Mireille Henry Laboratoire de Virologie Ho ˆ pital Timone Marseille Cedex, France Address correspondence to: Vale ´rie Moal, M.D., Service de Ne ´phrologie et d’He ´modialyse, Ho ˆ- pital La Conception, 147 boulevard Baille 13385, Marseille Cedex 05 France. E-mail: valerie.moal@mail.ap-hm.fr Received 26 July 2005. Accepted 7 December 2005. Copyright © 2006 by Lippincott Williams & Wilkins ISSN 0041-1337/06/8109-1358 DOI: 10.1097/01.tp.0000202731.01530.cb REFERENCES 1. Carman WF. The clinical significance of sur- face antigen variants of hepatitis B virus. J Viral Hepat 1997; 4(suppl 1): 11. 2. Carman WF, Trautwein C, Van Deursen FJ, et al. Hepatitis B virus envelope variation af- ter transplantation with and without hepati- tis B immune globulin prophylaxis. Hepatol- ogy 1996; 24: 489. 3. Wallace LA, Echevarria JE, Echevarria JM, et al. Molecular characterization of envelope antigenic variants of hepatitis B virus from Spain. J Infect Dis 1994; 170(5): 1300. 4. Ashton-Rickardt PG, Murray K. Mutants of the hepatitis B virus surface antigen that de- fine some antigenically essential residues in the immunodominant a region. J Med Virol 1989; 29(3): 196. 5. Carman WF, Korula J, Wallace L, et al. Ful- minant reactivation of hepatitis B due to en- velope protein mutant that escaped detec- tion by monoclonal HBsAg ELISA. Lancet 1995; 345: 1406. 6. Meier-Kriesche HU, Schold JD, Kaplan B. Long-term renal allograft survival: Have we made significant progress or is it time to re- think our analytic and therapeutic strategies? Am J Transplant 2004; 4: 1289. Rhabdomylysis Transference During Liver Transplantation Rhabdomyolysis can occur after many different types of acute muscle in- sults whereby the damaged muscle re- leases intracellular components that act as toxins, in particular, to the kidneys (1). Clinical sequelae include hypovole- mia, hyperkalemia, metabolic acidosis, and acute renal failure (2). We report an interesting case whereby the donor liver from a patient who had an anoxic brain injury caused by severe rhabdomyolysis led to the recurrence of rhabdomyolysis in the recipient. CASE PRESENTATION A 58-year-old man with end-stage liver disease secondary to autoimmune hepatitis was admitted to our center for an orthotropic liver transplantation. The cause of death to the donor was co- caine-induced cardiac failure along with severe rhabdomyolysis. The hepatic transaminases at the time of harvest were aspartate aminotransferase 65 mg/ dL, alanine aminotransaminase 58 mg/ dL, alkaline phosphatase 68 U/L, and to- tal bilirubin 0.1 mg/dL. Intraoperatively, the patient was placed on veno-venous bypass. Thereafter, the donor liver was transplanted with careful anastomosis. It was observed that the patient had gradual derangement in renal function tests with increasing blood urea nitrogen (BUN) and creatinine. Postoperatively, the BUN was 12 mg/dL and creatinine 0.8 mg/dL. However, during the next few days, it increased to 1.8 mg/dL. In- terestingly, this was not accompanied by a significant decrease in urine output. A careful review of the case and donor characteristics showed that the donor graft was retrieved from a patient with rhabdomyolysis who had an anoxic injury resulting in cardiopulmonary re- suscitation. This prompted the treating physicians to check for creatinine kinase (CK), which came back as high as 28,632 IU/L, CK, muscle, and brain 37.7 ng/mL, and troponin T 0.01 ng/mL. The transaminases were slightly increased as compared with the time of harvest. Elec- trocardiogram did not reveal evidence of cardiac ischemia or injury. The patient was diagnosed with rhabdomyolysis, and it was managed with aggressive hy- dration. We continued to watch the de- crease in CK; with that, the creatinine also started to normalize. (Fig. 1). DISCUSSION Rhabdomyolysis after organ trans- plantation does not occur more often than in other ill patients; however, trans- plant patients are exposed to many more medications and are at a greater risk for infections, which may increase the risk of developing rhabdomyolysis (3). The combination of cyclosporine and lova- statin has been found to be the prototype for rhabdomyolysis in these patients (4). Our patient was not receiving 3-hydroxy-3-methyl-glutaryl-CoA re- ductase inhibitors or cyclosporine. Therefore, the possibility of a drug-re- lated complication is very unlikely. Also, the rapid development of rhabdomyoly- sis within 6 hr of transplantation from a patient with cocaine-induced rhabdo- myolysis and anoxic injury makes this case interesting. One explanation might be the transference of cocaine into the recipient through the transplanted liver, where its effect were accentuated by acute surgical stress. Also, harvesting the liver from a donor could possibly have FIGURE 1. Rise and decline in creatinine kinase (CK) in relation to postoper- ative days. Transplantation • Volume 81, Number 9, May 15, 2006 1359