Evolution of trends in the live kidney transplant donor-recipient relationship.

OBJECTIVE: This study examined the changing demographics and age profile between living donors and their recipients. A 46-year review of living donor renal transplants in a single transplant center was performed. PATIENTS: The study included 923 consecutive living donor renal transplants from January 1966 until December 2011. RESULTS: These 923 living donor kidneys transplants represent 41% of all transplants performed during this 46-year review. The majority involved sibling donation (39.5%) followed by parent to child (32.5%). Dividing the 46-year timeframe into quartiles, the mean age of donors has remained stable at 39.3 ± 10.9 years. In contrast, the mean age of recipients has trended upwards, from 28 ± 10.7 years in the first quartile (1966-1978) to 37 ± 17.5 years in the latest quartile (2001-2011). This represents an increase every year of approximately 4 months (P < .001). Over the same period, the difference between a given donor's age and their recipient's has decreased every year by approximately 4 months (P < .001). In a linear regression model of donor-recipient categories and their age difference over time, we found that both the child-to-parent and grandchild-to-grandparent groups had the largest effect on the donor-recipient age difference when compared to the classic parent-to-child relationship. CONCLUSION: This review of center-specific data shows that the difference in the age of the donor to their recipient has been narrowing over time. We have determined that this is primarily due to changes in donor-recipient demographics with an increasing number of younger donors to older recipients. Although the medical risks to donors living with a single kidney have yet to be shown different than that of the general population, the increasing volume of donors who are younger and those with no relation to the recipient should prompt closer follow-up within the transplantation medical community.

IL-12 treatment of endogenously arising murine brain tumors.

A number of recent studies have indicated that T cells can be stimulated to attack transplanted brain tumors in rodent models. As IL-12 has been shown to activate cytotoxic T cell responses, we tested the idea that it might stimulate a T cell response against endogenous brain tumors that arise in SV40 large T Ag transgenic mice (SV11). SV11 mice develop tumors of the choroid plexus, a specialization of the ependymal lining of the brain ventricles. They are a particularly relevant model of human disease, because they are immunocompetent but immunologically tolerant of the tumors. SV11 mice were treated with recombinant murine IL-12 for 10 days. Tumors grew more slowly than in control treated mice, and in some cases were reduced in size, as assessed by magnetic resonance imaging before and after treatment. At the end of treatment, tumors, but not brain parenchyma, exhibited extensive infiltration of activated CD8(+) and CD4(+) T cells. Tumors also showed a reduction in vascular density. Mice treated with IL-12 lived significantly longer than control mice. Tumors that progressed were nearly devoid of T cells, indicating that the T cell response was not sustained. In addition, some mice that had a substantial tumor burden at the beginning of treatment displayed evidence of immunosuppression, which might be related to TGF-ss2 detected in tumors. We conclude that IL-12 treatment can initiate an anti-tumor response even against endogenously arising brain tumors, but factors that will allow a sustained and more effective anti-tumor response need to be determined.