Imaging pancreas transplants.

Pancreas transplants are performed in multiple centres across the UK with good graft survival rates. This places an increasing demand on radiology services, particularly as the complication rates are not insignificant. The imaging appearances of pancreas transplants and their complications can be difficult to interpret. This review provides an illustrative journey through the anatomical appearances of a graft and the imaging appearances of complications, as a reference tool for radiologists.

Pancreas transplantation, antibodies and rejection: where do we stand?

PURPOSE OF REVIEW: Antibody-mediated rejection (AMR) is acknowledged and defined in kidney transplantation, but where do we stand as far as pancreas transplantation is concerned? Here we appraise the most recent findings in pancreatic AMR and give suggestions for future research in the field by addressing currently unresolved issues. RECENT FINDINGS: Five main topics are discussed: chronological assessment of all literature on biopsy-proven pancreatic AMR; role of C4d and recent development in other markers; the use of sentinel organs, such as kidney biopsies and duodenal patch biopsies for diagnosis of pancreatic AMR; studies addressing islet pathology and its relevance in AMR; and protocol and follow-up pancreas biopsy practice in relation to pancreas transplant management and survival. SUMMARY: Antibody-mediated processes play a role in pancreas transplantation. However, sensitive markers, pathophysiological understanding, and adequate interventions have not yet been established. Much data are still lacking and we believe that studying protocol and follow-up biopsies along with serial donor-specific antibody data may improve pancreas transplant patient management and outcomes.

Fetal pancreas transplants are dependent on prolactin for their development and prevent type 1 diabetes in syngeneic but not allogeneic mice.

Transplantation of adult pancreatic islets has been proposed to cure type 1 diabetes (T1D). However, it is rarely considered in the clinic because of its transient effect on disease, the paucity of donors, and the requirement for strong immunosuppressive treatment to prevent allogeneic graft rejection. Transplantation of fetal pancreases (FPs) may constitute an attractive alternative because of potential abundant donor sources, possible long-term effects due to the presence of stem cells maintaining tissue integrity, and their supposed low immunogenicity. In this work, we studied the capacity of early FPs from mouse embryos to develop into functional pancreatic islets producing insulin after transplantation in syngeneic and allogeneic recipients. We found that as few as two FPs were sufficient to control T1D in syngeneic mice. Surprisingly, their development into insulin-producing cells was significantly delayed in male compared with female recipients, which may be explained by lower levels of prolactin in males. Finally, allogeneic FPs were rapidly rejected, even in the context of minor histocompatibility disparities, with massive graft infiltration with T and myeloid cells. This work suggests that FP transplantation as a therapeutic option of T1D needs to be further assessed and would require immunosuppressive treatment.

Upregulation of IL-1ß, IL-6, and CCL-2 by a novel mouse model of pancreatic ischemia-reperfusion injury.

BACKGROUND: Little is known about the immunologic events surrounding pancreatic ischemia-reperfusion injury (IRI) because of a lack of established experimental models. The purpose of this study was to develop a mouse model for pancreatic IRI to serve as a basis for the immunologic characterization of pancreatic organ damage at transplantation. METHODS: Reversible ischemia was surgically induced by vascular isolation of the distal pancreas for 0, 10, 20, or 30 min. Mice receiving laparotomy without clamping served as sham-operated controls. After reperfusion, mice were serially assayed for biochemical and histologic evidence of inflammation, proinflammatory cytokine and chemokine production, and inflammatory gene upregulation. RESULTS: After induction of pancreatic IRI, serum amylase and lactate dehydrogenase peaked at 6 hr and returned to baseline by 120 hr after injury in all groups. Mice undergoing 30 min of IRI demonstrated the greatest biochemical evidence of inflammation. Histologic scoring similarly demonstrated marked inflammation in mice subjected to 30-min IRI compared with controls. Serum cytokine/chemokine analysis demonstrated significant upregulation of granulocyte colony-stimulating factor, interferon γ, tumor necrosis factor α, interleukin (IL)-2, IL-1ß, IL-6, chemokine (C-C motif) ligand-2, chemokine (C-C motif) ligand-5, chemokine (C-X-C motif) ligand-1, and macrophage inflammatory protein 2. A similar upregulation of ccl2, il1b, il6, fos, hspa1a, hspd1, and cd14 gene expression was detected by real-time polymerase chain reaction analysis of pancreatic tissue. CONCLUSIONS: This novel model of distal pancreatic IRI in the mouse demonstrates time-limited pancreatic inflammation and injury by histologic and biochemical indices. Inflammation may be, in part, a result of the immunologic effects of IL-1ß, IL-6, and CCL-2. This model provides a method by which immunologic mechanisms of pancreatic IRI can be elucidated.

