ObjectiveTo compare the outcome of simultaneous pancreas-kidney transplantation (SPK) and living related donor renal transplantation (LRD) in patients with diabetes. Summary Background DataIt remains unanswered whether diabetic patients with endstage renal failure are better served by LRD or SPK. MethodsUsing a longitudinal database, data from all diabetic patients receiving LRD or cadaveric renal transplants or SPKs from January 1986 through January 1996 were analyzed. Patient and graft survival, early graft function, and the cause of patient and graft loss were compared for 43 HLA-identical LRDs, 87 haplotype-identical LRDs, 379 SPKs, and 296 cadaveric renal transplants. ResultsThe demographic composition of the SPK and LRD groups were similar, but because of less strict selection criteria in the cadaveric transplant group, patients were 10 years older, more patients received dialysis, and patients had been receiving dialysis longer before transplantation. Patient survival was similar for the SPK and LRD groups but was significantly lower for the cadaveric renal transplant group. Similarly, there was no difference in graft survival between SPK and LRD recipients, but it was significantly lower for recipients in the cadaveric renal transplant group. Delayed graft function was significantly more common in the cadaveric renal transplant group. Discharge creatinine, the strongest predictor of patient and graft survival, was highest in the SPK group and lowest in the HLA-identical LRD group. The rate of rejection within the first year was greatest in SPK patients (77%), intermediate in the haplotype-identical LRD and cadaveric transplant groups (57% and 48%, respectively), and lowest (16%) in the HLA-identical LRD group. Cardiovascular disease was the primary cause of death for all groups. Acute rejection, chronic rejection, and death with a functioning graft were the predominant causes of graft loss. ConclusionsThis study demonstrates that there was no difference in patient or graft survival in diabetic patients receiving LRD or SPK transplants. However, graft and patient survival rates in diabetic recipients of cadaveric renal transplants were significantly lower than in the other groups.

Experience with hepatic artery embolization for the treatment of symptomatic hepatic arteriovenous malformations (AVMs) in Rendu-OslerWeber disease is limited. We report 2 cases of hepatic AVMs that caused mesenteric angina-like symptoms that were treated with embolization. Both patients developed parenchymal and bile duct necrosis, intrahepatic bilomas, and refractory biliary sepsis, subsequently leading to liver failure. We hypothesize that the pathophysiological cause of biliary necrosis in this setting is similar to that which occurs in the setting of hepatic artery thrombosis of the liver allograft. Progressive liver failure in these patients was treated successfully by liver transplantation. Liver transplantation offers definitive therapy by removing the source of ongoing sepsis, restoring normal liver function, and eliminating the intrahepatic AV shunt.