Support for this project was provided by the Julie Henry Fund at Beth Israel Deaconess Medical Center.
Retransplantation After Post-Transplant Lymphoproliferative Disorders: An OPTN/UNOS Database Analysis
Version of Record online: 16 OCT 2006
American Journal of Transplantation
Volume 6, Issue 11, pages 2743–2749, November 2006
How to Cite
Johnson, S. R., Cherikh, W. S., Kauffman, H. M., Pavlakis, M. and Hanto, D. W. (2006), Retransplantation After Post-Transplant Lymphoproliferative Disorders: An OPTN/UNOS Database Analysis. American Journal of Transplantation, 6: 2743–2749. doi: 10.1111/j.1600-6143.2006.01543.x
- Issue online: 16 OCT 2006
- Version of Record online: 16 OCT 2006
- Received 30 May 2006, revised and accepted for publication 2 August 2006
- Epstein-Barr virus;
- lymphoproliferative disease;
- post-transplant lymphoproliferative disorder;
Post-transplant lymphoproliferative disorders (PTLD) are a life-threatening complication of immunosuppressive therapy. Retransplantation of survivors remains controversial. The Organ Procurement and Transplant Network/United Network for Organ Sharing database was reviewed for individuals who developed PTLD and underwent retransplant from 1987 through 2004. Sixty-nine retransplants have been performed: 27 kidney, 22 liver, 9 lung, 6 heart, 4 intestine and 1 pancreas. At first transplant, most subjects (63.8%) were <17 years of age and was similar at retransplant with 50.7% less than 17 years. Time from transplant to PTLD was <1 year in 33.3%, 1–3 years in 21.7%, 3–5 years in 21.7%, 5–10 years in 21.7% and >10 years in 1.4%. Time from PTLD to retransplant was <1 year in 24.6%, 1–3 years in 37.7%, 3–5 years in 17.4% and 5–10 years in 20.3%. Induction agents were used in 21.7% of first and 47.8% of retransplants. Immunosuppression for first transplant was cyclosporine (CSA) in 55.1%, tacrolimus (TAC) in 27.5% versus CSA in 26.1%, TAC in 66.7% of retransplants. At last follow-up, patient and graft survival are 85.5% and 73.9%, respectively. Most subjects retransplanted after PTLD are <17 years on TAC-based immunosuppression. Patient/graft survival is excellent and retransplantation in PTLD subjects should be considered acceptable.
De novo malignancies after organ transplantation remain a significant cause of morbidity and mortality. Malignancy as a cause of death after kidney transplantation has increased from 1.2% in the decade 1970–1979, to 5.2% between 1980 and 1989, and 13.2% in the last decade from 1990–1999, due in large part to the longer survival of transplant recipients (1). In some, series malignancies cause up to 24% of deaths occurring after 1 year post-transplant (2). In addition, the cancer rates in kidney transplant recipients are 2-fold higher than the general population for the most common malignancies, including colon, lung, prostate, breast, stomach, esophagus, pancreas and ovary (3).
Post-transplant lymphoproliferative diseases (PTLD) continue to be a significant cause of graft loss and death in spite of our better understanding of their pathogenesis and role of the Epstein-Barr virus (EBV), antiviral prophylaxis, monitoring of EBV viral load and preemptive antiviral therapy, and improvements in immunosuppressive therapy. Improved therapies, including reduction in immunosuppression, antiviral therapy, anti-CD20 monoclonal antibody therapy, surgical resection and radiation therapy, have led to improved long-term patient survival despite a high rate of graft loss and graft dysfunction (4–7). Successful retransplantation without recurrent PTLD has been reported in survivors of PTLD who have lost their graft or have poor graft function after a reduction in immunosuppression (8–12). In the present report, the authors reviewed the Organ Procurement and Transplant Network/United Network for Organ Sharing (OPTN/UNOS) database, for all retransplants performed after allograft loss as a complication of PTLD, to determine the safety and efficacy of current practices.