Pancreas retransplantation: a second chance for diabetic patients?

BACKGROUND: If pancreas transplantation is a validated alternative for type 1 diabetic patients with end-stage renal disease, the management of patients who have lost their primary graft is poorly defined. This study aims at evaluating pancreas retransplantation outcome. METHODS: Between 1976 and 2008, 569 pancreas transplantations were performed in Lyon and Geneva, including 37 second transplantations. Second graft survival was compared with primary graft survival of the same patients and the whole population. Predictive factors of second graft survival were sought. Patient survival and impact on kidney graft function and survival were evaluated. RESULTS: Second pancreas survival of the 17 patients transplanted from 1995 was close to primary graft survival of the whole population (71% vs. 79% at 1 year and 59% vs. 69% at 5 years; P=0.5075) and significantly better than their first pancreas survival (71% vs. 29% at 1 year and 59% vs. 7% at 5 years; P=0.0008) regardless of the cause of first pancreas loss. The same results were observed with all 37 retransplantations. Survival of second simultaneous pancreas and kidney transplantations was better than survival of second pancreas after kidney. Patient survival was excellent (89% at 5 years). Pancreas retransplantation had no impact on kidney graft function and survival (100% at 5 years). CONCLUSION: Pancreas retransplantation is a safe procedure with acceptable graft survival that should be proposed to diabetic patients who have lost their primary graft.

Immunological monitoring after pancreas transplantation.

PURPOSE OF REVIEW: After switching from bladder to enteric drainage, pancreas graft monitoring, particularly after solitary transplantation, has become an important issue. The aim of this work was to systematically review the relevant literature with regard to various biomarkers, imaging techniques, and pathologic evaluation of allograft tissue. RECENT FINDINGS: More recent studies including graft histology demonstrate the low specificity of pancreatic enzymes as a marker of acute rejection. On the other hand, most blood and serum markers are indicative of an activated immune status rather than rejection. Interestingly, the concomitantly transplanted kidney from the same donor does not seem to be a reliable surrogate marker. Although computed tomography or ultrasound-guided percutaneous biopsies of the pancreas are performed more frequently at present, the complication rate is still as high as 11%. In contrast, cystoscopic and enteroscopic biopsies of the duodenal part of the graft are associated with almost no complications. The few clinical studies dealing with the duodenum as surrogate marker for the pancreas report a high correlation between duodenum mucosal and pancreas parenchymal histology. SUMMARY: Pancreatic graft parenchymal biopsy remains the gold standard in diagnosing pancreatic rejection, as clinical parameters, pancreatic enzymes, noninvasive biomarkers, and surrogate renal biopsies are not reliable tools. Endoscopically obtained duodenal cuff biopsies are a less invasive alternative to percutaneous biopsies.

Pancreas-after-kidney versus synchronous pancreas-kidney transplantation: comparison of intermediate-term results.

BACKGROUND: Controversy persists over the safety and efficacy of pancreas transplantation in patients with insulin-dependent diabetes mellitus who have received a prior kidney transplant. METHODS: We compared the outcomes of recipients who received either Synchronous-Pancreas Kidney-Transplantation (SPK, n=123) or Pancreas-After-Kidney-Transplants(n=49)at our institution between August 2002 to January 2010. RESULTS: Donor and recipient demographics were similar. Time interval between kidney and pancreas transplantation was 5.9 ± 3.8 (4.8 [1.6-12.2]) years. The majority of kidney-recipients in PAK group were transplanted at outside institutions and referred to us for PAK. Most patients received thymoglobulin induction and were maintained on tacrolimus, MMF, and prednisone. For SPK versus PAK recipients, there was no difference in median of length of hospital stay or incidence of overall complications. All PAK recipients are alive with functioning kidney grafts, whereas the 1-, 3-, and 5-year SPK patient survival rates were 98%,96%,and 94%, P=0.09. The 1-,3-, and 5-yr uncensored pancreas survival rates for SPK versus PAK were 93% vs. 90%, 90% vs. 90%, and 82% versus 85%, respectively (P=0.4). CONCLUSION: Glycemic control and intermediate survival outcomes were similar in both groups. Pancreas-graft outcomes in SPK and PAK were equivalent in our study, but our specific population entailed among other factors a long K to PAK time interval; PAK could be a comparable option to SPK for patients with access to kidney grafts.

