POSTTRANSPLANT LYMPHOPROLIFERATIVE DISORDER IN RENAL-ALLOGRAFT RECIPIENTS - CLINICAL-EXPERIENCE AND RISK FACTOR-ANALYSIS IN A SINGLE-CENTER

Citation
Sm. Cockfield et al., POSTTRANSPLANT LYMPHOPROLIFERATIVE DISORDER IN RENAL-ALLOGRAFT RECIPIENTS - CLINICAL-EXPERIENCE AND RISK FACTOR-ANALYSIS IN A SINGLE-CENTER, Transplantation, 56(1), 1993, pp. 88-96
Citations number
40
Categorie Soggetti
Immunology,Surgery
Journal title
ISSN journal
00411337
Volume
56
Issue
1
Year of publication
1993
Pages
88 - 96
Database
ISI
SICI code
0041-1337(1993)56:1<88:PLDIRR>2.0.ZU;2-N
Abstract
Post-transplant lymphoproliferative disorder (PTLD) is a well-recogniz ed complication of solid organ transplantation. The University of Albe rta Renal Transplant Program had not experienced a case of PTLD occurr ing in the early post-transplant period until March 1989. Since then, 4 patients have developed this complication. To identify the major ris k factors for the recent appearance of PTLD, a retrospective analysis was carried out on 162 cadaveric renal transplants performed between J uly 1987 and December 1990. Four cases of polymorphic PTLD were seen. Two patients presented with fatal disseminated disease. Two others dev eloped PTLD confined to the renal allograft; both are disease free at >24 months of follow-up. Seventy-two (44.4%) of the cadaveric transpla nt recipients had received Minnestota antilymphocyte globulin (MALG) i nduction therapy during the study period. Twenty-four of these also re ceived OKT3 for steroid-resistant rejection. Of the 4 patients with PT LD, 3 had received both MALG induction and OKT3; the remaining patient had received MALG induction only. The incidence of PTLD in the MALG/O KT3 group was 12.5%, which is significantly higher than that of patien ts receiving other immunosuppressive regimes (0.7%, P=0.015). The inci dence of PTLD was also significantly greater in the 13 patients at ris k for primary EBV infection compared to the EBV seropositive patients (23.1 vs. 0.7%, P=0.002). Only 2 seronegative patients received sequen tial MALG/OKT3; both developed PTLD. Thus, the population most at risk is that receiving potent antilymphocyte preparations in the setting o f primary EBV infection. Allograft involvement with PTLD must be consi dered in the differential diagnosis of allograft dysfunction, as early diagnosis may permit the successful management of this complication.