IMMUNE HEMATOLOGIC DISEASE Hemolytic anemia after kidney transplantation: a prospective analysis Ruth Achkar, Akemi K. Chiba, José P. Zampieri-Filho, José O.M. Pestana, and José O. Bordin BACKGROUND: Hemolysis may occur in 9% to 40% of patients after solid organ transplantation and be caused by the passenger lymphocyte syndrome (PLS). STUDY DESIGN AND METHODS: We have prospec- tively examined 217 kidney transplant recipients before (Day -1) and after (up to Days +10, +20, and +30) surgery. ABO-identical transplant was performed in 180 (82.9%) patients, while 37 (17.1%) individuals received ABO-compatible nonidentical grafts. Direct antiglobulin tests (DATs) were performed by tube technique (polyspecific anti-human globulin [IgG + C3d]), positive DAT samples were further tested by gel agglutination (monospecific anti-IgG, -IgM, -IgA, or -C3), and eluates were prepared from DAT-positive red blood cells (RBCs) by the dichloromethane elution test. RESULTS: We observed that 34 of 217 (15.7%) patients developed a positive DAT up to Day +30. The percentage of patients with positive DATs was signifi- cantly higher in those having ABO-compatible nonidenti- cal transplants compared to those that received ABO- identical grafts (10/37 = 27.0% vs. 24/180 = 13.3%; p = 0.037). Specific RBC antibodies (anti-A or anti-B) were found in only 5 of 37 (13.5%) patients having ABO-compatible nonidentical transplants who presented with clinical hemolysis. We found only three reactive eluates from 24 patients with positive DATs who re- ceived ABO-identical transplants but had no hemolysis. CONCLUSIONS: Our data collected prospectively dem- onstrated that: 1) positive DATs occurred in 15.7% of all patients up to Day +30 after a kidney transplant; 2) the DAT positivity occurred up to Day +10 in 9.7% of all transplanted patients; 3) the majority of the transplant recipients with a positive DAT had a nonreactive RBC eluate; and 4) PLS was the cause of a positive DAT in 13.5% of patients submitted to ABO-compatible non- identical kidney transplants. R enal transplantation is still the treatment of choice for patients with dialysis-dependent chronic renal failure. A successful kidney engraftment corrects both excretion and endo- crine functions, such as the synthesis of erythropoietin and vitamin D. Anemia is still a common finding in renal transplanted patients, but the exact mechanisms involved in the anemia pathophysiology are still not completely understood. Some possible causes are imperfect graft function, age, host comorbidities, use of angiotensin- converting enzyme inhibitors, infections, use of antipro- liferative drugs such as azathioprine, changes in the immune system, and immune hemolytic anemia. The passenger lymphocyte syndrome (PLS) that has been described in solid organ transplantation is associated with the action of immunocompetent donor lymphocytes in the transplanted organ producing antibodies that react with the host red blood cells (RBCs). 1,2 This graft-versus- host disease (GVHD) may occur with minor ABO incom- patibility (compatible nonidentical) transplantations, when ABO antibodies produced by grafted lymphocytes against host RBCs cause hemolysis. 3,4 The incidence of a positive direct antiglobulin test (DAT) in patients after solid organ transplantation has been described to vary from 17% to 70%; 4 however, most of the reported data are from retrospective analysis of kidney transplantation cases that were associated with alterations in immunohe- matologic tests. 5-8 In this study we have prospectively ana- lyzed immunohematologic variables of kidney transplant recipients before and up to 30 days after surgery. ABBREVIATION: PLS = passenger lymphocyte syndrome. From the Universidade Federal São Paulo, São Paulo, SP; and Hospital do Rim e Hipertensão, Fundação Oswaldo Ramos, SP, Brazil. Address reprint requests to: Ruth Achkar, MD, PhD, Rua Edson, 953 ap83, Campo Belo, São Paulo, SP, Brasil, 04618-034; e-mail:ruth@verup.com.br. Received for publication July 13, 2010; revision received March 10, 2011, and accepted March 15, 2011. doi: 10.1111/j.1537-2995.2011.03192.x TRANSFUSION 2011;51:2495-2499. Volume 51, November 2011 TRANSFUSION 2495