Successful urgent transplantation of an adult kidney into a child with inferior vena cava thrombosis.

Poor venous drainage options following inferior vena cava (IVC) thrombosis have been considered to complicate or preclude renal transplantation of adult kidneys into pediatric patients. We describe urgent renal transplantation in a 5-year-old (15.3 kg) male with IVC thrombosis using an adult living donor. Preoperative magnetic resonance venography revealed a patent infrahepatic/suprarenal vena cava and portal system. In surgery, the right liver lobe was mobilized sufficiently to anastomose the graft renal vein to the native IVC at the confluence of the native left renal vein and proximal vena cava. Graft function has remained excellent with serum creatinine of 0.5 mg/dL at 36 months. IVC thrombosis need not preclude successful transplantation of adult-sized kidneys into children.

Increased primary non-function in transplanted deceased-donor kidneys flushed with histidine-tryptophan-ketoglutarate solution.

Histidine-Tryptophan-Ketoglutarate (HTK) solution is increasingly used to flush and preserve organ donor kidneys, with efficacy claimed equivalent to University of Wisconsin (UW) solution. We observed and reported increased graft pancreatitis in pancreata flushed with HTK solution, which prompted this review of transplanting HTK-flushed kidneys. We analyzed outcomes of deceased-donor kidneys flushed with HTK and UW solutions with a minimum of 12 months follow-up, excluding pediatric and multi-organ recipients. We evaluated patient and graft survival and rejection rates, variables that might constitute hazards to graft survival and renal function. Two-year patient survival, rejection, renal function and graft survival were not different, but early graft loss (<6 months) was worse in HTK-flushed kidneys (p < 0.03). A Cox analysis of donor grade, cold ischemic time, panel reactive antibodies (PRA), donor race, first vs. repeat transplant, rejection and flush solution showed that only HTK use predicted early graft loss (p < 0.04; relative risk = 3.24), almost exclusively attributable to primary non-function (HTK, n = 5 (6.30%); UW, n = 1 (0.65%); p = 0.02). Delayed graft function and early graft loss with HTK occurred only in lesser grade kidneys, suggesting it should be used with caution in marginal donors.

Increased pancreatitis in allografts flushed with histidine-tryptophan-ketoglutarate solution: a cautionary tale.

We reviewed pancreas transplantation outcomes after Histidine-Tryptophan-Ketoglutarate (HTK) and University of Wisconsin (UW) preservation solution use between 2001 and 2007 at two transplant centers. While equivalence has been claimed for kidney and liver transplant outcomes after the use of HTK or UW preservation solution, consensus has not been reached on equivalence when flushing pancreata. Others have reported comparable patient and graft survival rates, but found an association between the use of HTK and an increase in the incidence of acute rejection and pancreatitis. In reviewing our experiences, we found in pancreata flushed with HTK a higher incidence of postoperative complications including graft pancreatitis, use of octreotide and a decreased rate of insulin-independence at hospital discharge. These findings prompted us to critically review our centers' experience to determine if there is a basis for suspecting a causal relationship.

Hashimoto's encephalopathy after intensive lymphocyte depletion with rabbit anti-thymocyte globulin in a renal transplant patient.

There has been no reported case of Hashimoto's encephalopathy (HE) ('steroid-responsive encephalopathy associated with autoimmune thyroiditis', 'SREAT'), in the renal transplant recipient population. We describe the case of a 55-year-old female with Type-1 diabetes who presented 2 years posttransplantation in a comatose state that had developed over the preceding 24 h. The patient had received a short, intensive course of rATG induction at the time of transplantation and early steroid withdrawal. After 6 months she had been withdrawn from calcineurin inhibitors and was maintained on mycophenolate mofetil and sirolimus. Systematic workup determined the cause of her coma to be HE. High-dose steroid therapy resulted in complete resolution of the patient's symptoms. The literature regarding the diagnosis, course and treatment of HE is reviewed and the possibility that increased use of steroid-free immunosuppression and intensive lymphocyte depletion regimens may increase the prevalence of de novo autoimmune disease is discussed.