Ten-year experience of selective omission of the pretransplant crossmatch test in deceased donor kidney transplantation.

BACKGROUND: A pretransplant lymphocyte crossmatch (XM) test is usually considered mandatory but may delay deceased donor renal transplantation. We report on the safety and clinical efficacy of omitting the XM when it is predicted to be negative based on sensitization history and human leukocyte antigen-specific antibody screening. METHODS: From 1998 to 2008, 606 deceased donor kidney transplants were performed at our center and the prospective donor-recipient XM omitted in 257 (42%). In all cases, a negative XM was confirmed retrospectively. Four hundred fourteen (68%) kidneys were donated after brain death (DBD) and 192 (32%) after cardiac death (DCD). The effect of this policy on cold ischemia time (CIT), delayed graft function (DGF), and transplant survival was assessed. RESULTS: Mean CIT was 16.7 hr with a prospective XM and 14.3 hr when it was omitted (P<0.001). The beneficial effect of omitting the XM on DGF was only apparent in recipients of DBD kidneys, where the DGF rate was 28% with a prospective XM and 18% without a prospective XM (P=0.03). The corresponding DGF rate in recipients of DCD kidneys was 52% with a prospective XM and 54% without a prospective XM. Logistic regression analysis, after adjustment for variables that influenced DGF, showed that the odds on suffering DGF were lower when the pretransplant XM test was omitted (P=0.04). Neither acute rejection rate nor long-term graft survival was influenced by omission of the XM. CONCLUSION: Rigorous recording of potential allosensitizing events and comprehensive antibody screening allows the XM to be safely omitted in selected patients and this helps limit CIT and may reduce DGF.

Soluble CD30 levels in recipients undergoing heart transplantation do not predict post-transplant outcome.

BACKGROUND: The pre-transplant serum level of soluble CD30 (sCD30), a proteolytic derivative of the lymphocyte surface receptor CD30, has been suggested as a biomarker for immunologic risk after organ transplantation. METHODS: Pre-transplant serum sCD30 levels were determined in 200 consecutive adult heart transplant recipients undertaken at a single center. Transplant outcome (acute rejection in the first 12 months and patient survival up to 5 years post-transplant) was determined. RESULTS: Patients treated with a left ventricular assist device (LVAD) prior to transplantation (n = 28) had higher levels of sCD30 (median 64 U/ml, range 12 to 112 U/ml) than those (n = 172) with no LVAD (median 36 U/ml, range 1 to 158 U/ml, p < 0.0001). Recipients were categorized according to whether sCD30 levels were "low" (lower quartile, <24 U/ml, n = 50), "intermediate" (24 to 58 U/ml, n = 100) or "high" (upper quartile, >58 U/ml, n = 50). Neither acute rejection nor recipient survival differed according to sCD30 level, with values (mean +/- SEM) of 0.30 +/- 0.04, 0.23 +/- 0.03 and 0.30 +/- 0.05 acute rejection episodes per 100 days in the low, intermediate and high groups, respectively, with recipient survival rates at 1 year of 77.7%, 84.9% and 86% and at 5 years of 73.6%, 67.9% and 75.8%, respectively. CONCLUSIONS: Pre-transplant serum sCD30 level does not predict acute allograft rejection or recipient survival after heart transplantation, although sCD30 levels are increased by LVAD, possibly as a result of biomaterial-host immune interaction.

Monitoring systemic donor lymphocyte macrochimerism to aid the diagnosis of graft-versus-host disease after liver transplantation.

BACKGROUND: The diagnosis of graft-versus-host disease (GvHD) after liver transplantation can be difficult because early symptoms are often nonspecific. In this study, the presence of donor lymphocyte macrochimerism in recipient peripheral blood was examined as a diagnostic aid for GvHD after cadaveric donor liver transplantation. METHODS: Between 1996 and 2002, 33 liver transplant recipients with a clinical suspicion of GvHD (skin rash, diarrhea, pyrexia, pancytopenia, or anemia, without an obvious alternative cause) were investigated for peripheral blood donor lymphocyte macrochimerism. Donor macrochimerism was determined at the time of first clinical presentation by a low-sensitivity polymerase chain reaction (PCR) to detect donor human leukocyte antigen (HLA) alleles using genomic DNA extracted from recipient peripheral blood. Where donor HLA alleles were detected, the percentage of donor T cells was quantified by two-color flow cytometric analysis using antibodies specific for mismatched donor and recipient HLA alleles. The relationship between the presence or absence of donor lymphocyte macrochimerism and final diagnoses based on clinical and histological criteria was examined. RESULTS: Seven of the 33 patients were PCR positive for donor HLA alleles. All had macrochimerism, with donor T lymphocyte levels ranging from 4% to 50% of circulating lymphocytes. All seven patients had normal liver function tests, skin rash, and diagnosis of GvHD histologically confirmed by skin or gut biopsies. Twenty-six patients were PCR negative, and, in 23, an alternative diagnosis was eventually established. The remaining three patients made a rapid and spontaneous recovery with no further symptoms suggestive of GvHD. CONCLUSIONS: Donor lymphocyte macrochimerism was present in all patients in whom the diagnosis of GvHD was confirmed. In patients with symptoms consistent with GvHD and a negative PCR for donor HLA, an alternative diagnosis was eventually established or the patients recovered spontaneously. Detection of donor HLA alleles in recipient peripheral blood by PCR is a useful diagnostic tool for GvHD after liver transplantation.