Trends in immunosuppression after pancreas transplantation: what is in the pipeline?

PURPOSE OF REVIEW: To provide an overview of currently available immunosuppressive strategies and novel therapeutic developments in pancreas transplantation. RECENT FINDINGS: From 1966 through 2012 more than 30 000 pancreas transplantations have been performed around the world with excellent patient and graft survival. However, drug-related side effects and toxicities remain to negatively affect long-term outcomes. At present, more than 90% of pancreas transplant recipients receive induction therapy with depleting or nondepleting antibodies. The most widely used maintenance protocols are based on tacrolimus and mycophenolate mofetil with early or delayed corticosteroid withdrawal. In case of documented side effects related to this standard protocol, several regimens are actively pursued to switch to mammalian target of rapamycin inhibitors as well as to attempt initial calcineurin inhibitor avoidance and immunosuppression minimization. In addition, the recent documented negative impact of donor-specific antibodies on pancreas transplantation outcome has resulted in new treatment protocols for antibody-mediated rejection including intravenous immunoglobulins, anti-CD20 antibodies and protease inhibitors. SUMMARY: Implementation of novel therapeutic strategies and combination protocols to reduce or avoid drug toxicities and immune-related complications that are evaluated in prospective and randomized trials is requested to improve outcomes after pancreas transplantation.

The efficacy and safety of alemtuzumab and daclizumab versus antithymocyte globulin during organ transplantation: a meta-analysis.

OBJECTIVE: The objective of this study was to compare efficacy and safety of alemtuzumab, antithymocyte globulin (ATG), and daclizumab for induction therapy in organ transplantation. METHODS: We searched PUBMED, EMBASE, and Cochrane databases to identify randomized controlled trials that compared alemtzumab, ATG, and daclizumab for induction therapy in kidney as well as pancreas transplantation. According to the inclusion criteria, the collected data included general characteristics of the studies and their major outcomes. The meta-analysis was performed using RevMan 5.0.25 software. RESULTS: We identified 9 studies involving 777 patients. No differences between alemtuzumab, daclizumab, and ATG were observed in terms of patient survival, graft survival, or acute rejection episodes at a 24-month follow-up (P = .62, P = .55, and P = .08, respectively). Infections within 36 months were greater between the alemtuzumab and the ATG group (P = .03). There was no significant difference in terms of infection at 24 months. CONCLUSIONS: Alemtuzumab and daclizumab appeared to be as effective as ATG for induction therapy in kidney transplantation at a follow-up of 24 months. However, alemtuzumab showed a lower rate of infection at 36 months compared with ATG.

Simultaneous pancreas-kidney transplantation nine years after liver transplantation--a case report.

In this case report we have described a patient suffering from sclerosing cholangitis, diabetes mellitus type I, and consequent end-stage renal disease who was successfully treated with simultaneous pancreas and kidney transplantation 9 years after orthotopic liver transplantation.

Treatment of severe psoriasis with etanercept in a pancreas-kidney transplant recipient.

Severe psoriasis is a rare condition under immunosuppressive therapy. We describe a 42-years-old man with psoriasis since the age of 22 years. The patient underwent a combined pancreas-kidney transplantation at the age of 32 because of Goodpasture syndrome with renal and pulmonary involvments and type 1 diabetes mellitus. Seven years later a pancreas retransplantation was performed due to nonfunction of the original pancreas allograft. Despite intensive systemic immunosuppression, consisting of prednisone, tacrolimus, and mycofenolate mofetil, and topical treatment with dithranol and steroids, there was significant worsening of psoriasis. In October 2009 we initiated therapy with etanercept (25 mg s.c.) twice weekly under close clinical and laboratory monitoring. Improvement was rapid with a decrease in Psoriasis Area and Severity Index (PASI) from 25.2 to <5 during the first months of treatment without a severe infection or other adverse reaction. Graft functions were not affected by the treatment. The patient remains till now on the same regimen and is almost free of skin manifestations. To our knowledge so far only 2 cases of etanercept therapy in psoriasis have been reported in liver transplant recipients. In both cases the treatment was well tolerated and effective. Psoriasis therapy in organ transplant recipients represents a major challenge. Biological agents such as etanercept may provide an effective option for refractory cases.