Materials and Methods
The Institutional Review Board of Beth Israel Deaconess Medical Center approved this study. This is a retrospective review of the OPTN/UNOS database which was queried for individuals who received a solid organ transplant between October 1, 1987, and June 29, 2004, developed PTLD, lost the graft and subsequently underwent retransplantation. The database was queried for demographic information, organ transplanted, date of first and second transplant, date of diagnosis or report of PTLD, patient and graft survival, induction and maintenance immunosuppression, occurrence and treatment of rejection. Detailed data on location of PTLD, pathology, clonality and EBV status was also queried. However, since the OPTN/UNOS only started collecting the detailed data on PTLD from January 1, 1999, this information is not known for PTLD cases reported prior to that date. Data are summarized as mean ± standard error of the mean, or as median and range of values.
A total of 69 patients with a history of PTLD have undergone retransplantation, including 27 kidney, 22 liver, 9 lung, 6 heart, 4 intestine and 1 pancreas recipient(s). Recipient characteristics are noted in Table 1. Forty-four (63.8%) of first transplant recipients and 35 (50.7%) of retransplanted patients were less than 17 years of age. Patients more than 50 years of age accounted for only 5 (7.2%) of first transplants and 9 (13%) of retransplants performed. The time from transplant to PTLD is shown in Figure 1. Twenty-three subjects (33%) developed PTLD within the first year following transplant and 38 (55.1%) developed PTLD within 3 years of transplant. In general, the time periods for development of PTLD are equally represented, with the exception of a small percentage developing PTLD greater than 10 years from transplant (Figure 2). Induction immunosuppression was used in 15 (21.8%) of first transplants and 47.8% of retransplants (Table 1). Maintenance immunosuppression following the first transplant was cyclosporine (CSA) based in 38 (55.1%) and tacrolimus (TAC) in 19 (27.5%), whereas after retransplantation, maintenance immunosuppression was TAC-based in 46 (66.7%) and CSA in 18 (26.1%). The causes of graft loss for the first transplant are shown in Figure 3 and were primarily acute or chronic rejection. Fifty-nine (85.6%) of patients remain alive and 51 of 69 (73.9%) second allografts are functioning at the time of last follow-up (mean 784 ± 82 days). No patient has developed recurrent PTLD.
|African American||9 (13.0%)|
|Age at transplant (years)||17.3 ± 2.1 (range 0–61 years)|
|<17 years old||44 (63.8%)|
|Time from Txp to PTLD||1136 ± 125 days|
|≤ 1 year||23 (33%)|
|≤ 3 years||38 (55.1%)|
|Time from PTLD to ReTx||945 ± 104 days|
|Time from Tx to ReTx||2081 ± 160 days|
|Patient survival after ReTx||784 ± 82 days|
|Induction||15 (21.8%)||33 (47.8%)|
|IL-2R||5 (7.2%)||21 (30.4%)|
|ATG||7 (10.1%)||2 (2.9%)|
|CSA||38 (55.1%)||18 (26.1%)|
|TAC||19 (27.5%)||46 (66.7%)|
|Steroid/Other||12 (17.4%)||5 (7.2%)|
Twenty-seven kidney recipients, 18 (66.7%) males, developed PTLD and underwent retransplantation. The ethnicity of the group was Caucasian in 20 (74.1%), African American in 4 (14.8%), Hispanic in 1 (3.7%) and other in 2 (7.4%). The age at the time of first transplant was less than 18 years in 12 (44.4%), 18–34 years in 8 (29.6%), 35–49 years in 3 (11.1%) and 50–64 years in 4 (14.8%). End-stage renal disease was caused by glomerular disease in 13 (48.1%), tubular disease in 4 (14.8%), diabetes in 3 (11.1%), neoplasm in 1 (3.7%), hypertension in 1 (3.7%), polycystic kidney disease in 1 (3.7%) and other in 4 (14.8%).
