ABSTRACT
BACKGROUND: Concern that morbidly obese (body mass index [BMI] 35) kidney transplant recipients have worse outcomes than non-morbidly obese recipients leads many transplant centers to deny them the benefit of kidney transplantation. These concerns are supported by guidelines recently published by the American Society of Transplantation. However, successfully transplanted morbidly obese persons have a survival advantage over those that remain on dialysis. It is our practice to evaluate morbidly obese transplant candidates for transplantation under the same criteria used for nonobese candidates. This report reviews our experience with morbidly obese kidney transplant recipients having a three year follow-up. METHODS: Outcomes for 23 morbidly obese (BMI 35, range 37 to 56) kidney transplant recipients transplanted between January 1995 and February 2000 were compared with 224 nonobese (BMI 25) kidney recipients transplanted during the same period. RESULTS: Patient and graft survivals were similar between both groups. Although 3-year graft survival for morbidly obese recipients of cadaver organs was 75% compared with 90% for the nonobese group, this finding was not statistically significant, and 3-year graft survival was 100% for morbidly obese recipients of living donor organs compared with 91% for nonobese recipients. Morbidly obese recipients had significantly longer hospital stays, higher readmission rates, and a higher wound infection rate than nonobese recipients. CONCLUSIONS: We found that morbidly obese persons have 3-year graft and patient survivals similar to nonobese persons. Although they also have greater complications and greater numbers of days in the hospital, we believe these reasons are not sufficient to deny morbidly obese persons the survival and quality-of-life advantages of kidney transplantation.
Subject(s)
Kidney Failure, Chronic/surgery , Kidney Transplantation , Obesity, Morbid/complications , Actuarial Analysis , Adult , Body Mass Index , Case-Control Studies , Cause of Death , Contraindications , Female , Follow-Up Studies , Graft Rejection/epidemiology , Graft Rejection/etiology , Graft Survival , Humans , Kidney Failure, Chronic/complications , Kidney Failure, Chronic/mortality , Kidney Transplantation/mortality , Kidney Transplantation/psychology , Length of Stay/statistics & numerical data , Living Donors , Male , Middle Aged , Patient Readmission/statistics & numerical data , Patient Selection , Practice Guidelines as Topic , Quality of Life , Surgical Wound Infection/epidemiology , Surgical Wound Infection/etiology , Survival Analysis , Treatment Outcome , Washington/epidemiologyABSTRACT
We studied nonviral delivery, expression, and the effect of the human interleukin-10 (Hu IL-10) gene on the rat model of heterotopic auxiliary liver transplantation (HALT). Two previous pilot studies showed remarkable expression of the Hu IL-10 gene in donor and recipient rats, and a decreasing effect of acute rejection in certain cases. In this study, we focused on the efficacy of Hu IL-10 gene expression to decrease acute rejection compared with cyclosporine A (CyA) in a HALT model. Three study groups and one control group were designed. Each group consisted of 6 DA donor and 6 Lewis recipient rats, which underwent HALT. In the control group, donors and recipients were not treated at all. In group II, recipients were treated with one dose of CyA. In group III, donors were treated with Hu IL-10 plasmid. In group IV, donors were treated with Hu IL-10 plasmid, and recipients were treated with one dose of CyA. Rejection was established by histopathology: it revealed 100% rejection in control and 33.3% rejection in study groups II, III, and IV. Human IL-10 gene expression prevented acute rejection with the same efficacy as CyA in the HALT model in rats.
Subject(s)
Adjuvants, Immunologic/administration & dosage , Gene Expression/immunology , Genetic Therapy/methods , Graft Rejection/prevention & control , Interleukin-10/administration & dosage , Liver Transplantation/immunology , Acute Disease , Adjuvants, Immunologic/genetics , Animals , Cyclosporine/administration & dosage , Female , Genetic Vectors/immunology , Graft Rejection/immunology , Humans , Immunosuppressive Agents/administration & dosage , Interleukin-10/genetics , Interleukin-10/immunology , Liver Transplantation/methods , Male , Models, Animal , Rats , Rats, Inbred LewABSTRACT
Pyruvate carboxylase deficiency, complex form, presents in early infancy with lethal metabolic acidosis, resulting from ketoacidosis and lactic acidemia. Renal tubular acidosis, hyperammonemia, and citrullinemia complete the picture. In an infant with this disease, large amounts of glucose ameliorated the ketoacidosis, but worsened the lactic acidosis. Orthotopic hepatic transplantation completely reversed the ketoacidosis and the renal tubular abnormality and ameliorated the lactic acidemia. Concentrations of glutamine in cerebrospinal fluid were low and did not improve with liver transplantation.