Early findings of prospective anti-HLA donor specific antibodies monitoring study in pancreas transplantation: Indiana University Health Experience.

The significance of donor-specific antibodies (DSA) is not well known in the setting of pancreas transplantation. Since December 2009, we prospectively followed pancreas transplant patients with single-antigen-luminex-bead testing at one, two, three, six, and then every six months for the first two yr. Thirty-five of the 92 patients that underwent pancreas transplantation (13 pancreas-alone [PTA], 20 with a kidney [SPK], and two after a kidney [PAK]) agreed to participate in study. Median age at transplant was 45 yr and follow-up was 23 months. Majority were Caucasian (n = 33) and male (n = 18). Rabbit anti-thymocyte globulin induction was used. Median HLA-mismatch was 4.2 ± 1.1. Eight patients (7SPK, 1PAK) developed post-transplant DSA at median follow-up of 76 d (26-119), 1 SPK had pre-formed DSA. Seven patients had both class I and class II DSA, one with class I and one with class II only. Mean peak class I DSA-MFI was 3529 (±1456); class II DSA-MFI was 5734 (±3204) whereas cumulative DSA MFI (CI + CII) was 9264 (±4233). No difference was observed in the patient and donor demographics among patients with and without DSA. One patient in non-DSA group developed acute cellular rejection of pancreas. From our data it appears that post-transplant DSA in pancreas allograft recipients may not impact the early-pancreatic allograft outcomes. The utility of prospective DSA monitoring in pancreatic transplant patients needs further evaluation and long-term follow-up.

Pros and cons for C4d as a biomarker.

The introduction of C4d in daily clinical practice in the late nineties aroused an ever-increasing interest in the role of antibody-mediated mechanisms in allograft rejection. As a marker of classical complement activation, C4d made it possible to visualize the direct link between anti-donor antibodies and tissue injury at sites of antibody binding in a graft. With the expanding use of C4d worldwide several limitations of C4d were identified. For instance, in ABO-incompatible transplantations C4d is present in the majority of grafts but this seems to point at 'graft accommodation' rather than antibody-mediated rejection. C4d is now increasingly recognized as a potential biomarker in other fields where antibodies can cause tissue damage, such as systemic autoimmune diseases and pregnancy. In all these fields, C4d holds promise to detect patients at risk for the consequences of antibody-mediated disease. Moreover, the emergence of new therapeutics that block complement activation makes C4d a marker with potential to identify patients who may possibly benefit from these drugs. This review provides an overview of the past, present, and future perspectives of C4d as a biomarker, focusing on its use in solid organ transplantation and discussing its possible new roles in autoimmunity and pregnancy.

Distinctive morphological features of antibody-mediated and T-cell-mediated acute rejection in pancreas allograft biopsies.

PURPOSE OF REVIEW: Two main histopathological types of acute rejection are recognized in solid organ transplantation: T-cell-mediated rejection (TCMR) and antibody-mediated rejection (AMR). In pancreas allografts the contrasting morphological features of these entities have only recently been described. RECENT FINDINGS: Acute TCMR is characterized by active septal infiltrates composed predominantly of T cells and often involving veins (venulitis) and ducts (ductitis). Inflammation of the arterial endothelium (intimal arteritis or endarteritis) may be present. Focal or diffuse acinar inflammation (acinitis) is also typical of TCMR. Acute AMR in contrast, is characterized by predominantly macrophagic (±â€Šneutrophilic) inflammation, concentrated in, and around the interacinar microvasculature (interacinar inflammation, capillaritis) and typically shows focal or diffuse C4d staining of the interacinar capillaries. Architectural preservation is common in milder forms of AMR, whereas severe or untreated forms lead to extensive vascular injury and secondary parenchymal hemorrhagic necrosis. These morphological features strongly correlate with the presence of circulating donor-specific antibody (DSA)+. SUMMARY: Stereotypical TCMR and AMR, as well as mixed forms of rejection can be confidently diagnosed in pancreas allograft biopsies with the combination of three elements: systematic analysis of the histological features; evaluation of C4d staining; and determination of the DSA status.