Induction immunosuppression was used in 10 of 27 (37.0%) first transplants including antithymocyte globulin (ATG) in 5 (18.5%), IL-2 receptor antagonists in 3 (11.1%) and OKT3 in 2 (7.4%). At the time of retransplant, induction agents were used in 20 of 27 (74.1%) subjects including IL-2 receptor antagonists in 13 (48.1%), thymoglobulin in 5 (18.5%) and multiple agents in 2 (7.4%). No patient initially induced with a T-cell-depleting antibody underwent induction with a T-cell-depleting antibody at retransplant.
Maintenance immunosuppression was CSA-based in 22 of 27 (81.5%) of first transplants, TAC-based in 2 (7.4%) and other in 3 (11.1%). Maintenance immunosuppression after retransplantation was TAC-based in 17 of 27 (63.0%), CSA-based in 9 (33%) and rapamycin in 1 (3.7%). Azathioprine was used in 15 of 27 (55.6%) first transplants and in none of the retransplants. Mycophenolate mofetil was used in 20 of 27 (74.1%) patients undergoing retransplantation. CSA-based regimens were maintained in 8 of 22 (36.4%) subjects initially treated with CSA at first transplant and the remaining subjects were converted to TAC-based regimens 13 (59.1%), or rapamycin 1 (4.5%). Rejection was treated within the first 6 months in 13 (48.1%) first transplants.
The median times from first transplant to PTLD diagnosis and from first transplant to retransplant were 1042 days (range 31–4149 days) and 2717 days (range 722–4838 days), respectively (Figures 1 and 4). The median time from PTLD diagnosis to retransplant was 1337 days (Figure 5). The median first and retransplant graft survival times were 1746 days (range 201–4320 days) and 383 days (range 15–1716 days), respectively. The median patient survival time after retransplant was 728 days (range 15–1860 days). Most occurrences of PTLD were equally divided among the time periods noted in Figure 2, whereas most first allografts survived 3–10 years and most retransplants occurred more than 5 years after first transplant. This finding implies a lag period from the diagnosis of PTLD, graft survival and requirement for retransplant. The cause of first graft loss was chronic rejection in 13 (48.1%), acute rejection in 5 (18.5%), infection in 1 (3.7%), primary failure in 1 (3.7%) or urologic complication in 1 (3.7%), other in 4 (14.8%) and not reported in 2 (7.4%) (Figure 3).
All 27 patients remain alive and 24 of 27 (88.9%) of retransplants are functioning with a mean follow-up of 742 ± 107 days. The three retransplants were lost secondary to chronic rejection in two and graft thrombosis in one.
Twenty-two liver recipients underwent retransplantation after PTLD. Thirteen of 22 (59.1%) were males. The cohort included 13 (59.1%) Caucasian, 5 (22.7%) African American and 4 (18.2%) Hispanic. The ages at first transplant were <1 year in 5 (22.7%), 1–5 years in 7 (31.8%), 6–10 years in 2 (9.1%), 11–17 years in 2 (9.1%), 18–34 years in 1 (4.5%), 35–49 years in 4 (18.2%) and 50–64 years in 1 (4.5%). Thus, 16 of 22 (72.7%) liver retransplants were pediatric patients. Biliary atresia was the most frequent indication for first liver transplant occurring in 10 of 22 (45.5%), followed by noncholestatic liver disease in 6 (27.3%), acute hepatic necrosis in 3 (13.6%), and cholestatic liver disease, metabolic disease and other in 1 (4.5%) each.
Induction agents were used in only 2 (9.1%) first transplants (1 ATG and 1 IL-2 receptor antagonist) and 4 (18.2%) retransplants (IL-2 receptor antagonists in all). Maintenance immunosuppression in first transplants was CSA-based in 7 (31.8%), TAC-based in 11 (50%) and steroid or other in 4 (18.2%). After retransplantation, 17 (77.2%) were maintained on TAC-based regimens, 2 (9.1%) on CSA-based regimens and 3 (13.6%) on steroid or other-based regimens. None of the first or retransplants were treated for rejection.
