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Objective: We previously showed that kidney allografts have the ability to confer tolerance on a co-transplanted heart allograft procured from the same class I-disparate, miniature swine donor. However, kidney-induced cardiac allograft tolerance (KICAT) has not been tested in a more clinically relevant, full MHC disparate strain combination. Design: Heart allografts (n=3) or heart and kidney allografts (n=5) were transplanted into MHC-mismatched recipients treated with high-dose FK506 for 12 days. Setting: Transplantation Biology Research Center, Massachusetts General Hospital, Boston, MA. Patients: MHC-inbred miniature swine. Interventions: Heterotopic heart/kidney transplantation. Main Outcome Measures: Tolerance and cardiac allograft survival as measured by clinical exam, histology, and in vitro assays. Results: All isolated heart allografts rejected by POD 40. In contrast, heart and kidney allografts survived for >200 days with no evidence of rejection on serial cardiac biopsies. Heart and kidney recipients lost donor-specific responsiveness in CML and MLR assays, were free of alloantibody and exhibited prolonged survival of donor, but not third-party skin grafts. Late (>100 days) removal of the kidney allografts did not cause acute rejection of the heart allografts (n=2) and did not abrogate donor-specific unresponsiveness in vitro. Conclusions: KICAT can be extended to fully mismatched allografts in a consistent and robust manner. Elucidating the renal element responsible for KICAT could provide mechanistic information that leads to protocols which successfully induce tolerance in recipients of isolated heart allografts and other tolerance-resistant organs.