood type A to B and B to A). The subjects were six patients, including one case with graft loss, who had received ABO-incompatible kidney allografts more than ten years previously. As normal controls, four cases of ABO-compatible transplantation during the same period, including two recipient/donor pairs each with blood group A1 and blood group B were enrolled. Results Expression of the blood-type A or B antigens decreased gradually to 91.8% during the first three months after transplantation, 85.8% during the first five years, 64.1% during the first ten years, and 57.6% over ten years after transplantation on average in ABO-incompatible transplant recipients. In one patient with graft loss due to severe antibody-mediated rejection, the donor's type B blood-type antigens on the transplanted graft had changed but partially to the recipient's blood-type A antigen by 2582 days after the transplantation, suggestive of the occurrence of blood-type chimerism on the endothelium. In ABO-compatible transplant recipients, such changes in expression were not observed. The average percentage of blood-type antigen-positive vessels at more than ten years after the renal transplantation was 99.8%. Conclusions Decrease in the expression of the donor's blood-type antigen on the endothelium of the graft has been considered as one of the mechanisms underlying the accommodation occurring over the long-term after ABO-incompatible kidney transplantation. On the other hand, establishment of antigenic chimerism on the graft endothelium could be one of the hallmarks of the immunological reaction associated with antibody-mediated rejection.

ABO-incompatible renal transplantation: From saline flushes to antigen-specific immunoadsorption-Tools to overcome the barrier

On April 23, 1951, a 30-year-old woman received the first intentional ABOi (ABO incompatible) renal transplantation in Boston. At that time, it was commonly believed that intensely rinsing the graft to remove blood would be sufficient to overcome any immunological problems associated with blood type incompatibility. However, when the abovementioned patient and another ABOi transplant recipient died within a month, Humes and colleagues arrived at the same conclusion: "We do not feel that renal transplantation in the presence of blood incompatibility is wise." In the decades that followed, we learned that the oligosaccharide surface antigens representing the ABO-blood group antigens are expressed not only on erythrocytes but also on cells from various tissues, including the vascular endothelium. The growing gap between organ demand and availability has sparked efforts to overcome the ABO barrier. After its disappointing results in the early 1970s, Japan became the leader of this endeavor in the 1980s. All protocols are based on 2 strategies: removal of preformed antibodies with extracorporeal techniques and inhibition of ongoing antibody production. Successful ABOi renal transplantation became possible with the advent of splenectomy, new immunosuppressive drugs (e.g., rituximab, a monoclonal antibody against CD20), and extracorporeal methods such as antigen-specific immunoadsorption. This review summarizes the underlying pathophysiology of ABOi transplantation and the different protocols available. Further, we briefly touch potential short- and long-term problems, particularly the incidence of infectious complications and malignancies, that can arise with high-intensity immunosuppressive therapy.

Delayed hyperacute rejection in a patient who developed clostridium difficile infection after ABO-incompatible kidney transplantation

Over the past decade ABO incompatible transplantation has emerged as an important potential source for increasing living kidney transplantation in selected transplant centers. Early reports suggest that patients who have elevated serum anti-blood group antibody titers (anti-A/B) before transplantation and a rebound antibody production after antibody removal may be at high immunological risk. With currently available immune modulation protocols and immunosuppressive therapy, excellent short- and long-term patient and graft survival rates have been achieved even in those with high anti-A/B antibody titers before plasmapheresis or immunoadsorption. Nonetheless, acute infection with an organism possessing surface markers analogous to blood group antigens such as carbohydrate structures on the surface of bacterial cell wall occurring before the firm establishment of accommodation can trigger the onset of acute antibody-mediated rejection. We herein report a case of delayed hyperacute rejection in an A1 to O, ABO incompatible transplant recipient following an episode of Clostridium difficile infection.