The median time from first transplant to PTLD diagnosis and to retransplant was 336 days (range 25–3293 days) and 1042 days (range 0–4770 days), respectively (Figures 1 and 4). The median time from PTLD to retransplant was 435 days (range 0–2397 days) (Figure 5). The median first and retransplant graft survival times were 1042 days (range 0–4770 days) and 846 days (range 0–2276 days), respectively. The median patient survival time after retransplant was 846 days (range 0–2276 days). Slightly more than half of PTLD, 12/22 (54.5%) occurred within the first year of transplant. Almost all, 19/22 (86.4%) individuals retransplanted were done within 3 years of first transplant. Nineteen of 22 (86.4%) patients are alive following retransplantation with 15/22 (68.2%) grafts characterized as functioning, 6 (27.3%) as failed (1 vascular thrombosis, 1 biliary tract complication and 4 not reported) and 1 (4.5%) not reported with mean follow-up of 935 ± 167 days.
Nine patients underwent lung retransplantation after PTLD. All were Caucasian and 5 (55.6%) were males. The age at first transplant was 1–5 years in 2 (22.2%), 6–10 years in 1 (11.1%), 11–17 years in 3 (33.3%), 18–34 years in 2 (22.2%) and 35–49 years 1 (11.1%). The indication for lung transplantation was cystic fibrosis in 6 (66.7%), congenital heart disease in 1 (11.1%), primary pulmonary hypertension in 1 (11.1%) and idiopathic pulmonary fibrosis in 1 (11.1%).
Induction immunosuppression was used in only 1/9 (11.1%) first transplants (ATG) and in 1/9 (11.1%) retransplants (IL-2 receptor antagonist). Maintenance immunosuppression was CSA-based in 6 (66.7%), TAC in 2 (22.2%) and other in 1 (11.1%) first transplants. Retransplant maintenance immunosuppression was CSA-based in 4 (44.4%) and TAC-based in 5 (55.6%). No rejection was reported after first lung transplant and 1 (11.1%) experienced rejection after retransplants that was treated with ATG.
The median time from first transplant to PTLD diagnosis and to retransplantation was 746 days (range 321–3448 days) and 1870 days (range 395–4310 days), respectively (Figures 1 and 4). The median time from PTLD to retransplantation was 862 days (range 2–1993 days) (Figure 5). The median first and retransplant graft survival times were 2180 days (range 395–4310 days) and 412 days (range 2–1758 days), respectively. The median patient survival time after retransplant was 412 days (range 2–1758 days). Although most PTLDs occurred within 3 years of first transplant, several occurred as late as 10 years after the first transplant. In addition, the data suggest a several-year time lag between the diagnosis of PTLD and retransplantation. Only 5/9 (55.6%) retransplanted patients are alive and 3/9 (33.3%) grafts are functioning with a mean follow-up of 776 ± 249 days. The causes of death were multisystem organ failure in two patients, graft failure in one patient and viral sepsis in one patient.
Six heart recipients were retransplanted after developing PTLD. All six were pediatric patients with ages of <1 year in 2 (33.3%), 1–5 years in 3 (50%) and 6–10 years in 1 (16.7%). Four of six (66.7%) were females and 4 (66.7%) were Caucasian and 2 (33.3%) Hispanic. The diagnosis at first transplant was congenital heart disease in 4 (66.7%) and cardio-myopathy in 2 (33.3%). No induction agents were used in first transplant and in 2 (33.3%) retransplants (IL-2 receptor antagonists). Maintenance immunosuppression for first transplants was CSA-based in 2, TAC in 1 and steroid or other-based in 3. At retransplant, maintenance immunosuppression was TAC-based in 3, CSA in 2 and steroid or other-based in 1. No first transplant was treated for rejection within the first year and 1/6 (16.7%) of retransplants was treated for rejection with Thymoglobulin™ within the first post-transplant year.
