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To satisfy the increasing requests for renal grafts, elderly donors are increasingly accepted for kidney transplant at many centers. The main unresolved question is the long-term effect on graft survival of potential histological lesions due to donor age. We present a prospective histological study performed from January 1997 to December 2001 on 184 consecutively transplanted renal grafts in which the only criterion for graft acceptance was a normal value of serum creatinine upon admission to the intensive care unit independent of donor age. At the end of the study, 57 recipients (31%) of mean age 55 years (range 39 to 67 years) received a renal graft from donors aged more than 60 years (mean age 66 years; range 60 to 75 years), this cohort denoted as older donor kidney transplant group (ODKTG) and 127 recipients (69%) with a mean age of 49 years (range 21 to 63 years) received a renal graft from donors whose age was lower than 60 years (mean age 49 years; range 16 to 59 years), a cohort denoted as the younger donor kidney transplant group (YDKTG). The two groups were comparable for time of dialysis, cold ischemia time, immunosuppression therapy, grading of histological damage. At the end of the study with a mean follow-up of 5.6 years (range 3.5 to 7.5 years), primary graft nonfunction and delayed graft function were significantly more represented in the ODKTG than the YDKTG. Cumulative patient and graft survival was 84.3% and 79.4% in the ODKTG, respectively, and 93.8% and 85.9% in the YDKTG, respectively (P = NS). Cumulative serum creatinine values were 1.98 mg/100 mL in ODKTG and 1.65 mg/100 mL in YDKTG (P = NS). In conclusion, renal grafts from older donors presented histological damage comparable to that seen among renal grafts from younger donors.

Over the years, the frequency of heart transplant candidates with HLA sensitization has increased as a result of the number of patients bridged to transplant using left ventricular assist devices (LVAD). Here we have examined 119 patients who were bridged to transplant with LVAD for a relationship between HLA antibodies and early (30 days) and late (2 years or more) rejection, as evidenced by endomyocardial biopsies. Both cytotoxic panel-reactive antibody reactions against a panel of T lymphocytes (T-PRA) and the percentage of transplants that occurred across a positive class I flow cross-match were examined. Biopsies were scored using ISHLT criteria. At 30 days, patients who had a biopsy grade of 0 had a mean T-PRA at transplant of 2.2%, while the mean PRAs of the other biopsy grades were significantly higher (P < .001). A similar pattern was seen with the highest biopsy results at 2 years or later (P < .001). None of the patients who had a grade 0 biopsy at 30 days posttransplant had a positive flow cytometry class I cross-match (P = .02), although the same pattern did not occur later due to a small number of patients (n = 3) who had negative biopsies. Thus, when biopsy results were examined early or late posttransplant, patients with negative biopsy results tended to have less HLA sensitization. While the methods of HLA sensitization involve humoral responses, more aggressive immunosuppression might be warranted to attempt to reduce cellular rejection posttransplant if HLA class I antibodies are present at the time of transplant.