Rituximab: An emerging therapeutic agent for kidney transplantation

Rituximab: An emerging therapeutic agent for kidney transplantation Joseph Kahwaji, Chris Tong, Stanley C Jordan, Ashley A VoComprehensive Transplant Center, Transplant immunology Laboratory, HLA Laboratory, Cedars-Sinai Medical Center, Los Angeles, CA, USAAbstract: Rituximab (anti-CD20, anti-B-cell) is now emerging as an important drug for modification of B-cell and antibody responses in solid-organ transplant recipients. Its uses are varied and range from facilitating desensitization and ABO blood group-incompatible transplantation to the treatment of antibody-mediated rejection (AMR), post-transplant lymphoproliferative disorder (PTLD), and recurrent glomerular diseases in the renal allograft. Despite these uses, prospective randomized trials are lacking. Only case reports exist in regards to its use in de novo and recurrent diseases in the renal allograft. Recent reports suggests that the addition of rituximab to intravenous immunoglobulin (IVIG) may have significant benefits for desensitization and treatment of AMR and chronic rejection. Current dosing recommendations are based on data from United States Food and Drug Administration-approved indications for treatment of B-cell lymphomas and rheumatoid arthritis. From the initial reported experience in solid organ transplant recipients, the drug is well tolerated and not associated with increased infectious risks. However, close monitoring for viral infections is recommended with rituximab use. The occurrence of progressive multifocal leukoencephalopathy (PML) has been reported with rituximab use. However, this is rare and not reported in the renal transplant population. Here we will review current information regarding the effectiveness of rituximab as an agent for desensitization of highly human leukocyte antigen-sensitized and ABO-incompatible transplant recipients and its use in treatment of AMR. In addition, the post-transplant use of rituximab for treatment of PTLD and for recurrent and de novo glomerulonephritis in the allograft will be discussed. In summary, we will make recommendations based on existing literature and our extensive experience at Cedars-Sinai Medical Center for using rituximab in renal transplantation.Keywords: kidney transplant, rituximab, desensitization, rejection, review

The emerging role of rituximab in organ transplantation

Long-term acceptance of solid organ allografts remains a challenge. While many acute rejection episodes can be treated, new mechanisms of allograft damage are now being defined especially in kidney transplantation. Unexpected clusters of CD20(+) cells have been discovered in renal biopsies performed for clinical rejection. C4d deposition is now routinely seen in refractory rejection. Despite the rapid introduction of new immunosuppressive agents in transplantation, the search for an efficacious anti-B-cell agent remains. With novel mechanisms of allograft damage now being defined, it is important to consider how an anti-B-cell agent might fit into an immunosuppressive regimen. Rituximab is a high-affinity CD20 specific antibody that depletes the B-cell compartment by inducing cellular apoptosis. Thus, it is a rational choice for therapy in transplantation to abrogate B-cell mediated events. In this review, we will discuss the mechanisms of action of rituximab, and its use in for a variety of indications in solid organ transplantation. There are emerging case reports that show that rituximab may be an effective agent to treat antibody-mediated rejection, and post-transplant lymphoproliferative disorder. Rituximab has been frequently cited as an important adjunct therapy in desensitization protocols for highly sensitized transplant recipients as well as recipients of ABO incompatible transplants. Rituximab demonstrates promise in this regard and warrants additional consideration in prospective clinical trials.

Soluble type A substance in fresh-frozen plasma as a function of ABO and Secretor genotypes and Lewis phenotype

Soluble ABO blood group substance (SAS) in fresh-frozen plasma (FFP) and its cognate alloantibody titer reduction capacity (TRC) are not considered when prescribing this product for plasma exchange (PEX) therapy of ABO incompatible transplant recipients. SAS was quantified in 250 single FFPs using ELISA. Total and IgG class-specific anti-A TRCs of FFPs were measured using a microhemagglutination inhibition assay. SAS level depended not only on the A subtype ( p < 0.0001) and the Secretor status ( p < 0.0001), but also on the expression of ALe b in A 1 secretors ( p < 0.0001). The variation was as great as 137.6 arbitrary units (aU) for 14 A 1 Le(a−b−) secretors and 1.2 aU for 6 A 2 non-secretors. Homozygous expression of the A 1, A 2 and Secretor alleles did not increase SAS levels. Only total anti-A TRC, but not IgG class-specific TRC depended on the detected SAS level ( r = 0.566, p = 0.0003).

Excellent Long-term Outcome of ABO-Incompatible Living Donor Kidney Transplantation in Japan

Owing to the severe shortage of cadaveric grafts in Japan, we have performed ABO-incompatible living donor kidney transplantation since 1989. This study assessed short- and long-term outcomes in 441 patients who received ABO-incompatible living donor kidney transplants between January 1989 and December 2001. We compared our results with historical data from 1055 recipients of living kidney transplantation. Overall patient survival rates 1, 3, 5, 7, and 9 years after ABO-incompatible transplantation were 93%, 89%, 87%, 85%, and 84%, respectively. Corresponding overall graft survival rates were 84%, 80%, 71%, 65%, and 59%. After ABO-incompatible transplantation, graft survival rates were significantly higher in patients 29 years or younger than in those 30 years or older and in patients who received anticoagulation therapy than in those who did not receive such therapy. There were no significant differences between A-incompatible and B-incompatible recipients with respect to clinical outcomes. The graft survival rate at 1 year in the historical controls was slightly but not significantly higher than that in our recipients of ABO-incompatible transplants. We conclude that long-term outcome in recipients of ABO-incompatible living kidneys is excellent. Transplantation of ABO-incompatible kidneys from living donors is a radical, but effective treatment for end-stage renal disease.