The median time from first transplant to PTLD diagnosis and to retransplant was 2121 days (range 1429–2736 days) and 2679 days (range 2092–4734 days), respectively (Figures 1 and 4). The median time from PTLD to retransplant was 880 days (range 0–1998 days) (Figure 5). The median first and retransplant graft survival times were 2679 days (range 2092–4734 days) and 750 days (range 15–2137 days), respectively. The median patient survival time after retransplant was 750 days (range 15–2137 days). Most patients (n = 4) developed PTLD and were retransplanted within 5–10 years of initial transplant. Two of six retransplanted patients have died (cardiac arrest and cardiogenic shock) with mean follow-up of 982 ± 337 days.
Four patients (two males and two females) underwent intestinal retransplantation after PTLD. All were pediatric recipients: 2 (50%) aged 1–5 years, 1 (25%) aged 6–10 years and 1 (25%) aged 11–17 years. The indications for the first transplant were short gut syndrome in three patients and functional bowel disorder in one patient. All patients were on TAC-based immunosuppressive regimens after the first transplant and after retransplantation. None of the patients experienced rejection either after the first transplant or after retransplantation. Induction agents were used in two of four of the first transplants (IL-2 receptor antagonist and OKT3 in one each) and in three of four retransplants (Thymoglobulin™ in two and IL-2 antagonist in one).
The median times from the first transplant to PTLD diagnosis and to retransplantation were 237 days (range 61–712 days) and 776 days (range 291–2432 days), respectively (Figures 1 and 4). The median time from PTLD to retransplantation was 655 days (range 0–1720 days) (Figure 5). The median graft survival times of the first and retransplant were 776 days (range 291–2432 days) and 190 days (range 12–360 days), respectively. The median patient survival time after retransplantation was 190 days (range 12–360 days). Three of four patients are still alive and three of four retransplants are functioning with median follow-up of 190 ± 96 days. The cause of graft loss for the remaining one patient was a perioperative death.
Only one individual underwent pancreas retransplantation after a diagnosis of PTLD. The subject was a Caucasian male, 32 years old. The times from transplant to PTLD and from PTLD to retransplantation were 1445 and 3340 days, respectively. The PTLD diagnosis was made 1895 days after the first transplant (Figures 1–5). The initial and retransplant immunosuppressive regimens were CSA-based. Induction was only used in the retransplant (thymoglobulin). The patient remains alive with a functioning graft.
For the entire cohort, 44 (63.8%) of the PTLD cases were reported prior to January 1, 1999, and therefore detailed pathologic information about the PTLD was not known. Of the 25 PTLD cases reported after January 1, 1999, the most common diagnosis was polymorphic lymphoma in 11 (44%), followed by monomorphic lymphoma in 7 (28%), polymorphic hyperplasia in 2 (8%), Hodgkin's disease in 1 (4%) and unknown in 4 (5%). The clonality of the lesion was characterized as monoclonal in 4 (16%), polyclonal in 9 (36%) and unknown in 12 (48%). The origin of PTLD was reported as B cell in 15 (60%), unknown in 10 (40%). Tumors were reported in a single site in 14 (56%), multiple sites in 9 (36%) and unknown in 2 (8%). EBV was reported as positive in 18 (26.1%), negative in 3 (4.3%) and not reported in 48 (69.6%).
