Passenger Lymphocyte Syndrome After Simultaneous Pancreas-Kidney Transplantation: A Case Report of an Unusual Cause of Alloimmune Hemolytic Anemia.

BACKGROUND: Passenger lymphocyte syndrome (PLS) is a disease in which the donor's lymphocytes produce antibodies to the red blood cell antigens of the recipient, causing alloimmune hemolysis. CASE REPORT: We report the case of a 39-year-old woman with stage V chronic kidney disease on hemodialysis secondary to poorly controlled diabetes mellitus type 1. She received a simultaneous pancreas-kidney transplant from a cadaver donor. The donor was A- and the recipient was A+ without initial complications with normal renal and pancreatic function, and her hemoglobin (Hb) level was 10.2 g/dL at discharge. Four weeks later she was admitted with acute pyelonephritis of the renal graft, with a Hb level of 7.5 g/dL, creatinine level of 0.7 mg/dL, and glucose level of 80 mg/dL. The study of anemia showed direct polyspecific direct Coombs weakly positive (w/+), presenting 2 alloantibodies against the Rh system: anti-D, anti-E. We increased Prednisone dose to 1 mg/kg/d and then decreased it in a pattern. Eight days after discharge, without transfusion, her Hb level was 9.9 g/dL and then it normalized. CONCLUSIONS: PLS is a very rare condition and should be suspected in the first few weeks after transplantation. In our case anemia was probably due to a residual population of Rh-negative donor cells in the transplanted pancreas-kidney received. It is usually a sudden onset of hemolytic anemia in patients with a solid organ transplant and different Rh or ABO lower incompatibility.

Tyrosine-phosphatase and glutamate-decarboxylase antibodies after simultaneous pancreas kidney transplantation: do they have an impact on pancreas graft survival?

INTRODUCTION: The pathogenesis of type 1 diabetes mellitus (T1DM) is associated with auto-antibodies. These auto-antibodies contribute to pancreatic ß-cell destruction. Tyrosine-phosphatases (IA-2) and glutamic acid decarboxylase (GAD65) are the most frequently used by clinicians. When T1DM patients develops advanced chronic kidney disease, simultaneous pancreas-kidney (SPK) transplantation becomes the best option. However, pancreatic graft survival is limited. The role of the auto-antibodies on pancreas graft survival remains controversial. OBJECTIVE: The aim of this study was to assess pancreas graft survival according to the presence of GAD65 and IA-2 auto-antibodies after SPK transplantation. METHODS: We analyzed all SPK transplantations performed in our hospital since January 1990 to December 2013 with at least 30 days of pancreas graft survival. We collected demographic and clinical variables from donors and recipients. Graft failure was defined as complete insulin independence after transplantation. Pancreatic graft survival was analyzed using the Kaplan-Meier method. RESULTS: Overall, 152 SPK transplantations were performed during the period. One hundred sixteen were accessed for de novo post-transplantation auto-antibodies. Also, 17.8% (n = 27) were positive for anti-GAD65, 13.8% (n = 20) for IA-2, 3.9% (n = 6) were positive for both, and the rest were negative for any auto-antibody (n = 63). Kaplan-Meier survival curves estimated a worst pancreas graft survival for patients with positive IA-2 antibodies versus those patients with negative auto-antibodies and GAD65+auto-antibodies (P = .003 and .022, respectively, by log-rank). Mean pancreas graft survival rates at first and fifth year were 72% and 64%, respectively, for those patients with positive IA-2. CONCLUSIONS: IA-2 antibodies after SPK transplantation are associated with long-term graft lost compared with the rest of the groups. Monitoring of these auto-antibodies after SPK may help to identify patients with a higher risk of graft failure.

Short-term evolution of renal transplant with grafts from donation after cardiac death: Type III Maastricht category.

BACKGROUND: Kidney transplantation from donors after cardiac death (Type III Maastricht category) is a therapeutic option for patients with terminal renal failure. MATERIALS AND METHODS: We present a cohort of 8 patients who received a kidney transplant from donors after cardiac death (DCD). We analyzed the analytical results for the first 6 months after transplantation. RESULTS: We included 8 cases of kidney transplants with organs from DCD (Type III Maastricht category). The mean age of donors was 58.40 ± 4.39 years and 3 (60%) were male. The mean creatinine (Cr) level prior to death was 1.10 ± 0.36 mg/dL. The mean age of recipients was 59.88 ± 10.58 years and 7 (87.5%) were male. Seven patients (87.5%) were on hemodialysis, whereas only 1 (12.5%) was on peritoneal dialysis. The median time on renal replacement therapy was 18 months (range, 2-76). Mean total warm ischemia time (WIT) was 24.88 ± 6.72 minutes, whereas the mean real WIT was 20.13 ± 4.51 minutes. The mean cold ischemia time (CIT) was 6 hours and 12 minutes ± 2 hours. Preimplantation biopsy showed acute tubular necrosis (extensive 40%). Tubular atrophy was mild in 100% of cases. After transplantation, 6 patients (75%) had delayed graft function requiring dialysis sessions whereas 2 patients (25%) did not require renal replacement therapy. Mean Cr level at 1, 3, and 6 months after transplantation was 2.37, 1.75, and 1.17 mg/dL, respectively. CONCLUSION: Kidney transplantation with grafts from donors after cardiac arrest Maastricht Type III evolves favorably in the short term. According to preliminary results, controlled asystole donation could be an effective alternative to transplantation.