Long-term pancreatic allograft survival after renal retransplantation in prior simultaneous pancreas-kidney recipients.

Over a 23-year period, our center performed 82 renal retransplants in prior simultaneous pancreas-kidney recipients with functioning pancreatic allografts. All patients were insulin-independent at retransplantation. We aimed to quantify the risk of returning to insulin therapy and to identify factors that predispose patients to pancreatic allograft failure after renal retransplantation. Among these 82 patients, pancreatic allograft survival after renal retransplantation was 78%, 49% and 40% at 1, 5 and 10 years. When analyzing risk factors, we unexpectedly found no clear relationship between the cause of primary renal allograft failure, hemoglobin A1c (HbA1c) or fasting C-peptide level at retransplant and subsequent pancreatic allograft failure. An elevated HbA1c in the month after renal retransplant correlated with subsequent pancreatic graft loss and patients experiencing pancreatic graft loss were more likely to subsequently lose their renal retransplant. Although it is difficult to prospectively identify those patients who will return to insulin therapy after repeat renal transplantation, the relatively high frequency of this event mandates that this risk be conveyed to patients. Nonetheless, the survival benefit associated with renal retransplantation justifies pursuing retransplantation in this population.

Recurrence of type 1 diabetes after simultaneous pancreas-kidney transplantation in the absence of GAD and IA-2 autoantibodies.

We report herein the patterns of type 1 diabetes recurrence in a simultaneous pancreas-kidney transplant (SPK) recipient, in the absence of rejection. A 38-year-old female underwent SPK for end-stage nephropathy secondary to type 1 diabetes. Fasting blood glucose, HbA1c, fructosamine, C-peptide and autoantibodies (GAD-65, IA-2) were monitored throughout follow-up. At 3.5 years post-SPK, HbA1c and fructosamine increased sharply, indicating loss of perfect metabolic control, despite C-peptide levels in the normal-high range. Exogenous insulin was restarted 4 months later. C-peptide levels abruptly fell and became undetectable at 5.5 years. Autoantibody levels, which were undetectable at the time of SPK, never converted to positivity. Pancreas retranspantation was performed at 6 years. The failed pancreas graft had a normal macroscopic appearance. On histology, there were no signs of cellular or humoral rejection in the kidney or pancreas. A selective peri-islet lymphocytic infiltrate was observed, together with near-total destruction of ß cells. At 2.5 years post retransplantation, pancreatic graft function is perfect. This observation indicates unequivocally that pancreas graft can be lost to recurrence of type 1 diabetes in the absence of rejection. GAD-65 and IA-2 autoantibodies are not reliable markers of autoimmunity recurrence.

Quantitative in situ analysis of FoxP3+ T regulatory cells on transplant tissue using laser scanning cytometry.

There is abundant evidence that immune cells infiltrating into a transplanted organ play a critical role for destructive inflammatory or regulatory immune reactions. Quantitative in situ analysis (i.e., in tissue sections) of immune cells remains challenging due to a lack of objective methodology. Laser scanning cytometry (LSC) is an imaging-based methodology that performs quantitative measurements on fluorescently and/ or chromatically stained tissue or cellular specimens at a single-cell level. In this study, we have developed a novel objective method for analysis of immune cells, including Foxp3(+) T regulatory cells (Tregs), on formalin-fixed /paraffin-embedded (FFPE) transplant biopsy sections using iCys® Research Imaging Cytometer. The development of multiple immunofluorescent staining was established using FFPE human tonsil sample. The CD4/CD8 ratio and the population of Tregs among CD4(+) cells were analyzed using iCys and compared with the results from conventional flow cytometry analysis (FCM). Our multiple immunofluorescent staining techniques allow obtaining clear staining on FFPE sections. The CD4/CD8 ratio analyzed by iCys was concordant with those obtained by FCM. This method was also applicable for liver, small intestine, kidney, pancreas, and heart transplant biopsy sections and provide an objective quantification of Tregs within the grafts.

Tacrolimus monotherapy following alemtuzumab induction in combined kidney-pancreas transplantation: results of a prospective randomized trial.