PTLD remains a significant complication affecting solid organ transplant recipients with adverse effects on both graft and patient survival. The reported incidence of PTLD following transplantation varies by type of transplant. In a review of the European Collaborative Transplant database, the incidence of PTLD was greatest in thoracic transplant recipients. The combined heart-lung transplants were associated with the greatest risk of PTLD, followed by lung, heart and abdominal organs (13). Dharnidharka et al., in an extensive review of PTLD utilizing several national and international databases, found that the overall incidence of PTLD was 1.2% for kidney recipients, 2.4% for pediatric liver recipients, 2.3% for adult liver recipients, 3.9% for cardiac recipients and 8% for intestinal recipients (14). Other risk factors for the development of PTLD include pediatric recipient, the use of T-cell-depleting antibodies for induction or rejection, use of TAC, and transplantation of organs from an EBV+ donor into an EBV− recipient (13–16). Cherikh et al. showed that IL-2 receptor antibody induction was associated with the smallest risk of PTLD and with improved graft and patient survival. Other studies have demonstrated Caucasian race, male gender, CMV disease and liver transplantation for hepatitis C to be associated with an increased risk of PTLD (14,17). Given the myriad risk factors associated with PTLD, the common denominator is likely the overall degree of immunosuppression.
The treatment of PTLD includes restoration of EBV-specific immunity, cytotoxic chemotherapy, antiviral therapy, surgical resection, radiation, and, the use of anti-B-cell monoclonal antibody therapy (5,7,18,19). Reduction in immunosuppression has been reported to lead to remission or regression of disease in up to 50% and is a mainstay of therapy (20–22), but is associated with a high likelihood of allograft loss which is obviously fatal in heart, lung or liver transplant recipients unless the patients undergo retransplantation (7,23). The 1-year mortality rate after diagnosis of PTLD in kidney transplant recipients is 30–40% with a 57–75% rate of graft loss (10,11,13). In cardiac transplant recipients, outcomes are more ominous with a 1-year survival of only 45%. Acute cardiac decompensation after a reduction in immunosuppression is a frequent cause of death (24). Thus, many patients afflicted with PTLD will die of their disease, succumb to organ failure or return to dialysis.
The role of retransplantation of solid organ recipients after treatment for PTLD has been controversial because of the risk of recurrent PTLD with reintroduction of higher levels of immunosuppression. A number of case reports have cited data on a wide variety of solid organ recipients that have undergone retransplantation after a diagnosis of PTLD (8–12). Outcomes are generally best when EBV viral loads are undetectable, allograft nephrectomy had been performed, and 12–24 months have elapsed from PTLD diagnosis to retransplant. At the time of retransplant, a number of recommendations have been proposed, including use of prolonged antiviral agents, serial EBV monitoring, avoidance of over-immunosuppression and consideration of EBV-serostatus matching (25).
In this report, we have identified the largest cohort, to date, of individuals undergoing retransplantation after PTLD. Similar to previous studies on the prevalence of PTLD, pediatric recipients comprise the majority of individuals undergoing successful retransplantation after PTLD. The pediatric group comprised virtually all recipients of intestinal, heart, liver and lung transplants receiving retransplants for PTLD. Only in kidney transplants did adults outnumber children.
Immunosuppression favored CSA with the first transplant and conversion to TAC-based therapy at retransplant. Although no patient initially induced with antilymphocyte antibodies was re-induced at retransplantation, 10% of retransplanted recipients were induced with these agents in spite of the documented increased risk of PTLD. More reliance on IL-2R antagonists was noted at retransplant vs. first transplant and likely is reflective of a concern for the role of the overall level of immunosuppression and association with PTLD. Data demonstrating a lower risk of PTLD with IL-2R antagonists was published after the date of retransplantation for this series (15). Despite evidence demonstrating a higher rate of PTLD with TAC-based regimens, most retransplants were maintained on TAC (13). As with other immunosuppressive agents, therapeutic strategies reflect national trends in antirejection therapy rather than a concerted effort to lower the level of immunosuppression at the time of retransplantation. In Shapiro's review of immunosuppression trends, induction rates for renal transplant have increased from 25% in 1994 to 70% in 2003, with the agent of choice nationally being rabbit ATG, whereas in our subjects it was IL-2R antagonists (26). This is likely reflective of physician concern of over-immunosuppression and PTLD recurrence. The use of induction agents in liver recipients remains unusual and national trends demonstrate an increased utilization from 7% in 1997 to 20% in 2003. Their use is primarily for those with renal dysfunction, with expected delayed introduction of calcineurin inhibitors (26). In our series, the use of induction agents increased from 9.2% of first to 18.2% of retransplants with the agent of choice an IL-2R antagonist. Lastly, the national trend away from CSA- to TAC-based regimens (67% of kidneys and 86% of livers) was also exhibited. CSA was the predominant agent in first renal transplants, but TAC was used in 59% of retransplants. Similarly, in liver transplant recipients, CSA was used in 31.8% of first and in only 9.1% retransplants. These findings mirror those seen nationally with TAC-based therapies used in 67% of kidneys and in 86% of liver recipients (26). Furthermore, the trend toward elimination of azathioprine in favor of mycophenolic acid was seen in this review. These findings suggest that individuals retransplanted after PTLD receive similar induction and maintenance agents as the non-PTLD population. Thoracic organ transplants also followed national immunosuppression trends, including more frequent use of TAC-based therapies and use of mycophenolic acid in favor of azathioprine (26).
