Journal Information
Vol. 33. Issue. 4.July 2013
Pages 443-622
Vol. 33. Issue. 4.July 2013
Pages 443-622
DOI: 10.3265/Nefrologia.pre2013.May.11930
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Passenger lymphocyte syndrome: an uncommon form of anaemia in renal transplantation
Síndrome del linfocito pasajero: una rara forma de anemia en el trasplante renal
Verónica Pascual Péreza, Verónica Pascual-Pérezb, Nerea Gómez Larrambec, Nerea Gómez-Larrambed, Rocío Collantes Mateosa, Rocío Collantes-Mateosb, Teresa Visus Fernández de Manzanosc, Teresa Visus-Fernández de Manzanosd, José Manuel Urbizu Gallardoc, José M. Urbizu-Gallardod, Auxiliadora Mazuecos Blancaa, Auxiliadora Mazuecos-Blancab
a Servicio de Nefrolog??a, Hospital Universitario Puerta del Mar, C??diz, C??diz, Spain,
b Servicio de Nefrolog??a, Hospital Universitario Puerta del Mar, C??diz,
c Servicio de Nefrolog??a, Hospital Universitario de Cruces, Barakaldo, Vizcaya, Spain,
d Servicio de Nefrolog??a, Hospital Universitario de Cruces, Barakaldo, Vizcaya,
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To the Editor:

Passenger lymphocyte syndrome (PLS) is an alloimmune haemolytic anaemia in solid organ transplantation (SOT) caused by alloantibodies derived from a donor B cell clone, that are transferred with the graft, resulting in a secondary immune response against the recipient's red blood cells in SOT with compatible but not identical blood groups.1-5 It is an uncommon entity whose frequency has been related to the size (in terms of lymphoid content) of the transplanted organ and is much more common in heart/lung (70%) and liver (29%) than in renal transplantation (RT) (9%).2,3 The antibodies are normally anti-ABO, uncommonly anti-D, and there are isolated cases of anti-C, anti-E, anti-Kell, anti-Jk and anti-Fy.3

We report two cases of live donor RT with low ABO incompatibility who developed PLS.




A 23-year-old male with stage V chronic kidney disease (CKD-V) due to polycystic kidney disease. He received a live donor RT on 6 June 2011, with the donor being group O+ and the recipient being group A+, without initial complications and with functional graft at discharge (plasma creatinine [Pcr] 1.1mg/dl) and haemoglobin 10g/dl. Immunosuppressive therapy consisted of tacrolimus, mycophenolate, and steroids.

Fourteen days after transplantation, laboratory tests were performed and we observed haemoglobin of 5.8 g/dl with stable renal function (Pcr 1.2mg/dl) and the remaining complementary tests (including CT and abdominal ultrasound) were within the normal range.

The anaemia work-up showed haemolytic anaemia (low haptoglobin and high reticulocytes and direct bilirubin) with positive direct Coombs test and appearance of anti-A antibodies in the patient's red blood cell preparation, compatible with alloimmune haemolytic anaemia (PLS). The patient was treated with transfusion of 4 packed red blood cell units and methylprednisolone (1mg/kg/day) with subsequent gradually decreasing amounts. Tests at discharge: Pcr 0.7mg/dl and haemoglobin 9.6g/dl. In the following weeks, there was complete resolution and no recurrence.




A 42-year-old male with CKD-V due to diabetic nephropathy. He received a live donor RT on 10 September 2012. The donor was blood group O+ and the recipient was A+. The initial immunosuppression included tacrolimus, mycophenolate and steroids. After the RT progression was very good. At discharge he had haemoglobin of 11.4g/dl and Pcr of 1.4mg/dl.

Fourteen days later, he sought consultation due to general malaise and severe haemolytic anaemia was detected (haemoglobin 4.3g/dl). Complementary tests ruled out active bleeding. The blood smear did not show schistocytes and the direct Coombs test was positive with presence of anti-A antibodies. He was diagnosed with alloimmune haemolytic anaemia (PLS). He was treated with transfusion of 12 packed red blood cell units and high-dose steroids (methylprednisolone 1mg/kg/day) with a progressive decrease in dosage. The blood abnormalities cleared within ten days and there was haemoglobin stability, without further transfusions being required. 31 days after transplantation, he was diagnosed with II-B acute rejection with negative donor-specific antibodies, and treatment with thymoglobulin was required. Renal function subsequently stabilised, with Pcr of 3.2mg/dl.

PLS must be suspected for sudden anaemic symptoms in the first-second week after transplantation, in SOT with low ABO incompatibility or different Rh.1-5 Its duration is limited in time (about 3 months).1-3 Blood transfusion of the donor group and steroid administration are recommended. In severe cases, rituximab and/or plasmapheresis have been used.1-5 Immunosuppressive therapy with mycophenolate is recommended for its effect on B cells.1,5 Prevention measures, such as careful graft perfusion and removal of lymph nodes from perirenal fat1,3 are particularly important. In our cases, the two grafts came from living donors. It is possible that the lower cold ischaemia time and higher speed in the implantation process also favoured the development of PLS, due to the greater number and viability of the donor’s lymphocytes.


Conflicts of interest


The authors declare that they have no conflicts of interest related to the contents of this article.

Peces R, D??az Corte C, Navascu??s RA. Hemolytic anemia caused by graft-versus-host reaction in ABO-nonidentical renal transplants from blood group O donors. Nefrologia 2001;21(4):395-401. [Pubmed]
Ainsworth CD, Crowther MA, Treleaven D, Evanovitch D, Webert KE, Blajchman MA. Severe hemolytic anemia post-renal transplantation produced by donor anti-D passenger lymphocytes: case report and literature review. Transfus Med Rev 2009;23(2):155-9. [Pubmed]
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Debska-Slizie?? A, Chamienia A, Kr??l E, Zdrojewski Z, Pirski I, Zadrozny D, et al. Hemolytic anemia after renal transplantation: analysis of case reports. Transplant Proc 2003;35(6):2233-37.
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