BACKGROUND: We investigated the safety and efficacy of Campath induction and tacrolimus (TAC) maintenance therapy compared to ATG induction with TAC +MMF + steroids in de novo kidney-pancreas transplanted patients. MATERIAL/METHODS: 14 patients (Group A) received Campath 30 mg + methylprednisolone 500 mg before revascularization followed by TAC monotherapy, and 16 patients (Group B) ATG 8 mg/kg with TAC + MMF+ steroids (withdrawn at month 3). TAC trough levels (ng/mL) of 12-15 were aimed for in both groups until month 6 and thereafter 6-12. RESULTS: 1-year patient survival was 100% in both groups; kidney and pancreas survival in Group A was 93% each. In Group B 1-year kidney and pancreas survival was 100% and 87%, respectively. A total of three pancreas grafts were lost due to thrombosis of the graft vein within the first month. The only kidney loss was due to initial non-function. All biopsy-proven acute rejections of renal transplants (n=3 in Group A, n=0 in Group B) were reversible. No acute pancreas graft rejection was demonstrated. Infectious complications, lipid metabolism and blood pressure were comparable in both groups, as were other adverse events. No tumor occurred. At 12 months 13 patients in each group were steroid-free; the mean serum creatinine level was 1.44 mg/dL in Group A and 1.33 mg/dL in Group B. All patients were exogenous insulin-free. CONCLUSIONS: At one year efficacy and safety of Campath +TAC monotherapy were comparable to those of ATG + TAC + MMF + steroids in a limited number of combined kidney-pancreas transplant recipients.

Graft-versus-host disease after solid organ transplantation: a single center experience and review of literature.

BACKGROUND: Graft-versus-host disease (GVHD) is an uncommon cause of morbidity and mortality after solid organ transplantation that is most likely under-diagnosed. We describe our single center experience with three cases of GVHD diagnosed over a period of 15 years in a total of 2,271 solid organ transplant recipients. CASE REPORTS: We describe three case reports: (1) a 3-week old neonate who developed GVHD 16 months after living-related liver transplant, (2) a 14-year old adolescent who developed GVHD 4 months following an unrelated cadaveric pancreas transplant and; (3) a 27-year old male who developed GVHD 18 days after simultaneous kidney-pancreas transplant from an unrelated donor. GVHD was confirmed through skin biopsies, engraftment profile from bone marrow biopsy and variable number tandem repeat analysis. Treatment strategies included use of corticosteroids and sirolimus monotherapy, corticosteroids and mesenchymal stromal cell therapy and reduction of immunosuppression. We observed that African-American race, sexual and HLA mismatching and cytomegalovirus infection may be high risk factors for development of GVHD following solid organ transplant. CONCLUSIONS: GVHD continues to be a rare but fatal complication following solid organ transplantation that demands a high index of clinical suspicion for diagnosis and management. Future approaches may focus on early recognition of risk factors and improving treatment protocols using a combination of mesenchymal stromal cell transplantation with pharmacotherapy.

Thymoglobulin versus basiliximab induction therapy for simultaneous kidney-pancreas transplantation: impact on rejection, graft function, and long-term outcome.

BACKGROUND: Thymoglobulin (ATG) and basiliximab induction therapies are used by the majority of centers for pancreas transplantation today. Although both strategies have different mechanisms, there is a paucity of studies comparing them. We compared the efficacy and side effects of both methods in simultaneous pancreas-kidney (SPK) transplantation. METHODS: We analyzed 128 SPKs at our institution between January 2001 and August 2008. Forty-nine patients received basiliximab (40 mg), whereas 79 patients had ATG (5 mg/kg). Graft function, complications, rejection, and survival rates were analyzed. RESULTS: ATG versus basiliximab therapy was associated with decreased 3-month (6% vs. 21%; P=0.01) and 1-year (14% vs. 27%; P=0.049) rejection rate. Steroid-resistant rejections were decreased with ATG (3%) vs. basiliximab (14%) (P=0.01). In a univariate regression analysis, basiliximab induction was a risk factor for rejection (HR, 7.1; CI, 3.8-13). No differences were observed regarding complications and graft function up to 5 years. ATG versus basiliximab therapy resulted in identical 1-year (90% vs. 93%), 3-year (87% vs. 89%), and 5-year (78% vs. 83%) pancreas survival (P=0.7). No difference was observed in kidney survival after 1 year (99% vs. 98%), 3 years (97% vs. 98%), and 5 years (95% vs. 95%) (P=0.4). CONCLUSIONS: ATG versus basiliximab induction therapy results in decreased acute cellular rejection in the first year after SPK with similar side effects. Long-term graft function and survival are not affected by induction regimen.