Timing of retransplantation clearly is an important consideration to optimize successful outcomes. In Karras' review of six renal retransplants after PTLD, all recipients had 2 years of documented PTLD remission prior to listing, and all had undergone allograft nephrectomy. The median delay from PTLD to retransplant was 77 months (9). Our report demonstrates comparable waiting periods for renal retransplant recipients of whom 16 (59.3%) waited at least 3 years. Most recipients of retransplantation waited more than 1-year from diagnosis of PTLD to retransplant. Shorter time periods from diagnosis to retransplant were observed for liver and lung recipients of whom 18 of 22 (81.8%) and 8 of 9 (88.9%), respectively, were retransplanted within 3 years of diagnosis. This is likely reflective of urgency of medical need, but may also result from shorter wait times for deceased donor organs as compared to kidney and cardiac allografts.
In summary, retransplantation after graft loss following a diagnosis of PTLD has been reported in 69 recipients, the majority of whom are children and recipients of liver or renal allografts. Surprisingly, immunosuppressive therapy following retransplantation closely mirrored that reported nationally, suggesting more concern on the part of transplant physicians for acute rejection than recurrent PTLD. Of the 69 retransplants performed, only 10 (14.4%) patients have died, with the greatest mortality seen after thoracic organ retransplant where 7 of 15 (46.7%) have died. In contrast, no deaths were reported after 27 renal retransplants and in only 3 of 22 (13.6%) liver retransplants, suggesting improved outcomes for abdominal retransplantation after PTLD as compared to thoracic organ retransplantation. While most waited more than 1 year from PTLD diagnosis to retransplant, a number of them were transplanted at less than 1 year from diagnosis, suggesting that individualization of timing of retransplant based on need can be done with acceptable results. Improved data reporting for histopathology, EBV serostatus and clonality would permit improved determination of prognostic factors.
- 7Analysis of factors that influence survival with post-transplant lymphoproliferative disorder in renal transplant recipients: The Israel Penn International Transplant Tumor Registry experience. Am J Transplant 2005; 5(4 Pt 1): 775–780., , et al.
- 10Long-term follow-up of kidney transplant patients with posttransplant lymphoproliferative disorder: Duration of posttransplant lymphoproliferative disorder-induced operational graft tolerance, interleukin-18 course, and results of retransplantation. Transplantation 2003; 76: 153–158., , .
- 11Renal retransplantation in patients who lost their allografts during management of previous post-transplant lymphoproliferative disease. Clin Transplantation 1990; 4: 187–190., , et al.
- 18Treatment of posttransplant lymphoproliferative disorder with the anti-CD20 monoclonal antibody rituximab alone in an adult after liver transplantation: A new drug in therapy of patients with posttransplant lymphoproliferative disorder after solid organ transplantation? Transplantation 2000; 69: 430–432., , , , .